Hiperparatyreoza
Etiologia i przyczyny

Hiperparatyreoza to zaburzenie charakteryzujące się nadmierną produkcją parathormonu (PTH) przez gruczoły przytarczyczne, obejmujące trzy główne typy: pierwotną, wtórną i trzeciorzędową. Pierwotna hiperparatyreoza (PHPT) najczęściej wynika z gruczolaka przytarczyc (80-85% przypadków), hiperplazji (15-20%) lub rzadko raka (<1%), z poziomem wapnia w surowicy często przekraczającym 14 mg/dl i PTH 5-10-krotnie powyżej normy. Etiologia może mieć podłoże genetyczne (np. mutacje MEN1, CDC73, CASR) lub być związana z czynnikami środowiskowymi, takimi jak długotrwałe leczenie litem czy napromieniowanie szyi. Wtórna hiperparatyreoza rozwija się w odpowiedzi na hipokalcemię, najczęściej w przebiegu przewlekłej choroby nerek, niedoboru witaminy D lub zaburzeń wchłaniania wapnia, prowadząc do kompensacyjnego wzrostu PTH. Trzeciorzędowa hiperparatyreoza to stan autonomicznej, niekontrolowanej produkcji PTH po długotrwałej wtórnej hiperparatyreozie, skutkujący hiperkalcemią mimo korekty pierwotnej przyczyny.

Etiologia hiperparatyreozy

Hiperparatyreoza (nadczynność przytarczyc) to zaburzenie charakteryzujące się nadmierną produkcją parathormonu (PTH) przez gruczoły przytarczyczne. Możemy wyróżnić trzy główne typy hiperparatyreozy: pierwotną, wtórną i trzeciorzędową, z których każda ma odmienną etiologię.123

Pierwotna hiperparatyreoza

Pierwotna hiperparatyreoza (PHPT) występuje, gdy jeden lub więcej gruczołów przytarczycznych produkuje nadmierną ilość PTH z powodu problemu zlokalizowanego bezpośrednio w gruczołach przytarczycznych. Jest to trzecie najczęstsze zaburzenie endokrynologiczne po cukrzycy i chorobach tarczycy.45 Najczęstszymi przyczynami pierwotnej hiperparatyreozy są:

Gruczolak przytarczyc

Gruczolak przytarczyc (adenoma) jest najczęstszą przyczyną pierwotnej hiperparatyreozy, występującą w około 80-85% przypadków. Jest to łagodny (nienowotworowy) guz powstający w jednym z gruczołów przytarczycznych, powodujący jego nadmierną aktywność i zwiększoną produkcję PTH.678 Gruczolak rozwija się, gdy dochodzi do zaburzenia działania czujnika wapniowego (CaSR) w komórkach przytarczyc, prowadząc do zwiększonej proliferacji klonalnej tkanki przytarczyc.910

W około 10% przypadków gruczolaki przytarczyc mogą znajdować się w lokalizacji ektopowej, poza typowym położeniem gruczołów przytarczycznych, co może utrudniać ich diagnostykę i leczenie. Potencjalne ektopowe lokalizacje obejmują grasicę, tarczycę, osierdzie, przestrzeń pozaprzełykową lub górne śródpiersie. Rzadziej spotykane lokalizacje mogą obejmować gardło, boczną część szyi lub przełyk.11

Rozrost przytarczyc

Hiperplazja przytarczyc (rozrost) występuje w około 15-20% przypadków pierwotnej hiperparatyreozy i charakteryzuje się powiększeniem dwóch lub więcej gruczołów przytarczycznych.1213 W przeciwieństwie do pojedynczego gruczolaka, hiperplazja może dotyczyć wszystkich czterech gruczołów przytarczycznych, które stają się powiększone i produkują nadmierne ilości PTH.14

Rak przytarczyc

Rak przytarczyc jest bardzo rzadką przyczyną pierwotnej hiperparatyreozy, występującą w mniej niż 1% przypadków.1516 Pacjenci z rakiem przytarczyc mają tendencję do młodszego wieku w porównaniu z pacjentami z gruczolakami przytarczyc, cechują się bardziej nasiloną hiperkalcemią i ekstremalnie wysokimi poziomami PTH. Stężenie wapnia w surowicy często przekracza 14 mg/dl, a poziomy PTH są 5-10 razy wyższe od górnej granicy normy.17

Przyczyny genetyczne

Do 10% przypadków pierwotnej hiperparatyreozy ma podłoże genetyczne.18 Mutacje genetyczne związane z hiperparatyreozą obejmują:

  • Zespół mnogiej gruczolakowatości wewnątrzwydzielniczej (MEN) typu 1, 2A i 4 – zespoły dziedziczone autosomalnie dominująco, w których hiperparatyreoza współistnieje z innymi zaburzeniami endokrynologicznymi1920
  • Zespół guza szczęki i hiperparatyreozy (hyperparathyroidism-jaw tumor syndrome) – rzadki stan występujący najczęściej u nastolatków lub młodych dorosłych, objawiający się pojedynczym gruczolakiem przytarczyc i zmianami kostnymi w szczęce, a także guzem Wilmsa lub torbielami nerek21
  • Rodzinna izolowana hiperparatyreoza (FIHP) – może być spowodowana mutacjami w genach MEN1, CDC73 lub CASR22
  • Noworodkowa ciężka hiperparatyreoza – objawia się ciężką hiperkalcemią w okresie noworodkowym23
  • Rodzinna hipokalciuryczna hiperkalcemia – spowodowana pojedynczą mutacją w receptorze wyczuwającym wapń, co prowadzi do niewrażliwości na hamowanie wydzielania PTH24
Inne przyczyny pierwotnej hiperparatyreozy

Inne czynniki, które mogą przyczynić się do rozwoju pierwotnej hiperparatyreozy, obejmują:

  • Leczenie litem – długotrwałe stosowanie litu, szczególnie przez ponad 10 lat, może prowadzić do hiperparatyreozy u około 40% pacjentów. Lit może powodować oporność receptora wyczuwającego wapń, wymagając wyższego poziomu wapnia w surowicy, aby zahamować wydzielanie PTH.252627
  • Napromieniowanie szyi – wcześniejsza ekspozycja na promieniowanie w okolicy szyi i głowy, np. w ramach leczenia nowotworów lub schorzeń łagodnych, zwiększa ryzyko rozwoju hiperparatyreozy.282930
  • Parathyromatoza – niezwykle rzadki stan charakteryzujący się obecnością wielu małych, funkcjonalnych gniazd tkanki przytarczycznej, zazwyczaj po chirurgicznym usunięciu gruczołów przytarczycznych. Może naśladować obraz raka przytarczyc.31

W niektórych przypadkach pierwotnej hiperparatyreozy przyczyna pozostaje nieznana, a schorzenie występuje sporadycznie, bez wyraźnej przyczyny czy historii rodzinnej.3233

Wtórna hiperparatyreoza

Wtórna hiperparatyreoza rozwija się jako odpowiedź na inne schorzenie powodujące obniżenie poziomu wapnia we krwi. W tym przypadku gruczoły przytarczyczne reagują fizjologicznie na hipokalcemię, zwiększając produkcję PTH w celu normalizacji stężenia wapnia.3435

Przewlekła choroba nerek

Przewlekła choroba nerek jest najczęstszą przyczyną wtórnej hiperparatyreozy.3637 W miarę pogarszania się funkcji nerek, dochodzi do kilku zaburzeń metabolicznych prowadzących do wtórnej hiperparatyreozy:

  • Zmniejszona zdolność nerek do aktywacji witaminy D, co prowadzi do obniżonego wchłaniania wapnia w jelitach3839
  • Zwiększone stężenie fosforanów we krwi (hiperfosfatemia) z powodu zmniejszonego wydalania fosforanów przez nerki4041
  • Zmniejszone stężenie wapnia we krwi (hipokalcemia) w wyniku powyższych zaburzeń42

Te zmiany biochemiczne stymulują gruczoły przytarczyczne do zwiększonej produkcji PTH, co z czasem może prowadzić do ich rozrostu.4344

Niedobór witaminy D

Niedobór witaminy D jest kolejną częstą przyczyną wtórnej hiperparatyreozy.4546 Witamina D jest niezbędna do prawidłowego wchłaniania wapnia w jelitach i utrzymania prawidłowego stężenia wapnia we krwi. Niedobór witaminy D może wynikać z:

  • Niewystarczającej ekspozycji na światło słoneczne47
  • Niedostatecznej podaży witaminy D w diecie48
  • Zaburzeń wchłaniania jelitowego witaminy D, np. po operacji bariatrycznej49

Długotrwały niedobór witaminy D prowadzi do obniżenia stężenia wapnia we krwi, co stymuluje gruczoły przytarczyczne do zwiększonej produkcji PTH.50

Zaburzenia wchłaniania wapnia

Wtórna hiperparatyreoza może być również spowodowana zaburzeniami wpływającymi na wchłanianie wapnia w przewodzie pokarmowym:51

  • Choroby zapalne jelit i inne entropatie powodujące zespół złego wchłaniania52
  • Celiakia prowadząca do zaburzenia wchłaniania wapnia i witaminy D53
  • Niedostateczna podaż wapnia w diecie5455
Inne przyczyny wtórnej hiperparatyreozy

Inne, rzadsze przyczyny wtórnej hiperparatyreozy to:

  • Stosowanie niektórych leków, takich jak leki moczopędne pętlowe, które mogą zwiększać wydalanie wapnia przez nerki56
  • Bisfosfoniany – inhibicja resorpcji kości spowodowana stosowaniem bisfosfonianów może prowadzić do wtórnej hiperparatyreozy57
  • Nerkowy wyciek wapnia – stan, w którym nerki wydalają nadmierne ilości wapnia z moczem58

Trzeciorzędowa hiperparatyreoza

Trzeciorzędowa hiperparatyreoza rozwija się w wyniku długotrwałej wtórnej hiperparatyreozy, szczególnie u pacjentów z przewlekłą chorobą nerek.5960

W trzeciorzędowej hiperparatyreozie gruczoły przytarczyczne, po długotrwałej stymulacji, stają się autonomiczne i kontynuują nadmierną produkcję PTH nawet po skorygowaniu pierwotnej przyczyny hipokalcemii.6162 Gruczoły przytarczyczne przestają reagować na mechanizmy regulacyjne i produkują PTH niezależnie od stężenia wapnia we krwi, co prowadzi do hiperkalcemii.6364

Etiologia trzeciorzędowej hiperparatyreozy może obejmować:

  • Przeroślnięte gruczoły przytarczyczne po latach wtórnej hiperparatyreozy65
  • Zmianę wartości progowej czujnika wapniowego do poziomów hiperkalcemicznych66
  • Monoklonalną ekspansję komórek przytarczyc prowadzącą do tworzenia guzków w przerosłych gruczołach67

Trzeciorzędowa hiperparatyreoza może utrzymywać się nawet po przeszczepie nerki.68

Normokalcemiczna pierwotna hiperparatyreoza

Normokalcemiczna pierwotna hiperparatyreoza jest stanem charakteryzującym się trwale podwyższonym poziomem PTH przez co najmniej 6 miesięcy, pomimo prawidłowego skorygowanego stężenia wapnia w surowicy i stężenia wapnia zjonizowanego, po wykluczeniu wszystkich przyczyn wtórnej hiperparatyreozy, w tym niedoborów wapnia i witaminy D.6970

Badania obrazowe mające na celu identyfikację nadczynnych gruczołów przytarczycznych są mniej skuteczne u pacjentów z normokalcemiczną pierwotną hiperparatyreozą niż u pacjentów z klasyczną hiperkalcemiczną pierwotną hiperparatyreozą.71 Normokalcemiczna hiperparatyreoza jest uważana za wczesną postać pierwotnej hiperparatyreozy.72

Prawie połowa pacjentów z rozpoznaną normokalcemiczną pierwotną hiperparatyreozą ma osteoporozę, co wskazuje na istotny wpływ tego stanu na metabolizm kostny, mimo prawidłowego stężenia wapnia.73

Hiperparatyreoza związana z nowotworem

Hiperkalcemia związana z nowotworem może wystąpić u 20-30% wszystkich pacjentów z chorobą nowotworową i może być mylona z pierwotną hiperparatyreozą, szczególnie jeśli objawy hiperkalcemii są pierwszym klinicznym objawem nowotworu.74

Najczęstszą przyczyną hiperkalcemii związanej z nowotworem jest produkcja i wydzielanie białka podobnego do parathormonu (PTHrP), najczęściej z powodu raka płaskonabłonkowego płuc i nowotworów nerek.7576

Czynniki ryzyka hiperparatyreozy

Istnieje kilka czynników, które mogą zwiększać ryzyko rozwoju hiperparatyreozy:

Czynniki demograficzne

  • Płeć – kobiety są narażone na hiperparatyreozę 3-4 razy częściej niż mężczyźni7778
  • Wiek – częstość występowania hiperparatyreozy wzrasta z wiekiem, średni wiek w momencie diagnozy to 55-65 lat7980
  • Status po menopauzie – kobiety po menopauzie są szczególnie narażone na rozwój pierwotnej hiperparatyreozy8182

Ekspozycja na promieniowanie

  • Wcześniejsza radioterapia głowy i szyi, szczególnie w dzieciństwie lub okresie dojrzewania8384
  • Ekspozycja na promieniowanie po wypadkach w elektrowniach jądrowych85

Czynniki genetyczne i rodzinne

  • Historia rodzinna hiperparatyreozy lub zespołów endokrynologicznych86
  • Zespoły dziedziczne, takie jak MEN1, MEN2A, MEN487
  • Rodzinna izolowana hiperparatyreoza88
  • Zespół guza szczęki i hiperparatyreozy89

Leki i stany chorobowe

  • Długotrwałe stosowanie litu, szczególnie powyżej 10 lat9091
  • Przewlekła choroba nerek, szczególnie zaawansowana niewydolność nerek92
  • Ciężki niedobór wapnia w diecie93
  • Ciężki niedobór witaminy D94
  • Stosowanie tiazydowych leków moczopędnych95

Mechanizmy patofizjologiczne

W patogenezie hiperparatyreozy istotną rolę odgrywają różne mechanizmy molekularne i komórkowe:

Zaburzenia regulacji wydzielania PTH

Pierwotna hiperparatyreoza charakteryzuje się nieprawidłową regulacją wydzielania PTH przez wapń, co prowadzi do nadmiernego wydzielania PTH w stosunku do stężenia wapnia w surowicy.96 Kluczowe mechanizmy patofizjologiczne obejmują:

  • Zaburzenia receptora wyczuwającego wapń (CaSR) – zmniejszenie wrażliwości CaSR prowadzi do wyższego progu wapnia wymaganego do zahamowania wydzielania PTH9798
  • Zwiększona proliferacja klonalna tkanki przytarczyc, prowadząca do powstania gruczolaka lub hiperplazji99

Zaburzenia genetyczne i molekularne

Badania genetyczne i molekularne zidentyfikowały szereg genów i mechanizmów związanych z rozwojem hiperparatyreozy:

  • Gen MEN1 – koduje białko menin, które działa jako supresor nowotworów. Inaktywujące mutacje tego genu prowadzą do zespołu MEN1 i hiperparatyreozy100101
  • Gen RET – koduje receptor kinazy tyrozynowej, a jego mutacje prowadzą do zespołu MEN2A102103
  • Gen CDC73/HRPT2 – koduje parafibrominę, białko jądrowe działające jako supresor nowotworów. Mutacje tego genu są związane z zespołem guza szczęki i hiperparatyreozy104105
  • Gen CDKN1B – koduje inhibitor kinazy zależnej od cykliny, a jego mutacje prowadzą do zespołu MEN4106107
  • Gen cykliny D1/PRAD1 – jego nadekspresja może przyczyniać się do rozwoju gruczolaków przytarczyc108
  • Gen CASR – koduje receptor wyczuwający wapń, a jego mutacje mogą prowadzić do rodzinnej hipokalciurycznej hiperkalcemii lub normokalcemicznej pierwotnej hiperparatyreozy109

Zaburzenia gospodarki wapniowo-fosforanowej

We wtórnej hiperparatyreozie kluczową rolę odgrywają zaburzenia gospodarki wapniowo-fosforanowej:

  • Obniżone stężenie wapnia – stymuluje gruczoły przytarczyczne do zwiększonej produkcji PTH110
  • Podwyższone stężenie fosforanów – bezpośrednio stymuluje wydzielanie PTH111
  • Niedobór aktywnej witaminy D – zmniejsza wchłanianie wapnia w jelitach i zwiększa wydzielanie PTH112
  • Oporność na czynnik wzrostu fibroblastów 23 (FGF-23) – FGF-23 normalnie hamuje wydzielanie PTH, ale w przewlekłej chorobie nerek mechanizm ten jest zaburzony113

Autonomizacja gruczołów przytarczycznych

W trzeciorzędowej hiperparatyreozie dochodzi do autonomizacji gruczołów przytarczycznych:

  • Długotrwała stymulacja gruczołów przytarczycznych prowadzi do ich trwałego przerostu114
  • Utrata wrażliwości na wapń – gruczoły przytarczyczne stają się niewrażliwe na hamujące działanie podwyższonego stężenia wapnia115
  • Rozwój guzków w obrębie przerosłych gruczołów przytarczycznych116

Wpływ czynników środowiskowych

Różne czynniki środowiskowe mogą przyczyniać się do rozwoju hiperparatyreozy:

  • Promieniowanie jonizujące – może powodować mutacje w komórkach przytarczyc, prowadząc do ich niekontrolowanego wzrostu117
  • Lit – zaburza działanie receptora wyczuwającego wapń, prowadząc do oporności na mechanizmy hamujące wydzielanie PTH118
  • Czynniki chemiczne – niektóre związki chemiczne mogą wpływać na funkcję gruczołów przytarczycznych119

Hiperparatyreoza a układ sercowo-naczyniowy

Hiperparatyreoza może wpływać na układ sercowo-naczyniowy poprzez kilka mechanizmów:

  • Bezpośredni wpływ PTH na ścianę tętnic – prowadzi do zwiększonej sztywności aorty i innych dużych tętnic120
  • Wpływ na układ renina-angiotensyna-aldosteron – PTH ma działanie sekrecyjne na aldosteron, co może prowadzić do hiperalosteronizmu121
  • Odkładanie wapnia w ścianie naczyń – przyspiesza rozwój miażdżycy i zwiększa ryzyko chorób sercowo-naczyniowych122

Zrozumienie złożonych mechanizmów patofizjologicznych hiperparatyreozy jest kluczowe dla opracowania skutecznych strategii diagnostycznych i terapeutycznych, dostosowanych do indywidualnych potrzeb pacjentów z różnymi typami tego schorzenia.123124

Kolejne rozdziały

Zapraszamy do dalszego czytania naszego leksykonu.

Wybierz kolejny rozdział z menu poniżej, aby otworzyć nową podstronę kompedium wiedzy i uzyskać szczegółowe informację o leku, substancji lub chorobie.

  1. 10.04.2026
  2. www.leksykon.com.pl

Materiały źródłowe

  • #1 Hyperparathyroidism – Symptoms & causes – Mayo Clinic
    https://www.mayoclinic.org/diseases-conditions/hyperparathyroidism/symptoms-causes/syc-20356194
    Hyperparathyroidism is caused by factors that increase the production of parathyroid hormone. […] Primary hyperparathyroidism occurs because of a problem with one or more of the four parathyroid glands: A noncancerous growth (adenoma) on a gland is the most common cause. […] Secondary hyperparathyroidism is the result of another condition that lowers the blood calcium, which then affects the gland’s function. This causes your parathyroid glands to overwork and produce high amounts of parathyroid hormone to maintain or restore the calcium level to the standard range. […] Factors that may result in secondary hyperparathyroidism include: Severe calcium deficiency. Your body may not get enough calcium from your diet, often because your digestive system doesn’t absorb the calcium from food.
  • #2 Hyperparathyroidism: What It Is, Symptoms & Treatment
    https://my.clevelandclinic.org/health/diseases/14454-hyperparathyroidism
    Hyperparathyroidism can be primary (caused by growths or enlarged glands) or secondary (caused by kidney disease or low calcium levels). […] Growths on your parathyroid glands, parathyroid gland enlargement, and conditions that cause low levels of calcium or high levels of phosphate can all cause hyperparathyroidism. Primary, secondary and tertiary hyperparathyroidism have different causes. […] When you have a growth on a parathyroid gland or one or more of the glands are enlarged, it produces more PTH and doesn’t respond to signals that tell it to stop making hormones. This causes primary hyperparathyroidism. Specific causes of primary hyperparathyroidism include: Adenomas noncancerous (benign) growths are the most common cause of primary hyperparathyroidism. […] The most common cause of secondary hyperparathyroidism is kidney disease. When your kidneys aren’t working properly, your phosphate levels go up and your vitamin D levels go down. Low vitamin D levels lead to low calcium levels. Your parathyroid glands adjust by making more PTH to get rid of phosphate in your blood and increase the amount of calcium. […] Secondary hyperparathyroidism causes tertiary hyperparathyroidism. Your parathyroid glands become enlarged from working much more than they should. This causes them to stop responding to signals that tell them not to make more PTH.
  • #3 Hyperparathyroidism > Fact Sheets > Yale Medicine
    https://www.yalemedicine.org/conditions/hyperparathyroidism
    Hyperparathyroidism is a condition in which the parathyroid glands produce too much parathyroid hormone (PTH). […] There are primary, secondary, and tertiary forms of hyperparathyroidism. Each has a different cause. […] There are different possible causes of hyperparathyroidism, depending on whether the condition is primary, secondary, or tertiary. […] Primary hyperparathyroidism: The condition is usually due to a benign (non-cancerous) tumor or growth, called an adenoma, arising in one of the four parathyroid glands. […] Secondary hyperparathyroidism: The condition occurs because of chronically low levels of calcium or vitamin D in the blood, which causes the parathyroid glands to chronically release high levels of PTH. […] Tertiary hyperparathyroidism: The condition occurs among people who have had secondary hyperparathyroidism for a long time, particularly among people who have had chronic kidney disease for many years.
  • #4 Primary Hyperparathyroidism – StatPearls – NCBI Bookshelf
    https://www.ncbi.nlm.nih.gov/books/NBK441895/
    Primary hyperparathyroidism is a disorder characterized by excessive production of PTH. It is the third most common endocrine disorder after diabetes and thyroid disorders. Eighty percent of patients will present with a single adenoma, approximately 15% with hyperplasia of all 4 glands, 2% to 4% with multiple adenomas, and fewer than 1% with parathyroid carcinoma. A combination of increased clonal proliferation of parathyroid tissue with reduced CaSR usually causes primary hyperparathyroidism. Most of these adenomas will be located in the parathyroid glands, but in up to 10% of cases, they may be in an ectopic location. Potential ectopic locations include the thymus, thyroid, pericardium, retro-esophageal space, or superior mediastinum. More unusual locations to find ectopic parathyroid glands would be in the pharynx, lateral neck, or esophagus. […]
  • #5 Hyperparathyroidism | AAFP
    https://www.aafp.org/pubs/afp/issues/2004/0115/p333.html
    Primary hyperparathyroidism is caused by the inappropriate secretion of PTH, which results in hypercalcemia. The condition usually occurs sporadically, although familial forms are well recognized. In 85 percent of patients with primary hyperparathyroidism, the underlying cause is an adenoma in a single parathyroid gland. Hypertrophy of all four parathyroid glands and multiple adenomas within the parathyroid glands account for the remainder of cases. Fewer than 0.5 percent of cases are caused by parathyroid malignancies. Most patients with primary hyperparathyroidism are postmenopausal women. The incidence of the condition increases with age, and the average age at diagnosis is 55 years. A small percentage of patients presents years after external neck irradiation. Lithium therapy also can be responsible for overactive parathyroid glands, with the excess activity persisting even after discontinuation of the drug. In 10 to 20 percent of patients, primary hyperparathyroidism is caused by an inherited hyperfunction of multiple parathyroid glands. These patients tend to be diagnosed at a younger age. Although rare, familial disorders should be considered in patients diagnosed with primary hyperparathyroidism. With several of these familial disorders, patients should be evaluated for significant associated abnormalities. Familial forms of primary hyperparathyroidism include multiple endocrine neoplasia type I and type II, neonatal severe primary hyperparathyroidism, hyperparathyroidism-jaw tumor syndrome, familial hypocalciuric hypercalcemia, and familial isolated hyperparathyroidism. Approximately 95 percent of patients with multiple endocrine neoplasia type I, or Werner’s syndrome, have associated primary hyperparathyroidism. This syndrome is associated with various tumors, including pancreatic and pituitary adenomas. Patients with multiple endocrine neoplasia type II, or Sipple’s syndrome, may develop a milder form of primary hyperparathyroidism. This syndrome is characterized primarily by medullary thyroid carcinoma and pheochromocytoma. Genetic testing for both syndromes is available in some medical centers. Neonatal severe primary hyperparathyroidism presents with severe hypercalcemia during the newborn period. Hyperparathyroidism-jaw tumor syndrome is a rare condition that usually presents in adolescents or young adults as a solitary adenoma associated with bone lesions in the jaw and with Wilms’ tumor or renal cysts. Familial hypocalciuric hypercalcemia is caused by a single mutation in the calcium-sensing receptor, resulting in insensitivity to feedback inhibition of PTH secretion. In affected patients, the calcium/creatinine clearance ratio is less than 0.01, compared with a calcium/creatinine clearance ratio of greater than 0.02 in patients with primary hyperparathyroidism. Patients with familial hypocalciuric hypercalcemia are asymptomatic and require no treatment. Familial isolated hyperparathyroidism has no specific features. It is usually thought to be an expression of occult multiple endocrine neoplasia type I.
  • #6 Primary Hyperparathyroidism – StatPearls – NCBI Bookshelf
    https://www.ncbi.nlm.nih.gov/books/NBK441895/
    Primary hyperparathyroidism is a disorder characterized by excessive production of PTH. It is the third most common endocrine disorder after diabetes and thyroid disorders. Eighty percent of patients will present with a single adenoma, approximately 15% with hyperplasia of all 4 glands, 2% to 4% with multiple adenomas, and fewer than 1% with parathyroid carcinoma. A combination of increased clonal proliferation of parathyroid tissue with reduced CaSR usually causes primary hyperparathyroidism. Most of these adenomas will be located in the parathyroid glands, but in up to 10% of cases, they may be in an ectopic location. Potential ectopic locations include the thymus, thyroid, pericardium, retro-esophageal space, or superior mediastinum. More unusual locations to find ectopic parathyroid glands would be in the pharynx, lateral neck, or esophagus. […]
  • #7 Primary Hyperparathyroidism – NIDDK
    https://www.niddk.nih.gov/health-information/endocrine-diseases/primary-hyperparathyroidism
    In about 8 out of 10 people with primary hyperparathyroidism, a benign, or noncancerous, tumor called an adenoma has formed in one of the parathyroid glands. The tumor causes the gland to become overactive. […] In most other cases, extra PTH comes from two or more adenomas or from hyperplasia, a condition in which all four parathyroid glands are enlarged. People with rare inherited conditions that affect the parathyroid glands, such as multiple endocrine neoplasia type 1 or familial hypocalciuric hypercalcemia, are more likely to have more than one gland affected. […] Rarely, primary hyperparathyroidism is caused by cancer of a parathyroid gland.
  • #8 Hyperparathyroidism: Symptoms, Causes, & Treatment
    https://patient.info/hormones/thyroid-and-parathyroid-glands/hyperparathyroidism
    Hyperparathyroidism is either primary, secondary or tertiary. […] In primary hyperparathyroidism, one or more of your parathyroid glands become enlarged and overactive. The gland, or glands, release too much parathyroid hormone. This results in a high level of calcium in your blood. […] Causes include: A single parathyroid adenoma. This is the most common cause of primary hyperparathyroidism. There is a non-cancerous (benign) tumour of one of your parathyroid glands. This causes the gland to release more parathyroid hormone than it should. […] Hyperplasia affecting more than one parathyroid gland. This accounts for most other cases of primary hyperparathyroidism. Hyperplasia means that the parathyroid gland has become bigger. It usually affects more than one gland at the same time. As a result of the increase in size, more parathyroid hormone is released.
  • #9 Primary Hyperparathyroidism – StatPearls – NCBI Bookshelf
    https://www.ncbi.nlm.nih.gov/books/NBK441895/
    Primary hyperparathyroidism is a disorder characterized by excessive production of PTH. It is the third most common endocrine disorder after diabetes and thyroid disorders. Eighty percent of patients will present with a single adenoma, approximately 15% with hyperplasia of all 4 glands, 2% to 4% with multiple adenomas, and fewer than 1% with parathyroid carcinoma. A combination of increased clonal proliferation of parathyroid tissue with reduced CaSR usually causes primary hyperparathyroidism. Most of these adenomas will be located in the parathyroid glands, but in up to 10% of cases, they may be in an ectopic location. Potential ectopic locations include the thymus, thyroid, pericardium, retro-esophageal space, or superior mediastinum. More unusual locations to find ectopic parathyroid glands would be in the pharynx, lateral neck, or esophagus. […]
  • #10 Hyperparathyroidism Causes & Treatment Options | Dr. Babak Larian
    https://www.hyperparathyroidmd.com/hyperparathyroidism/
    Hyperparathyroidism happens when one or more parathyroid glands over produce their hormone (PTH) and cause an imbalance in the blood calcium level. […] In primary hyperparathyroidism tumor develops within a parathyroid gland when there is a disturbance on the calcium sensor of a single parathyroid cell; this changes the setting for the calcium to a higher number for that particular cell, while the remaining normal cells stay at the proper level. […] The majority of the time, a parathyroid tumor is located in 1 of the 4 parathyroid glands. It is usually a benign tumor, called a parathyroid adenoma, which grows to an abnormal size. As it grows it releases greater amounts of PTH, thus causing Primary Hyperparathyroidism (PHPT). […] Primary hyperparathyroidism, is called primary because the source of the problem is primarily in the parathyroid gland itself. The causes include: A noncancerous growth on one or two of the parathyroid glands, Abnormal growth (hyperplasia) of all parathyroid cells in all parathyroid glands, Very rarely a cancerous tumor in one the parathyroid gland.
  • #11 Primary Hyperparathyroidism – StatPearls – NCBI Bookshelf
    https://www.ncbi.nlm.nih.gov/books/NBK441895/
    Primary hyperparathyroidism is a disorder characterized by excessive production of PTH. It is the third most common endocrine disorder after diabetes and thyroid disorders. Eighty percent of patients will present with a single adenoma, approximately 15% with hyperplasia of all 4 glands, 2% to 4% with multiple adenomas, and fewer than 1% with parathyroid carcinoma. A combination of increased clonal proliferation of parathyroid tissue with reduced CaSR usually causes primary hyperparathyroidism. Most of these adenomas will be located in the parathyroid glands, but in up to 10% of cases, they may be in an ectopic location. Potential ectopic locations include the thymus, thyroid, pericardium, retro-esophageal space, or superior mediastinum. More unusual locations to find ectopic parathyroid glands would be in the pharynx, lateral neck, or esophagus. […]
  • #12 Hyperparathyroidism | AAFP
    https://www.aafp.org/pubs/afp/issues/2004/0115/p333.html
    Primary hyperparathyroidism is caused by the inappropriate secretion of PTH, which results in hypercalcemia. The condition usually occurs sporadically, although familial forms are well recognized. In 85 percent of patients with primary hyperparathyroidism, the underlying cause is an adenoma in a single parathyroid gland. Hypertrophy of all four parathyroid glands and multiple adenomas within the parathyroid glands account for the remainder of cases. Fewer than 0.5 percent of cases are caused by parathyroid malignancies. Most patients with primary hyperparathyroidism are postmenopausal women. The incidence of the condition increases with age, and the average age at diagnosis is 55 years. A small percentage of patients presents years after external neck irradiation. Lithium therapy also can be responsible for overactive parathyroid glands, with the excess activity persisting even after discontinuation of the drug. In 10 to 20 percent of patients, primary hyperparathyroidism is caused by an inherited hyperfunction of multiple parathyroid glands. These patients tend to be diagnosed at a younger age. Although rare, familial disorders should be considered in patients diagnosed with primary hyperparathyroidism. With several of these familial disorders, patients should be evaluated for significant associated abnormalities. Familial forms of primary hyperparathyroidism include multiple endocrine neoplasia type I and type II, neonatal severe primary hyperparathyroidism, hyperparathyroidism-jaw tumor syndrome, familial hypocalciuric hypercalcemia, and familial isolated hyperparathyroidism. Approximately 95 percent of patients with multiple endocrine neoplasia type I, or Werner’s syndrome, have associated primary hyperparathyroidism. This syndrome is associated with various tumors, including pancreatic and pituitary adenomas. Patients with multiple endocrine neoplasia type II, or Sipple’s syndrome, may develop a milder form of primary hyperparathyroidism. This syndrome is characterized primarily by medullary thyroid carcinoma and pheochromocytoma. Genetic testing for both syndromes is available in some medical centers. Neonatal severe primary hyperparathyroidism presents with severe hypercalcemia during the newborn period. Hyperparathyroidism-jaw tumor syndrome is a rare condition that usually presents in adolescents or young adults as a solitary adenoma associated with bone lesions in the jaw and with Wilms’ tumor or renal cysts. Familial hypocalciuric hypercalcemia is caused by a single mutation in the calcium-sensing receptor, resulting in insensitivity to feedback inhibition of PTH secretion. In affected patients, the calcium/creatinine clearance ratio is less than 0.01, compared with a calcium/creatinine clearance ratio of greater than 0.02 in patients with primary hyperparathyroidism. Patients with familial hypocalciuric hypercalcemia are asymptomatic and require no treatment. Familial isolated hyperparathyroidism has no specific features. It is usually thought to be an expression of occult multiple endocrine neoplasia type I.
  • #13 Hyperparathyroidism: Symptoms, Causes, & Treatment
    https://patient.info/hormones/thyroid-and-parathyroid-glands/hyperparathyroidism
    Hyperparathyroidism is either primary, secondary or tertiary. […] In primary hyperparathyroidism, one or more of your parathyroid glands become enlarged and overactive. The gland, or glands, release too much parathyroid hormone. This results in a high level of calcium in your blood. […] Causes include: A single parathyroid adenoma. This is the most common cause of primary hyperparathyroidism. There is a non-cancerous (benign) tumour of one of your parathyroid glands. This causes the gland to release more parathyroid hormone than it should. […] Hyperplasia affecting more than one parathyroid gland. This accounts for most other cases of primary hyperparathyroidism. Hyperplasia means that the parathyroid gland has become bigger. It usually affects more than one gland at the same time. As a result of the increase in size, more parathyroid hormone is released.
  • #14 Hyperparathyroidism: Understanding Parathyroid Disease and Treatment Options
    https://www.parathyroid.com/parathyroid-disease.htm
    Hyperparathyroidism is caused the over-production of parathyroid hormone (PTH) by one or more parathyroid tumors. […] The most common cause of excess hormone production (hyperparathyroidism or parathyroid disease) is the development of a benign tumor in one of the parathyroid glands. This enlargement of one parathyroid gland is called a parathyroid adenoma which accounts for about 70 percent of all patients with primary hyperparathyroidism. […] In most cases we don’t know WHY parathyroid tumors form. But this is HOW a parathyroid tumor forms: The normal parathyroid gland is made up of about 80,000 very small parathyroid cells. […] Around 5% of all patients with primary hyperparathyroidism will have an enlargement of all four parathyroid glands, a term called parathyroid hyperplasia. In this instance, all of the parathyroid glands become enlarged and produce too much parathyroid hormone.
  • #15 Primary Hyperparathyroidism – StatPearls – NCBI Bookshelf
    https://www.ncbi.nlm.nih.gov/books/NBK441895/
    Parathyroid carcinoma is relatively rare, constituting fewer than 1% of all cases of hyperparathyroidism. Compared to patients with parathyroid adenomas, those with parathyroid carcinomas tend to be younger, more hypercalcemic, and with extremely high levels of PTH. The serum calcium often exceeds 14 mg/dL, with PTH levels 5 to 10 times the upper limit of the reference range. These cancers tend to be relatively aggressive and potentially life-threatening, usually due to severe and intractable hypercalcemia rather than direct invasion by malignant tissue. […] […] Parathyromatosis is the presence of multiple small functional nests of parathyroid tissue, usually after surgical removal of the parathyroid glands. This exceedingly rare condition can mimic the appearance of parathyroid carcinoma due to the nests being surrounded by fibrous post-surgical tissue. Parathyromatosis can be distinguished from parathyroid carcinoma by histologic criteria. Parathyromatosis is thought to have 2 etiologies: proliferation of parathyroid tissue residual from embryologic development and, more frequently, seeding during parathyroidectomy or percutaneous ablation, which often occurs in patients with CKD who have persistently elevated PTH. This can be a cause of recurrent, persistent, or intractable hyperparathyroidism. […]
  • #16 Hyperparathyroidism | AAFP
    https://www.aafp.org/pubs/afp/issues/2004/0115/p333.html
    Primary hyperparathyroidism is caused by the inappropriate secretion of PTH, which results in hypercalcemia. The condition usually occurs sporadically, although familial forms are well recognized. In 85 percent of patients with primary hyperparathyroidism, the underlying cause is an adenoma in a single parathyroid gland. Hypertrophy of all four parathyroid glands and multiple adenomas within the parathyroid glands account for the remainder of cases. Fewer than 0.5 percent of cases are caused by parathyroid malignancies. Most patients with primary hyperparathyroidism are postmenopausal women. The incidence of the condition increases with age, and the average age at diagnosis is 55 years. A small percentage of patients presents years after external neck irradiation. Lithium therapy also can be responsible for overactive parathyroid glands, with the excess activity persisting even after discontinuation of the drug. In 10 to 20 percent of patients, primary hyperparathyroidism is caused by an inherited hyperfunction of multiple parathyroid glands. These patients tend to be diagnosed at a younger age. Although rare, familial disorders should be considered in patients diagnosed with primary hyperparathyroidism. With several of these familial disorders, patients should be evaluated for significant associated abnormalities. Familial forms of primary hyperparathyroidism include multiple endocrine neoplasia type I and type II, neonatal severe primary hyperparathyroidism, hyperparathyroidism-jaw tumor syndrome, familial hypocalciuric hypercalcemia, and familial isolated hyperparathyroidism. Approximately 95 percent of patients with multiple endocrine neoplasia type I, or Werner’s syndrome, have associated primary hyperparathyroidism. This syndrome is associated with various tumors, including pancreatic and pituitary adenomas. Patients with multiple endocrine neoplasia type II, or Sipple’s syndrome, may develop a milder form of primary hyperparathyroidism. This syndrome is characterized primarily by medullary thyroid carcinoma and pheochromocytoma. Genetic testing for both syndromes is available in some medical centers. Neonatal severe primary hyperparathyroidism presents with severe hypercalcemia during the newborn period. Hyperparathyroidism-jaw tumor syndrome is a rare condition that usually presents in adolescents or young adults as a solitary adenoma associated with bone lesions in the jaw and with Wilms’ tumor or renal cysts. Familial hypocalciuric hypercalcemia is caused by a single mutation in the calcium-sensing receptor, resulting in insensitivity to feedback inhibition of PTH secretion. In affected patients, the calcium/creatinine clearance ratio is less than 0.01, compared with a calcium/creatinine clearance ratio of greater than 0.02 in patients with primary hyperparathyroidism. Patients with familial hypocalciuric hypercalcemia are asymptomatic and require no treatment. Familial isolated hyperparathyroidism has no specific features. It is usually thought to be an expression of occult multiple endocrine neoplasia type I.
  • #17 Primary Hyperparathyroidism – StatPearls – NCBI Bookshelf
    https://www.ncbi.nlm.nih.gov/books/NBK441895/
    Parathyroid carcinoma is relatively rare, constituting fewer than 1% of all cases of hyperparathyroidism. Compared to patients with parathyroid adenomas, those with parathyroid carcinomas tend to be younger, more hypercalcemic, and with extremely high levels of PTH. The serum calcium often exceeds 14 mg/dL, with PTH levels 5 to 10 times the upper limit of the reference range. These cancers tend to be relatively aggressive and potentially life-threatening, usually due to severe and intractable hypercalcemia rather than direct invasion by malignant tissue. […] […] Parathyromatosis is the presence of multiple small functional nests of parathyroid tissue, usually after surgical removal of the parathyroid glands. This exceedingly rare condition can mimic the appearance of parathyroid carcinoma due to the nests being surrounded by fibrous post-surgical tissue. Parathyromatosis can be distinguished from parathyroid carcinoma by histologic criteria. Parathyromatosis is thought to have 2 etiologies: proliferation of parathyroid tissue residual from embryologic development and, more frequently, seeding during parathyroidectomy or percutaneous ablation, which often occurs in patients with CKD who have persistently elevated PTH. This can be a cause of recurrent, persistent, or intractable hyperparathyroidism. […]
  • #18 Primary Hyperparathyroidism – StatPearls – NCBI Bookshelf
    https://www.ncbi.nlm.nih.gov/books/NBK441895/
    Malignancy-related hypercalcemia can be found in as many as 20% to 30% of all cancer patients. It can be confused with primary hyperparathyroidism, especially if hypercalcemia symptoms are the first clinical sign of the malignancy. The most common cause of malignancy-related hypercalcemia is the production and secretion of PTH-related protein, most often due to squamous cell carcinoma of the lung and renal cancers. […] […] Up to 10% of primary hyperparathyroidism cases have a genetic basis. Genetic mutations associated with hyperparathyroidism include multiple endocrine neoplasia types 1, 2A, and 4, hyperparathyroidism-jaw tumor syndrome, familial isolated hyperparathyroidism, neonatal severe hyperparathyroidism, and familial hypocalciuric hypercalcemia. A familial syndrome should be considered when primary hyperparathyroidism is diagnosed at an early age or there is a family history of hypercalcemia, pituitary adenomas, pancreatic islet cell tumors, pheochromocytomas, or medullary thyroid cancer.
  • #19 Hyperparathyroidism | AAFP
    https://www.aafp.org/pubs/afp/issues/2004/0115/p333.html
    Primary hyperparathyroidism is caused by the inappropriate secretion of PTH, which results in hypercalcemia. The condition usually occurs sporadically, although familial forms are well recognized. In 85 percent of patients with primary hyperparathyroidism, the underlying cause is an adenoma in a single parathyroid gland. Hypertrophy of all four parathyroid glands and multiple adenomas within the parathyroid glands account for the remainder of cases. Fewer than 0.5 percent of cases are caused by parathyroid malignancies. Most patients with primary hyperparathyroidism are postmenopausal women. The incidence of the condition increases with age, and the average age at diagnosis is 55 years. A small percentage of patients presents years after external neck irradiation. Lithium therapy also can be responsible for overactive parathyroid glands, with the excess activity persisting even after discontinuation of the drug. In 10 to 20 percent of patients, primary hyperparathyroidism is caused by an inherited hyperfunction of multiple parathyroid glands. These patients tend to be diagnosed at a younger age. Although rare, familial disorders should be considered in patients diagnosed with primary hyperparathyroidism. With several of these familial disorders, patients should be evaluated for significant associated abnormalities. Familial forms of primary hyperparathyroidism include multiple endocrine neoplasia type I and type II, neonatal severe primary hyperparathyroidism, hyperparathyroidism-jaw tumor syndrome, familial hypocalciuric hypercalcemia, and familial isolated hyperparathyroidism. Approximately 95 percent of patients with multiple endocrine neoplasia type I, or Werner’s syndrome, have associated primary hyperparathyroidism. This syndrome is associated with various tumors, including pancreatic and pituitary adenomas. Patients with multiple endocrine neoplasia type II, or Sipple’s syndrome, may develop a milder form of primary hyperparathyroidism. This syndrome is characterized primarily by medullary thyroid carcinoma and pheochromocytoma. Genetic testing for both syndromes is available in some medical centers. Neonatal severe primary hyperparathyroidism presents with severe hypercalcemia during the newborn period. Hyperparathyroidism-jaw tumor syndrome is a rare condition that usually presents in adolescents or young adults as a solitary adenoma associated with bone lesions in the jaw and with Wilms’ tumor or renal cysts. Familial hypocalciuric hypercalcemia is caused by a single mutation in the calcium-sensing receptor, resulting in insensitivity to feedback inhibition of PTH secretion. In affected patients, the calcium/creatinine clearance ratio is less than 0.01, compared with a calcium/creatinine clearance ratio of greater than 0.02 in patients with primary hyperparathyroidism. Patients with familial hypocalciuric hypercalcemia are asymptomatic and require no treatment. Familial isolated hyperparathyroidism has no specific features. It is usually thought to be an expression of occult multiple endocrine neoplasia type I.
  • #20 Primary Hyperparathyroidism – Parathyroid UK
    https://parathyroiduk.org/hyperparathyroidism/primary-hyperparathyroidism/
    In Primary Hyperparathyroidism (PHPT or Hyperpara), too much parathyroid hormone is produced by one or more of the parathyroid glands because they have become enlarged or overactive. This in turn causes the body to release calcium from the bones into the blood and results in high calcium levels (hypercalcaemia). […] The most common cause of PHPT is a parathyroid gland becoming enlarged due to the development of a benign (non-cancerous) tumour called an adenoma. This is more commonly diagnosed in women, particularly postmenopausal women, but can affect both men and women and all ages, including, less commonly, children. […] Sometimes all four parathyroid glands may become enlarged – this is called parathyroid hyperplasia. This may occur sporadically (without a family history) or as part of three familial (inherited) syndromes: multiple endocrine neoplasia 1 (MEN 1) and MEN 2A, and isolated familial hyperparathyroidism. In MEN 1, the problems in the parathyroid glands are associated with other tumours in the pituitary and the pancreas. In MEN 2A, overactivity of the parathyroid glands is associated with tumours in the adrenal gland or thyroid. […] Radiotherapy treatment to your head or neck may increase the risk of developing a parathyroid adenoma or carcinoma (cancer). Only in extremely rare cases indeed will the tumour be due to parathyroid cancer. If you have been diagnosed with parathyroid cancer please go to our Parathyroid Cancer.
  • #21 Hyperparathyroidism | AAFP
    https://www.aafp.org/pubs/afp/issues/2004/0115/p333.html
    Primary hyperparathyroidism is caused by the inappropriate secretion of PTH, which results in hypercalcemia. The condition usually occurs sporadically, although familial forms are well recognized. In 85 percent of patients with primary hyperparathyroidism, the underlying cause is an adenoma in a single parathyroid gland. Hypertrophy of all four parathyroid glands and multiple adenomas within the parathyroid glands account for the remainder of cases. Fewer than 0.5 percent of cases are caused by parathyroid malignancies. Most patients with primary hyperparathyroidism are postmenopausal women. The incidence of the condition increases with age, and the average age at diagnosis is 55 years. A small percentage of patients presents years after external neck irradiation. Lithium therapy also can be responsible for overactive parathyroid glands, with the excess activity persisting even after discontinuation of the drug. In 10 to 20 percent of patients, primary hyperparathyroidism is caused by an inherited hyperfunction of multiple parathyroid glands. These patients tend to be diagnosed at a younger age. Although rare, familial disorders should be considered in patients diagnosed with primary hyperparathyroidism. With several of these familial disorders, patients should be evaluated for significant associated abnormalities. Familial forms of primary hyperparathyroidism include multiple endocrine neoplasia type I and type II, neonatal severe primary hyperparathyroidism, hyperparathyroidism-jaw tumor syndrome, familial hypocalciuric hypercalcemia, and familial isolated hyperparathyroidism. Approximately 95 percent of patients with multiple endocrine neoplasia type I, or Werner’s syndrome, have associated primary hyperparathyroidism. This syndrome is associated with various tumors, including pancreatic and pituitary adenomas. Patients with multiple endocrine neoplasia type II, or Sipple’s syndrome, may develop a milder form of primary hyperparathyroidism. This syndrome is characterized primarily by medullary thyroid carcinoma and pheochromocytoma. Genetic testing for both syndromes is available in some medical centers. Neonatal severe primary hyperparathyroidism presents with severe hypercalcemia during the newborn period. Hyperparathyroidism-jaw tumor syndrome is a rare condition that usually presents in adolescents or young adults as a solitary adenoma associated with bone lesions in the jaw and with Wilms’ tumor or renal cysts. Familial hypocalciuric hypercalcemia is caused by a single mutation in the calcium-sensing receptor, resulting in insensitivity to feedback inhibition of PTH secretion. In affected patients, the calcium/creatinine clearance ratio is less than 0.01, compared with a calcium/creatinine clearance ratio of greater than 0.02 in patients with primary hyperparathyroidism. Patients with familial hypocalciuric hypercalcemia are asymptomatic and require no treatment. Familial isolated hyperparathyroidism has no specific features. It is usually thought to be an expression of occult multiple endocrine neoplasia type I.
  • #22 Familial isolated hyperparathyroidism: MedlinePlus GeneticsLock
    https://medlineplus.gov/genetics/condition/familial-isolated-hyperparathyroidism/
    Familial isolated hyperparathyroidism can be caused by mutations in the MEN1, CDC73, or CASR gene. […] In familial isolated hyperparathyroidism, MEN1 gene mutations result in an altered menin protein that is no longer able to control cell growth and division. […] The CDC73 gene mutations that cause familial isolated hyperparathyroidism likely result in decreased activity of the parafibromin protein. […] CASR gene mutations associated with familial isolated hyperparathyroidism lead to the production of a less sensitive CaSR that requires an abnormally high concentration of calcium to trigger signaling. […] Mutations in the MEN1 gene and the CDC73 gene are involved in other conditions in which hyperparathyroidism is just one of many features. […] In many individuals with the signs and symptoms of familial isolated hyperparathyroidism, a mutation in the MEN1, CDC73, or CASR gene has not been identified, indicating that other genes may be involved in this condition.
  • #23 Hyperparathyroidism | AAFP
    https://www.aafp.org/pubs/afp/issues/2004/0115/p333.html
    Primary hyperparathyroidism is caused by the inappropriate secretion of PTH, which results in hypercalcemia. The condition usually occurs sporadically, although familial forms are well recognized. In 85 percent of patients with primary hyperparathyroidism, the underlying cause is an adenoma in a single parathyroid gland. Hypertrophy of all four parathyroid glands and multiple adenomas within the parathyroid glands account for the remainder of cases. Fewer than 0.5 percent of cases are caused by parathyroid malignancies. Most patients with primary hyperparathyroidism are postmenopausal women. The incidence of the condition increases with age, and the average age at diagnosis is 55 years. A small percentage of patients presents years after external neck irradiation. Lithium therapy also can be responsible for overactive parathyroid glands, with the excess activity persisting even after discontinuation of the drug. In 10 to 20 percent of patients, primary hyperparathyroidism is caused by an inherited hyperfunction of multiple parathyroid glands. These patients tend to be diagnosed at a younger age. Although rare, familial disorders should be considered in patients diagnosed with primary hyperparathyroidism. With several of these familial disorders, patients should be evaluated for significant associated abnormalities. Familial forms of primary hyperparathyroidism include multiple endocrine neoplasia type I and type II, neonatal severe primary hyperparathyroidism, hyperparathyroidism-jaw tumor syndrome, familial hypocalciuric hypercalcemia, and familial isolated hyperparathyroidism. Approximately 95 percent of patients with multiple endocrine neoplasia type I, or Werner’s syndrome, have associated primary hyperparathyroidism. This syndrome is associated with various tumors, including pancreatic and pituitary adenomas. Patients with multiple endocrine neoplasia type II, or Sipple’s syndrome, may develop a milder form of primary hyperparathyroidism. This syndrome is characterized primarily by medullary thyroid carcinoma and pheochromocytoma. Genetic testing for both syndromes is available in some medical centers. Neonatal severe primary hyperparathyroidism presents with severe hypercalcemia during the newborn period. Hyperparathyroidism-jaw tumor syndrome is a rare condition that usually presents in adolescents or young adults as a solitary adenoma associated with bone lesions in the jaw and with Wilms’ tumor or renal cysts. Familial hypocalciuric hypercalcemia is caused by a single mutation in the calcium-sensing receptor, resulting in insensitivity to feedback inhibition of PTH secretion. In affected patients, the calcium/creatinine clearance ratio is less than 0.01, compared with a calcium/creatinine clearance ratio of greater than 0.02 in patients with primary hyperparathyroidism. Patients with familial hypocalciuric hypercalcemia are asymptomatic and require no treatment. Familial isolated hyperparathyroidism has no specific features. It is usually thought to be an expression of occult multiple endocrine neoplasia type I.
  • #24 Hyperparathyroidism | AAFP
    https://www.aafp.org/pubs/afp/issues/2004/0115/p333.html
    Primary hyperparathyroidism is caused by the inappropriate secretion of PTH, which results in hypercalcemia. The condition usually occurs sporadically, although familial forms are well recognized. In 85 percent of patients with primary hyperparathyroidism, the underlying cause is an adenoma in a single parathyroid gland. Hypertrophy of all four parathyroid glands and multiple adenomas within the parathyroid glands account for the remainder of cases. Fewer than 0.5 percent of cases are caused by parathyroid malignancies. Most patients with primary hyperparathyroidism are postmenopausal women. The incidence of the condition increases with age, and the average age at diagnosis is 55 years. A small percentage of patients presents years after external neck irradiation. Lithium therapy also can be responsible for overactive parathyroid glands, with the excess activity persisting even after discontinuation of the drug. In 10 to 20 percent of patients, primary hyperparathyroidism is caused by an inherited hyperfunction of multiple parathyroid glands. These patients tend to be diagnosed at a younger age. Although rare, familial disorders should be considered in patients diagnosed with primary hyperparathyroidism. With several of these familial disorders, patients should be evaluated for significant associated abnormalities. Familial forms of primary hyperparathyroidism include multiple endocrine neoplasia type I and type II, neonatal severe primary hyperparathyroidism, hyperparathyroidism-jaw tumor syndrome, familial hypocalciuric hypercalcemia, and familial isolated hyperparathyroidism. Approximately 95 percent of patients with multiple endocrine neoplasia type I, or Werner’s syndrome, have associated primary hyperparathyroidism. This syndrome is associated with various tumors, including pancreatic and pituitary adenomas. Patients with multiple endocrine neoplasia type II, or Sipple’s syndrome, may develop a milder form of primary hyperparathyroidism. This syndrome is characterized primarily by medullary thyroid carcinoma and pheochromocytoma. Genetic testing for both syndromes is available in some medical centers. Neonatal severe primary hyperparathyroidism presents with severe hypercalcemia during the newborn period. Hyperparathyroidism-jaw tumor syndrome is a rare condition that usually presents in adolescents or young adults as a solitary adenoma associated with bone lesions in the jaw and with Wilms’ tumor or renal cysts. Familial hypocalciuric hypercalcemia is caused by a single mutation in the calcium-sensing receptor, resulting in insensitivity to feedback inhibition of PTH secretion. In affected patients, the calcium/creatinine clearance ratio is less than 0.01, compared with a calcium/creatinine clearance ratio of greater than 0.02 in patients with primary hyperparathyroidism. Patients with familial hypocalciuric hypercalcemia are asymptomatic and require no treatment. Familial isolated hyperparathyroidism has no specific features. It is usually thought to be an expression of occult multiple endocrine neoplasia type I.
  • #25 Primary Hyperparathyroidism – StatPearls – NCBI Bookshelf
    https://www.ncbi.nlm.nih.gov/books/NBK441895/
    Normocalcemic primary hyperparathyroidism is the presence of persistently elevated PTH levels over at least 6 months despite normal corrected serum calcium and ionized calcium concentrations after excluding all causes of secondary hyperparathyroidism, including calcium and vitamin D deficiencies. Imaging studies to identify hyperfunctioning parathyroid glands are less likely to be positive than those with classical hypercalcemic primary hyperparathyroidism. Evaluation and treatment are similar to primary hyperparathyroidism. […] […] Lithium use can cause a degree of CaSR resistance, requiring higher serum calcium levels to suppress PTH secretion. The incidence of this effect is unknown, as PTH levels are not routinely checked in patients on lithium therapy, and cases are often asymptomatic. Lab values will generally show hypercalcemia, non-suppressed PTH, normal serum phosphorus, and hypocalciuria similar to familial hypocalciuric hypercalcemia. Lithium-related hyperparathyroidism is considered secondary hyperparathyroidism but can be associated with parathyroid gland hypertrophy requiring surgery and can present similarly to primary hyperparathyroidism. […]
  • #26 Causes of Parathyroid Disease, Tumors and Hyperparathyroidism
    https://www.parathyroid.com/causes.htm
    Radiation treatments to the neck and face as a youth or teenager, or as an adult for the treatment of certain cancers. […] These people are also at a much higher risk of developing a parathyroid tumor (always benign, not cancer). […] Long term use of Lithium. […] Many patients (as many as 40%) who have taken Lithium on a daily basis for 10 or more years will develop parathyroid problems. […] Familial (Hereditary) Forms of Hyperparathyroidism. This is just under 1% of all parathyroid patients. […] Hyperparathyroidism that occurs in families can occur in women and men, however, it can show up at any age. […] All four of the parathyroid glands grow big. […] These are not true tumors, but just bigger, juicy parathyroid glands. […] Multiple Endocrine Neoplasia Syndromes (MEN Syndromes). This is far less than 1% of all parathyroid patients. […] All of these patients have 4-gland hyperplasia. […] Kidney Disease. This is actually a different disease — Secondary Hyperparathyroidism. […] The term „Secondary” simply is a descriptive term, implying that the parathyroid glands grew big and juicy and are overproducing PTH in response to the kidney disease.
  • #27 Primary hyperparathyroidism and psychiatry: manifestations, causes and management | BJPsych Advances | Cambridge Core
    https://www.cambridge.org/core/journals/bjpsych-advances/article/primary-hyperparathyroidism-and-psychiatry-manifestations-causes-and-management/244AE2F2C49F37C671A725650E8BD8BF
    The mechanisms underlying the occurrence of hyperparathyroidism with lithium use are poorly understood. There are three theories currently in contention. According to the set-point theory, lithium disrupts calcium-sensing receptors (CaSR) on the parathyroid glands, increasing the calcium set point at which suppression of parathyroid hormone release occurs. […] Another theory suggests that lithium aggressively unmasks a parathyroid gland’s existing predisposition for disease. Finally, a third theory suggests that lithium directly stimulates increased parathyroid hormone secretion which, over time, results in gland hyperplasia. […] Studies have correlated lithium use with increased serum calcium and parathyroid hormone levels. […] The largest comprehensive review monitored 423 lithium users in two different locations. Of these, 18% were identified as suffering from LAH. Those with LAH had a median age of 65 years and the majority were women. […] The absolute risk of PHPT is 100 times greater with lithium use compared with risk in the general population.
  • #28 Patient education: Primary hyperparathyroidism (Beyond the Basics) – UpToDate
    https://www.uptodate.com/contents/primary-hyperparathyroidism-beyond-the-basics
    PHPT has been reported in people who have had past radiation to the head and neck (eg, to treat childhood cancer, to treat certain benign conditions, or after nuclear power plant accidents). People who have been exposed to radiation are more likely to have thyroid nodules (growths on the thyroid gland) as well as PHPT. If thyroid nodules are also present, they may impact the interpretation of some tests and the choice of treatment of PHPT.
  • #29 Causes of Parathyroid Disease, Tumors and Hyperparathyroidism
    https://www.parathyroid.com/causes.htm
    Radiation treatments to the neck and face as a youth or teenager, or as an adult for the treatment of certain cancers. […] These people are also at a much higher risk of developing a parathyroid tumor (always benign, not cancer). […] Long term use of Lithium. […] Many patients (as many as 40%) who have taken Lithium on a daily basis for 10 or more years will develop parathyroid problems. […] Familial (Hereditary) Forms of Hyperparathyroidism. This is just under 1% of all parathyroid patients. […] Hyperparathyroidism that occurs in families can occur in women and men, however, it can show up at any age. […] All four of the parathyroid glands grow big. […] These are not true tumors, but just bigger, juicy parathyroid glands. […] Multiple Endocrine Neoplasia Syndromes (MEN Syndromes). This is far less than 1% of all parathyroid patients. […] All of these patients have 4-gland hyperplasia. […] Kidney Disease. This is actually a different disease — Secondary Hyperparathyroidism. […] The term „Secondary” simply is a descriptive term, implying that the parathyroid glands grew big and juicy and are overproducing PTH in response to the kidney disease.
  • #30 Hyperparathyroidism – Wikipedia
    https://en.wikipedia.org/wiki/Hyperparathyroidism
    Causes of primary hyperparathyroidism include parathyroid adenoma (80% of patients), multiglandular disease usually seen as hyperplasia of the 4 parathyroid glands (15-20% of patients), parathyroid carcinoma (less than 1% of patients). […] Primary hyperparathyroidism occurs sporadically and most patients do not have a family history. […] Radiation exposure increases the risk of primary hyperparathyroidism. […] Additional risk factors include lithium and thiazide diuretics exposure. […] A number of genetic conditions including multiple endocrine neoplasia syndromes, hyperparathyroidism-jaw tumor syndrome, familial hypocalciuric hypercalcemia, neonatal severe hyperparathyroidism also increase the risk. […] The most common causes for secondary hyperparathyroidism include vitamin D deficiency, chronic kidney disease, inadequate calcium intake, malabsorption. […] Tertiary hyperparathyroidism most commonly occurs from prolonged secondary hyperparathyroidism.
  • #31 Primary Hyperparathyroidism – StatPearls – NCBI Bookshelf
    https://www.ncbi.nlm.nih.gov/books/NBK441895/
    Parathyroid carcinoma is relatively rare, constituting fewer than 1% of all cases of hyperparathyroidism. Compared to patients with parathyroid adenomas, those with parathyroid carcinomas tend to be younger, more hypercalcemic, and with extremely high levels of PTH. The serum calcium often exceeds 14 mg/dL, with PTH levels 5 to 10 times the upper limit of the reference range. These cancers tend to be relatively aggressive and potentially life-threatening, usually due to severe and intractable hypercalcemia rather than direct invasion by malignant tissue. […] […] Parathyromatosis is the presence of multiple small functional nests of parathyroid tissue, usually after surgical removal of the parathyroid glands. This exceedingly rare condition can mimic the appearance of parathyroid carcinoma due to the nests being surrounded by fibrous post-surgical tissue. Parathyromatosis can be distinguished from parathyroid carcinoma by histologic criteria. Parathyromatosis is thought to have 2 etiologies: proliferation of parathyroid tissue residual from embryologic development and, more frequently, seeding during parathyroidectomy or percutaneous ablation, which often occurs in patients with CKD who have persistently elevated PTH. This can be a cause of recurrent, persistent, or intractable hyperparathyroidism. […]
  • #32 Hyperparathyroidism – Wikipedia
    https://en.wikipedia.org/wiki/Hyperparathyroidism
    Causes of primary hyperparathyroidism include parathyroid adenoma (80% of patients), multiglandular disease usually seen as hyperplasia of the 4 parathyroid glands (15-20% of patients), parathyroid carcinoma (less than 1% of patients). […] Primary hyperparathyroidism occurs sporadically and most patients do not have a family history. […] Radiation exposure increases the risk of primary hyperparathyroidism. […] Additional risk factors include lithium and thiazide diuretics exposure. […] A number of genetic conditions including multiple endocrine neoplasia syndromes, hyperparathyroidism-jaw tumor syndrome, familial hypocalciuric hypercalcemia, neonatal severe hyperparathyroidism also increase the risk. […] The most common causes for secondary hyperparathyroidism include vitamin D deficiency, chronic kidney disease, inadequate calcium intake, malabsorption. […] Tertiary hyperparathyroidism most commonly occurs from prolonged secondary hyperparathyroidism.
  • #33 So you have primary hyperparathyroidism – Harvard Health
    https://www.health.harvard.edu/newsletter_article/so_you_have_primary_hyperparathyroidism
    Primary hyperparathyroidism is a disorder of the parathyroids, four tiny pea-sized glands located behind the thyroid gland in the neck. […] The usual cause is an adenoma a noncancerous tumor. […] In primary hyperparathyroidism, one or more parathyroid glands produce more PTH than needed, raising calcium levels above the normal range. Usually, the cause is a benign (noncancerous) tumor, or adenoma, in a single parathyroid gland. […] Parathyroid glands may become overactive because of lithium therapy, past radiation to the neck, or certain gene defects. […] Roughly 3% to 5% of cases are linked to inherited syndromes. […] In some cases, the cause is simply unknown.
  • #34 Hyperparathyroidism – Symptoms & causes – Mayo Clinic
    https://www.mayoclinic.org/diseases-conditions/hyperparathyroidism/symptoms-causes/syc-20356194
    Severe vitamin D deficiency. Vitamin D helps maintain appropriate calcium levels in the blood. […] Chronic kidney failure. Your kidneys convert vitamin D into a form that your body can use. If your kidneys work poorly, usable vitamin D may decrease and calcium levels drop. This causes parathyroid hormone levels to go up. […] Hyperparathyroidism may occur because of primary hyperparathyroidism or secondary hyperparathyroidism.
  • #35 Hyperparathyroidism | AAFP
    https://www.aafp.org/pubs/afp/issues/2004/0115/p333.html
    Secondary hyperparathyroidism is the result of a physiologic or pathophysiologic parathyroid response to hypocalcemia in an attempt to maintain calcium homeostasis. The condition can occur because of vitamin D deficiency or low calcium intake. The serum PTH level is elevated, and the serum calcium level may be normal or low, because of a diet that is limited in vitamin D or calcium, or because of deficiency secondary to malabsorption. In most instances, secondary hyperparathyroidism is caused by chronic renal failure, which results in a low concentration of 1,25-dihydroxyvitamin D3 because of decreased renal production. Tertiary hyperparathyroidism occurs because of prolonged hypocalcemia (usually secondary to chronic renal failure) that causes parathyroid gland hyperplasia. Autonomous oversecretion of PTH by the parathyroid glands results in hypercalcemia.
  • #36 Hyperparathyroidism: Symptoms, Causes, & Treatment
    https://patient.info/hormones/thyroid-and-parathyroid-glands/hyperparathyroidism
    Parathyroid carcinoma. Very rarely, primary hyperparathyroidism is caused by cancer in one of the parathyroid glands. […] Secondary hyperparathyroidism is caused by other diseases or deficiencies that are affecting your body. These other conditions are ones that cause a long-standing, low level of calcium in your blood. This means that your parathyroid glands are being stimulated all the time to try to increase your blood calcium level. […] Some of the causes of secondary hyperparathyroidism include: Chronic kidney disease (CKD) – the most common cause of secondary hyperparathyroidism. […] Vitamin D deficiency (rickets/osteomalacia) – another common cause. Vitamin D deficiency causes a long-standing low level of calcium in your blood. […] Gut (intestinal) malabsorption – there are various diseases that can affect your gut and prevent the calcium that you eat from being taken up (absorbed) into your blood. This can cause your blood calcium level to become low and stay low.
  • #37 Secondary hyperparathyroidism: causes, symptoms and treatment
    https://www.kidneyresearchuk.org/conditions-symptoms/secondary-hyperparathyroidism/
    Secondary hyperparathyroidism occurs as a result of chronic kidney disease (CKD). […] Three things cause increased production of PTH: low blood calcium, low levels of activated vitamin D, and high phosphate levels. All three occur in chronic kidney disease. […] This triggers the parathyroid glands to overproduce PTH in an attempt to increase the amount of calcium in the blood. […] If left for too long, the parathyroid glands can remain overactive all the time. This is known as tertiary hyperparathyroidism. […] Treatment for secondary hyperparathyroidism includes: Changes to diet to control the intake of phosphate, Tablets including phosphate binders and vitamin D supplements, Surgery to remove the parathyroid glands, either completely or leaving a small amount of gland in place, A newer class of drugs called calcimimetics (cinacalcet, etelcalcitide) that mimic the action of calcium on tissues and suppress the production of PTH.
  • #38 Hyperparathyroidism – Symptoms & causes – Mayo Clinic
    https://www.mayoclinic.org/diseases-conditions/hyperparathyroidism/symptoms-causes/syc-20356194
    Severe vitamin D deficiency. Vitamin D helps maintain appropriate calcium levels in the blood. […] Chronic kidney failure. Your kidneys convert vitamin D into a form that your body can use. If your kidneys work poorly, usable vitamin D may decrease and calcium levels drop. This causes parathyroid hormone levels to go up. […] Hyperparathyroidism may occur because of primary hyperparathyroidism or secondary hyperparathyroidism.
  • #39 Hyperparathyroidism: Background, Anatomy and Embryology, Primary Hyperparathyroidism
    https://emedicine.medscape.com/article/127351-overview
    Secondary hyperparathyroidism results from a chronic stimulus of the parathyroid gland to release parathyroid hormone. Parathyroid hormone release is increased in the setting of hypocalcemia and hyperphosphatemia and is decreased by fibroblast growth factor 23 (FGF-23). […] Tertiary disease is characterized by the development of autonomous hypersecretion of parathyroid hormone, causing hypercalcemia. The etiology is unknown but may be due to monoclonal expansion of parathyroid cells (nodule formation within hyperplastic glands). A change may occur in the set point of the calcium-sensing mechanism to hypercalcemic levels. Four-gland involvement occurs in most patients.
  • #40 Secondary hyperparathyroidism: causes, symptoms and treatment
    https://www.kidneyresearchuk.org/conditions-symptoms/secondary-hyperparathyroidism/
    Secondary hyperparathyroidism occurs as a result of chronic kidney disease (CKD). […] Three things cause increased production of PTH: low blood calcium, low levels of activated vitamin D, and high phosphate levels. All three occur in chronic kidney disease. […] This triggers the parathyroid glands to overproduce PTH in an attempt to increase the amount of calcium in the blood. […] If left for too long, the parathyroid glands can remain overactive all the time. This is known as tertiary hyperparathyroidism. […] Treatment for secondary hyperparathyroidism includes: Changes to diet to control the intake of phosphate, Tablets including phosphate binders and vitamin D supplements, Surgery to remove the parathyroid glands, either completely or leaving a small amount of gland in place, A newer class of drugs called calcimimetics (cinacalcet, etelcalcitide) that mimic the action of calcium on tissues and suppress the production of PTH.
  • #41 Secondary hyperparathyroidism: symptoms, causes & treatment | American Kidney Fund
    https://www.kidneyfund.org/living-kidney-disease/health-problems-caused-kidney-disease/secondary-hyperparathyroidism-symptoms-causes-treatment
    Secondary hyperparathyroidism (SHPT) is common in people who have kidney failure (stage 5 kidney disease). […] SHPT happens when another disease you have causes low levels of calcium in your blood. The most common cause of SHPT is end-stage renal disease (ESRD), also known as kidney failure. […] As your kidneys fail, they are no longer able to change inactive vitamin D to active vitamin D. This creates low levels of vitamin D in your body. When you have low levels of vitamin D, your body absorbs less calcium, and the level of calcium in your blood becomes low. This signals your parathyroid glands to make more PTH and grow larger, which causes SHPT. Your doctor may also call this „renal secondary hyperparathyroidism”.
  • #42 Secondary hyperparathyroidism: symptoms, causes & treatment | American Kidney Fund
    https://www.kidneyfund.org/living-kidney-disease/health-problems-caused-kidney-disease/secondary-hyperparathyroidism-symptoms-causes-treatment
    Secondary hyperparathyroidism (SHPT) is common in people who have kidney failure (stage 5 kidney disease). […] SHPT happens when another disease you have causes low levels of calcium in your blood. The most common cause of SHPT is end-stage renal disease (ESRD), also known as kidney failure. […] As your kidneys fail, they are no longer able to change inactive vitamin D to active vitamin D. This creates low levels of vitamin D in your body. When you have low levels of vitamin D, your body absorbs less calcium, and the level of calcium in your blood becomes low. This signals your parathyroid glands to make more PTH and grow larger, which causes SHPT. Your doctor may also call this „renal secondary hyperparathyroidism”.
  • #43 Hyperparathyroidism: What It Is, Symptoms & Treatment
    https://my.clevelandclinic.org/health/diseases/14454-hyperparathyroidism
    Hyperparathyroidism can be primary (caused by growths or enlarged glands) or secondary (caused by kidney disease or low calcium levels). […] Growths on your parathyroid glands, parathyroid gland enlargement, and conditions that cause low levels of calcium or high levels of phosphate can all cause hyperparathyroidism. Primary, secondary and tertiary hyperparathyroidism have different causes. […] When you have a growth on a parathyroid gland or one or more of the glands are enlarged, it produces more PTH and doesn’t respond to signals that tell it to stop making hormones. This causes primary hyperparathyroidism. Specific causes of primary hyperparathyroidism include: Adenomas noncancerous (benign) growths are the most common cause of primary hyperparathyroidism. […] The most common cause of secondary hyperparathyroidism is kidney disease. When your kidneys aren’t working properly, your phosphate levels go up and your vitamin D levels go down. Low vitamin D levels lead to low calcium levels. Your parathyroid glands adjust by making more PTH to get rid of phosphate in your blood and increase the amount of calcium. […] Secondary hyperparathyroidism causes tertiary hyperparathyroidism. Your parathyroid glands become enlarged from working much more than they should. This causes them to stop responding to signals that tell them not to make more PTH.
  • #44 Secondary Hyperparathyroidism | Columbia Surgery
    https://columbiasurgery.org/conditions-and-treatments/secondary-hyperparathyroidism
    Secondary hyperparathyroidism is a condition in which a disease outside of the parathyroid glands causes all of the parathyroid glands to become enlarged and hyperactive. The most common causes of secondary hyperparathyroidism are kidney failure and vitamin D deficiency. […] In kidney failure, the kidney is no longer able to make enough vitamin D or remove all of the phosphorus that is made by the body, which leads to low calcium levels. These low calcium levels stimulate the parathyroid glands to make more PTH. Over time, this constant stimulation causes the parathyroid glands to grow and become hyperactive and patients can progress to develop secondary hyperparathyroidism. […] For patients with secondary hyperparathyroidism from vitamin D deficiency, the best treatment is to raise the vitamin D levels to the normal range. For patients with secondary hyperparathyroidism from kidney failure, the only treatment is to have a kidney transplant. […] The main reasons for an operation include: worsening bone density, severe pruritus (i.e. uncontrollable itching), calciphylaxis, PTH levels that are consistently higher than 800 pg/ml, and inability to control calcium and phosphorus levels in the blood by dialysis.
  • #45 Hyperparathyroidism: Symptoms, Causes, & Treatment
    https://patient.info/hormones/thyroid-and-parathyroid-glands/hyperparathyroidism
    Parathyroid carcinoma. Very rarely, primary hyperparathyroidism is caused by cancer in one of the parathyroid glands. […] Secondary hyperparathyroidism is caused by other diseases or deficiencies that are affecting your body. These other conditions are ones that cause a long-standing, low level of calcium in your blood. This means that your parathyroid glands are being stimulated all the time to try to increase your blood calcium level. […] Some of the causes of secondary hyperparathyroidism include: Chronic kidney disease (CKD) – the most common cause of secondary hyperparathyroidism. […] Vitamin D deficiency (rickets/osteomalacia) – another common cause. Vitamin D deficiency causes a long-standing low level of calcium in your blood. […] Gut (intestinal) malabsorption – there are various diseases that can affect your gut and prevent the calcium that you eat from being taken up (absorbed) into your blood. This can cause your blood calcium level to become low and stay low.
  • #46 Hyperparathyroidism – Wikipedia
    https://en.wikipedia.org/wiki/Hyperparathyroidism
    Causes of primary hyperparathyroidism include parathyroid adenoma (80% of patients), multiglandular disease usually seen as hyperplasia of the 4 parathyroid glands (15-20% of patients), parathyroid carcinoma (less than 1% of patients). […] Primary hyperparathyroidism occurs sporadically and most patients do not have a family history. […] Radiation exposure increases the risk of primary hyperparathyroidism. […] Additional risk factors include lithium and thiazide diuretics exposure. […] A number of genetic conditions including multiple endocrine neoplasia syndromes, hyperparathyroidism-jaw tumor syndrome, familial hypocalciuric hypercalcemia, neonatal severe hyperparathyroidism also increase the risk. […] The most common causes for secondary hyperparathyroidism include vitamin D deficiency, chronic kidney disease, inadequate calcium intake, malabsorption. […] Tertiary hyperparathyroidism most commonly occurs from prolonged secondary hyperparathyroidism.
  • #47 Hyperparathyroidism: MedlinePlus Medical EncyclopediaLock
    https://medlineplus.gov/ency/article/001215.htm
    Hyperparathyroidism is a condition in which 1 or more of the parathyroid glands in your neck produce too much parathyroid hormone (PTH). […] If one or more of the parathyroid glands grow larger, it may lead to too much PTH. Most often, the cause is a benign tumor of the parathyroid glands (parathyroid adenoma). These benign tumors are common and happen without a known cause. […] Some genetic syndromes (multiple endocrine neoplasia I) make it more likely to have hyperparathyroidism. […] In very rare cases, hyperparathyroidism is caused by parathyroid cancer. […] Medical conditions that cause low blood calcium or increased phosphate can also lead to hyperparathyroidism. Common conditions include: […] Kidney damage or failure […] Vitamin D disorders (may occur in children who do not eat a variety of foods, and in older adults who do not get enough sunlight on their skin or who have poor absorption of vitamin D from food such as after bariatric surgery) […] If hyperparathyroidism is caused by kidney disease or failure, treatment may include: […] Parathyroid surgery, if the PTH level becomes uncontrollably high. […] Outlook depends on the cause of hyperparathyroidism.
  • #48 Hyperparathyroidism: MedlinePlus Medical EncyclopediaLock
    https://medlineplus.gov/ency/article/001215.htm
    Hyperparathyroidism is a condition in which 1 or more of the parathyroid glands in your neck produce too much parathyroid hormone (PTH). […] If one or more of the parathyroid glands grow larger, it may lead to too much PTH. Most often, the cause is a benign tumor of the parathyroid glands (parathyroid adenoma). These benign tumors are common and happen without a known cause. […] Some genetic syndromes (multiple endocrine neoplasia I) make it more likely to have hyperparathyroidism. […] In very rare cases, hyperparathyroidism is caused by parathyroid cancer. […] Medical conditions that cause low blood calcium or increased phosphate can also lead to hyperparathyroidism. Common conditions include: […] Kidney damage or failure […] Vitamin D disorders (may occur in children who do not eat a variety of foods, and in older adults who do not get enough sunlight on their skin or who have poor absorption of vitamin D from food such as after bariatric surgery) […] If hyperparathyroidism is caused by kidney disease or failure, treatment may include: […] Parathyroid surgery, if the PTH level becomes uncontrollably high. […] Outlook depends on the cause of hyperparathyroidism.
  • #49 Hyperparathyroidism: MedlinePlus Medical EncyclopediaLock
    https://medlineplus.gov/ency/article/001215.htm
    Hyperparathyroidism is a condition in which 1 or more of the parathyroid glands in your neck produce too much parathyroid hormone (PTH). […] If one or more of the parathyroid glands grow larger, it may lead to too much PTH. Most often, the cause is a benign tumor of the parathyroid glands (parathyroid adenoma). These benign tumors are common and happen without a known cause. […] Some genetic syndromes (multiple endocrine neoplasia I) make it more likely to have hyperparathyroidism. […] In very rare cases, hyperparathyroidism is caused by parathyroid cancer. […] Medical conditions that cause low blood calcium or increased phosphate can also lead to hyperparathyroidism. Common conditions include: […] Kidney damage or failure […] Vitamin D disorders (may occur in children who do not eat a variety of foods, and in older adults who do not get enough sunlight on their skin or who have poor absorption of vitamin D from food such as after bariatric surgery) […] If hyperparathyroidism is caused by kidney disease or failure, treatment may include: […] Parathyroid surgery, if the PTH level becomes uncontrollably high. […] Outlook depends on the cause of hyperparathyroidism.
  • #50 Hyperparathyroidism – Symptoms & causes – Mayo Clinic
    https://www.mayoclinic.org/diseases-conditions/hyperparathyroidism/symptoms-causes/syc-20356194
    Severe vitamin D deficiency. Vitamin D helps maintain appropriate calcium levels in the blood. […] Chronic kidney failure. Your kidneys convert vitamin D into a form that your body can use. If your kidneys work poorly, usable vitamin D may decrease and calcium levels drop. This causes parathyroid hormone levels to go up. […] Hyperparathyroidism may occur because of primary hyperparathyroidism or secondary hyperparathyroidism.
  • #51 Hyperparathyroidism: Symptoms, Causes, & Treatment
    https://patient.info/hormones/thyroid-and-parathyroid-glands/hyperparathyroidism
    Parathyroid carcinoma. Very rarely, primary hyperparathyroidism is caused by cancer in one of the parathyroid glands. […] Secondary hyperparathyroidism is caused by other diseases or deficiencies that are affecting your body. These other conditions are ones that cause a long-standing, low level of calcium in your blood. This means that your parathyroid glands are being stimulated all the time to try to increase your blood calcium level. […] Some of the causes of secondary hyperparathyroidism include: Chronic kidney disease (CKD) – the most common cause of secondary hyperparathyroidism. […] Vitamin D deficiency (rickets/osteomalacia) – another common cause. Vitamin D deficiency causes a long-standing low level of calcium in your blood. […] Gut (intestinal) malabsorption – there are various diseases that can affect your gut and prevent the calcium that you eat from being taken up (absorbed) into your blood. This can cause your blood calcium level to become low and stay low.
  • #52
    https://www.alliedacademies.org/articles/secondary-hyperparathyroidism-causes-and-clinical-implications-31752.html
    Secondary hyperparathyroidism is a condition where the parathyroid glands produce excess Parathyroid Hormone (PTH) in response to low calcium levels or other underlying health issues. […] The most common cause of secondary hyperparathyroidism is Chronic Kidney Disease (CKD). […] Another common cause of secondary hyperparathyroidism is vitamin D deficiency. […] Secondary hyperparathyroidism can also be associated with malabsorption conditions such as celiac disease or Inflammatory Bowel Disease (IBD). […] Common causes include chronic kidney disease, vitamin D deficiency, and malabsorption conditions.
  • #53
    https://www.alliedacademies.org/articles/secondary-hyperparathyroidism-causes-and-clinical-implications-31752.html
    Secondary hyperparathyroidism is a condition where the parathyroid glands produce excess Parathyroid Hormone (PTH) in response to low calcium levels or other underlying health issues. […] The most common cause of secondary hyperparathyroidism is Chronic Kidney Disease (CKD). […] Another common cause of secondary hyperparathyroidism is vitamin D deficiency. […] Secondary hyperparathyroidism can also be associated with malabsorption conditions such as celiac disease or Inflammatory Bowel Disease (IBD). […] Common causes include chronic kidney disease, vitamin D deficiency, and malabsorption conditions.
  • #54 Hyperparathyroidism – Symptoms & causes – Mayo Clinic
    https://www.mayoclinic.org/diseases-conditions/hyperparathyroidism/symptoms-causes/syc-20356194
    Hyperparathyroidism is caused by factors that increase the production of parathyroid hormone. […] Primary hyperparathyroidism occurs because of a problem with one or more of the four parathyroid glands: A noncancerous growth (adenoma) on a gland is the most common cause. […] Secondary hyperparathyroidism is the result of another condition that lowers the blood calcium, which then affects the gland’s function. This causes your parathyroid glands to overwork and produce high amounts of parathyroid hormone to maintain or restore the calcium level to the standard range. […] Factors that may result in secondary hyperparathyroidism include: Severe calcium deficiency. Your body may not get enough calcium from your diet, often because your digestive system doesn’t absorb the calcium from food.
  • #55 Hyperparathyroidism Information | Mount Sinai – New York
    https://www.mountsinai.org/health-library/diseases-conditions/hyperparathyroidism
    Hyperparathyroidism is a condition in which 1 or more of the parathyroid glands in your neck produce too much parathyroid hormone (PTH). […] If one or more of the parathyroid glands grow larger, it may lead to too much PTH. Most often, the cause is a benign tumor of the parathyroid glands (parathyroid adenoma). These benign tumors are common and happen without a known cause. […] Some genetic syndromes (multiple endocrine neoplasia I) make it more likely to have hyperparathyroidism. […] In very rare cases, hyperparathyroidism is caused by parathyroid cancer. […] Medical conditions that cause low blood calcium or increased phosphate can also lead to hyperparathyroidism. Common conditions include: […] Not enough calcium in the diet […] Vitamin D disorders (may occur in children who do not eat a variety of foods, and in older adults who do not get enough sunlight on their skin or who have poor absorption of vitamin D from food such as after bariatric surgery) […] Hyperparathyroidism is often diagnosed by common blood tests before symptoms occur.
  • #56 Hyperparathyroidism – Endocrine and Metabolic Disorders – Merck Manual Professional Edition
    https://www.merckmanuals.com/professional/endocrine-and-metabolic-disorders/parathyroid-disorders/hyperparathyroidism
    Other less common causes of secondary hyperparathyroidism include decreased calcium intake, poor calcium absorption in the intestine due to vitamin D deficiency, excessive renal calcium loss due to loop diuretic use, and inhibition of bone resorption due to bisphosphonate use. […] Tertiary hyperparathyroidism results when PTH secretion becomes autonomous of serum calcium concentration. […] Tertiary hyperparathyroidism generally occurs in patients with long-standing secondary hyperparathyroidism, as in patients with end-stage renal disease of several years duration.
  • #57 Hyperparathyroidism – Endocrine and Metabolic Disorders – Merck Manual Professional Edition
    https://www.merckmanuals.com/professional/endocrine-and-metabolic-disorders/parathyroid-disorders/hyperparathyroidism
    Other less common causes of secondary hyperparathyroidism include decreased calcium intake, poor calcium absorption in the intestine due to vitamin D deficiency, excessive renal calcium loss due to loop diuretic use, and inhibition of bone resorption due to bisphosphonate use. […] Tertiary hyperparathyroidism results when PTH secretion becomes autonomous of serum calcium concentration. […] Tertiary hyperparathyroidism generally occurs in patients with long-standing secondary hyperparathyroidism, as in patients with end-stage renal disease of several years duration.
  • #58 Secondary Hyperparathyroidism
    https://www.southwestparathyroid.com/secondary-hyperparathyroidism
    Secondary hyperparathyroidism causes hyperplasia, an enlargement of all four parathyroid glands. […] In secondary hyperparathyroidism (sHPT), the parathyroids are overactive, and parathyroid hormone (PTH) levels are high. […] The most common cause of secondary hyperparathyroidism is chronic kidney disease, usually at the point where it requires dialysis. […] For patients who are not on dialysis, the most common cause of sHPT is calcium malabsorption in the intestines. […] Finally, an often-overlooked cause of secondary HPT is renal calcium leak.
  • #59 Hyperparathyroidism > Fact Sheets > Yale Medicine
    https://www.yalemedicine.org/conditions/hyperparathyroidism
    Hyperparathyroidism is a condition in which the parathyroid glands produce too much parathyroid hormone (PTH). […] There are primary, secondary, and tertiary forms of hyperparathyroidism. Each has a different cause. […] There are different possible causes of hyperparathyroidism, depending on whether the condition is primary, secondary, or tertiary. […] Primary hyperparathyroidism: The condition is usually due to a benign (non-cancerous) tumor or growth, called an adenoma, arising in one of the four parathyroid glands. […] Secondary hyperparathyroidism: The condition occurs because of chronically low levels of calcium or vitamin D in the blood, which causes the parathyroid glands to chronically release high levels of PTH. […] Tertiary hyperparathyroidism: The condition occurs among people who have had secondary hyperparathyroidism for a long time, particularly among people who have had chronic kidney disease for many years.
  • #60 Hyperparathyroidism: Symptoms, Causes, & Treatment
    https://patient.info/hormones/thyroid-and-parathyroid-glands/hyperparathyroidism
    Tertiary hyperparathyroidism occurs as a result of long-standing secondary hyperparathyroidism. In tertiary hyperparathyroidism, the condition that was causing your low blood calcium level and the secondary hyperparathyroidism, has been treated (or your blood calcium level has been brought back to normal). […] However, your parathyroid glands continue to produce large amounts of parathyroid hormone. This is because they start to act by themselves (autonomously) and are no longer sensitive to your blood calcium level. They are not 'switched off’ when your blood calcium level rises. This results in a high calcium level in your blood.
  • #61 Hyperparathyroidism: Background, Anatomy and Embryology, Primary Hyperparathyroidism
    https://emedicine.medscape.com/article/127351-overview
    Secondary hyperparathyroidism results from a chronic stimulus of the parathyroid gland to release parathyroid hormone. Parathyroid hormone release is increased in the setting of hypocalcemia and hyperphosphatemia and is decreased by fibroblast growth factor 23 (FGF-23). […] Tertiary disease is characterized by the development of autonomous hypersecretion of parathyroid hormone, causing hypercalcemia. The etiology is unknown but may be due to monoclonal expansion of parathyroid cells (nodule formation within hyperplastic glands). A change may occur in the set point of the calcium-sensing mechanism to hypercalcemic levels. Four-gland involvement occurs in most patients.
  • #62 Hyperparathyroidism: Symptoms, Causes, & Treatment
    https://patient.info/hormones/thyroid-and-parathyroid-glands/hyperparathyroidism
    Tertiary hyperparathyroidism occurs as a result of long-standing secondary hyperparathyroidism. In tertiary hyperparathyroidism, the condition that was causing your low blood calcium level and the secondary hyperparathyroidism, has been treated (or your blood calcium level has been brought back to normal). […] However, your parathyroid glands continue to produce large amounts of parathyroid hormone. This is because they start to act by themselves (autonomously) and are no longer sensitive to your blood calcium level. They are not 'switched off’ when your blood calcium level rises. This results in a high calcium level in your blood.
  • #63 Hyperparathyroidism: What It Is, Symptoms & Treatment
    https://my.clevelandclinic.org/health/diseases/14454-hyperparathyroidism
    Hyperparathyroidism can be primary (caused by growths or enlarged glands) or secondary (caused by kidney disease or low calcium levels). […] Growths on your parathyroid glands, parathyroid gland enlargement, and conditions that cause low levels of calcium or high levels of phosphate can all cause hyperparathyroidism. Primary, secondary and tertiary hyperparathyroidism have different causes. […] When you have a growth on a parathyroid gland or one or more of the glands are enlarged, it produces more PTH and doesn’t respond to signals that tell it to stop making hormones. This causes primary hyperparathyroidism. Specific causes of primary hyperparathyroidism include: Adenomas noncancerous (benign) growths are the most common cause of primary hyperparathyroidism. […] The most common cause of secondary hyperparathyroidism is kidney disease. When your kidneys aren’t working properly, your phosphate levels go up and your vitamin D levels go down. Low vitamin D levels lead to low calcium levels. Your parathyroid glands adjust by making more PTH to get rid of phosphate in your blood and increase the amount of calcium. […] Secondary hyperparathyroidism causes tertiary hyperparathyroidism. Your parathyroid glands become enlarged from working much more than they should. This causes them to stop responding to signals that tell them not to make more PTH.
  • #64 Hyperparathyroidism – Endocrine and Metabolic Disorders – Merck Manual Professional Edition
    https://www.merckmanuals.com/professional/endocrine-and-metabolic-disorders/parathyroid-disorders/hyperparathyroidism
    The most common cause of hyperparathyroidism is parathyroid adenoma. […] Parathyroid adenomas are most often isolated solitary adenomas. However, parathyroid adenoma may be hereditary in patients with other endocrine tumors, particularly certain multiple endocrine neoplasia syndromes. […] Another cause is hyperplasia of the parathyroid glands. […] Primary hyperparathyroidism is a generalized disorder resulting from excessive secretion of parathyroid hormone by one or more parathyroid glands. […] Primary hyperparathyroidism causes hypercalcemia, hypophosphatemia, and excessive bone resorption (leading to osteoporosis). […] Secondary hyperparathyroidism occurs most commonly in advanced chronic kidney disease when decreased formation of active vitamin D in the kidneys and other factors lead to hypocalcemia and chronic stimulation of PTH secretion.
  • #65 Hyperparathyroidism | AAFP
    https://www.aafp.org/pubs/afp/issues/1998/0415/p1795.html
    Hyperparathyroidism is a common cause of hypercalcemia. […] In 85 percent of the persons affected, hyperparathyroidism is the result of an adenoma in a single parathyroid gland. Hypertrophy of all four parathyroid glands causes hyperparathyroidism in 15 percent of patients. A very small number of cases of hyperparathyroidism result from parathyroid malignancies. […] In addition, the incidence of hyperparathyroidism is higher in patients with type I and type II multiple endocrine neoplasia syndromes, in patients with familial hyperparathyroidism and in patients who received radiation therapy to the head and neck area for benign diseases during childhood. […] Secondary hyperparathyroidism occurs when the parathyroid glands are chronically stimulated to release parathyroid hormone. A decrease in circulating calcium is the stimulus for this release. Chronic renal failure, rickets and malabsorption syndromes are the most frequent conditions leading to secondary hyperparathyroidism. […] In some cases of prolonged secondary hyperparathyroidism, the glands take on an autonomous function manifested by continued high levels of parathyroid hormone despite resolution of the original stimulus. This state is referred to as tertiary hyperparathyroidism.
  • #66 Hyperparathyroidism: Background, Anatomy and Embryology, Primary Hyperparathyroidism
    https://emedicine.medscape.com/article/127351-overview
    Secondary hyperparathyroidism results from a chronic stimulus of the parathyroid gland to release parathyroid hormone. Parathyroid hormone release is increased in the setting of hypocalcemia and hyperphosphatemia and is decreased by fibroblast growth factor 23 (FGF-23). […] Tertiary disease is characterized by the development of autonomous hypersecretion of parathyroid hormone, causing hypercalcemia. The etiology is unknown but may be due to monoclonal expansion of parathyroid cells (nodule formation within hyperplastic glands). A change may occur in the set point of the calcium-sensing mechanism to hypercalcemic levels. Four-gland involvement occurs in most patients.
  • #67 Hyperparathyroidism: Background, Anatomy and Embryology, Primary Hyperparathyroidism
    https://emedicine.medscape.com/article/127351-overview
    Secondary hyperparathyroidism results from a chronic stimulus of the parathyroid gland to release parathyroid hormone. Parathyroid hormone release is increased in the setting of hypocalcemia and hyperphosphatemia and is decreased by fibroblast growth factor 23 (FGF-23). […] Tertiary disease is characterized by the development of autonomous hypersecretion of parathyroid hormone, causing hypercalcemia. The etiology is unknown but may be due to monoclonal expansion of parathyroid cells (nodule formation within hyperplastic glands). A change may occur in the set point of the calcium-sensing mechanism to hypercalcemic levels. Four-gland involvement occurs in most patients.
  • #68 Hyperparathyroidism (Types, Causes, Symptoms and Treatment)
    https://patient.info/doctor/hyperparathyroidism-pro
    Secondary hyperparathyroidism is seen in almost all patients with dialysis-dependent CKD. Most patients with CKD stage 5 develop SHPT. […] Several studies have documented that PTH levels are increased in CKD (stages 3 and 4) before there are changes in calcium and phosphate. […] Secondary hyperparathyroidism can, however, occur in any condition with chronic hypocalcaemia such as deficiency in vitamin D or malabsorption. […] […] […] Tertiary hyperparathyroidism causes […] Tertiary hyperparathyroidism (THPT) usually occurs after prolonged SHPT. […] The glands become autonomous, producing excessive PTH even after the cause of hypocalcaemia has been corrected. […] This results in hypercalcaemia. […] Long-standing kidney disease is the most common cause. […] It can persist after a renal transplant.
  • #69 Primary Hyperparathyroidism – StatPearls – NCBI Bookshelf
    https://www.ncbi.nlm.nih.gov/books/NBK441895/
    Normocalcemic primary hyperparathyroidism is the presence of persistently elevated PTH levels over at least 6 months despite normal corrected serum calcium and ionized calcium concentrations after excluding all causes of secondary hyperparathyroidism, including calcium and vitamin D deficiencies. Imaging studies to identify hyperfunctioning parathyroid glands are less likely to be positive than those with classical hypercalcemic primary hyperparathyroidism. Evaluation and treatment are similar to primary hyperparathyroidism. […] […] Lithium use can cause a degree of CaSR resistance, requiring higher serum calcium levels to suppress PTH secretion. The incidence of this effect is unknown, as PTH levels are not routinely checked in patients on lithium therapy, and cases are often asymptomatic. Lab values will generally show hypercalcemia, non-suppressed PTH, normal serum phosphorus, and hypocalciuria similar to familial hypocalciuric hypercalcemia. Lithium-related hyperparathyroidism is considered secondary hyperparathyroidism but can be associated with parathyroid gland hypertrophy requiring surgery and can present similarly to primary hyperparathyroidism. […]
  • #70 Normocalcemic Primary Hyperparathyroidism – Endocrine Surgery | UCLA Health
    https://www.uclahealth.org/medical-services/surgery/endocrine-surgery/conditions-treated/parathyroid/normocalcemic-primary-hyperparathyroidism
    Normocalcemic primary hyperparathyroidism (nPHPT) is suspected when patients calcium level is within the normal range, but parathyroid hormone level is too high. […] Normocalcemic primary hyperparathyroidism (nPHPT) is hypothesized to be an early type of primary hyperparathyroidism. […] Proper diagnosis of normocalcemic primary hyperparathyroidism is challenging, because there are several other causes of high parathyroid hormone levels and normal calcium levels. Because several other conditions may mimic normocalcemic primary hyperparathyroidism, detailed blood and sometimes urine testing is required to establish the definitive diagnosis. […] Nearly half of patients diagnosed with normocalcemic primary hyperparathyroidism have been found to have osteoporosis. […] The short answer is that we do not know for sure.
  • #71 Primary Hyperparathyroidism – StatPearls – NCBI Bookshelf
    https://www.ncbi.nlm.nih.gov/books/NBK441895/
    Normocalcemic primary hyperparathyroidism is the presence of persistently elevated PTH levels over at least 6 months despite normal corrected serum calcium and ionized calcium concentrations after excluding all causes of secondary hyperparathyroidism, including calcium and vitamin D deficiencies. Imaging studies to identify hyperfunctioning parathyroid glands are less likely to be positive than those with classical hypercalcemic primary hyperparathyroidism. Evaluation and treatment are similar to primary hyperparathyroidism. […] […] Lithium use can cause a degree of CaSR resistance, requiring higher serum calcium levels to suppress PTH secretion. The incidence of this effect is unknown, as PTH levels are not routinely checked in patients on lithium therapy, and cases are often asymptomatic. Lab values will generally show hypercalcemia, non-suppressed PTH, normal serum phosphorus, and hypocalciuria similar to familial hypocalciuric hypercalcemia. Lithium-related hyperparathyroidism is considered secondary hyperparathyroidism but can be associated with parathyroid gland hypertrophy requiring surgery and can present similarly to primary hyperparathyroidism. […]
  • #72 Normocalcemic Primary Hyperparathyroidism – Endocrine Surgery | UCLA Health
    https://www.uclahealth.org/medical-services/surgery/endocrine-surgery/conditions-treated/parathyroid/normocalcemic-primary-hyperparathyroidism
    Normocalcemic primary hyperparathyroidism (nPHPT) is suspected when patients calcium level is within the normal range, but parathyroid hormone level is too high. […] Normocalcemic primary hyperparathyroidism (nPHPT) is hypothesized to be an early type of primary hyperparathyroidism. […] Proper diagnosis of normocalcemic primary hyperparathyroidism is challenging, because there are several other causes of high parathyroid hormone levels and normal calcium levels. Because several other conditions may mimic normocalcemic primary hyperparathyroidism, detailed blood and sometimes urine testing is required to establish the definitive diagnosis. […] Nearly half of patients diagnosed with normocalcemic primary hyperparathyroidism have been found to have osteoporosis. […] The short answer is that we do not know for sure.
  • #73 Normocalcemic Primary Hyperparathyroidism – Endocrine Surgery | UCLA Health
    https://www.uclahealth.org/medical-services/surgery/endocrine-surgery/conditions-treated/parathyroid/normocalcemic-primary-hyperparathyroidism
    Normocalcemic primary hyperparathyroidism (nPHPT) is suspected when patients calcium level is within the normal range, but parathyroid hormone level is too high. […] Normocalcemic primary hyperparathyroidism (nPHPT) is hypothesized to be an early type of primary hyperparathyroidism. […] Proper diagnosis of normocalcemic primary hyperparathyroidism is challenging, because there are several other causes of high parathyroid hormone levels and normal calcium levels. Because several other conditions may mimic normocalcemic primary hyperparathyroidism, detailed blood and sometimes urine testing is required to establish the definitive diagnosis. […] Nearly half of patients diagnosed with normocalcemic primary hyperparathyroidism have been found to have osteoporosis. […] The short answer is that we do not know for sure.
  • #74 Primary Hyperparathyroidism – StatPearls – NCBI Bookshelf
    https://www.ncbi.nlm.nih.gov/books/NBK441895/
    Malignancy-related hypercalcemia can be found in as many as 20% to 30% of all cancer patients. It can be confused with primary hyperparathyroidism, especially if hypercalcemia symptoms are the first clinical sign of the malignancy. The most common cause of malignancy-related hypercalcemia is the production and secretion of PTH-related protein, most often due to squamous cell carcinoma of the lung and renal cancers. […] […] Up to 10% of primary hyperparathyroidism cases have a genetic basis. Genetic mutations associated with hyperparathyroidism include multiple endocrine neoplasia types 1, 2A, and 4, hyperparathyroidism-jaw tumor syndrome, familial isolated hyperparathyroidism, neonatal severe hyperparathyroidism, and familial hypocalciuric hypercalcemia. A familial syndrome should be considered when primary hyperparathyroidism is diagnosed at an early age or there is a family history of hypercalcemia, pituitary adenomas, pancreatic islet cell tumors, pheochromocytomas, or medullary thyroid cancer.
  • #75 Primary Hyperparathyroidism – StatPearls – NCBI Bookshelf
    https://www.ncbi.nlm.nih.gov/books/NBK441895/
    Malignancy-related hypercalcemia can be found in as many as 20% to 30% of all cancer patients. It can be confused with primary hyperparathyroidism, especially if hypercalcemia symptoms are the first clinical sign of the malignancy. The most common cause of malignancy-related hypercalcemia is the production and secretion of PTH-related protein, most often due to squamous cell carcinoma of the lung and renal cancers. […] […] Up to 10% of primary hyperparathyroidism cases have a genetic basis. Genetic mutations associated with hyperparathyroidism include multiple endocrine neoplasia types 1, 2A, and 4, hyperparathyroidism-jaw tumor syndrome, familial isolated hyperparathyroidism, neonatal severe hyperparathyroidism, and familial hypocalciuric hypercalcemia. A familial syndrome should be considered when primary hyperparathyroidism is diagnosed at an early age or there is a family history of hypercalcemia, pituitary adenomas, pancreatic islet cell tumors, pheochromocytomas, or medullary thyroid cancer.
  • #76 Hypercalcemia in Dogs and Cats – Endocrine System – Merck Veterinary Manual
    https://www.merckvetmanual.com/endocrine-system/the-parathyroid-glands-and-disorders-of-calcium-regulation-in-dogs-and-cats/hypercalcemia-in-dogs-and-cats
    Secondary hyperparathyroidism (SHPT) is characterized by increased PTH concentrations and low or normal calcium. […] Tertiary hyperparathyroidism (THPT) is a condition reflecting the development of abnormal parathyroid function after a period of secondary hyperparathyroidism, resulting in increased concentrations of PTH and ionized calcium. Patients with THPT typically have hypercalcemia, hyperphosphatemia, and increased PTH concentrations. […] Paraneoplastic syndrome, hypoadrenocorticism, nutritional deficiencies and renal disease are other common causes of hypercalcemia in dogs and cats. […] The cancers most commonly associated with hypercalcemia are lymphoma, anal gland adenocarcinoma (dogs) and squamous cell carcinoma (cats). […] Hypercalcemia in cats is most often idiopathic.
  • #77 Hyperparathyroidism Causes, Symptoms and Natural Remedies – Dr. Axe
    https://draxe.com/health/hyperparathyroidism/
    In about 90 percent of people with primary hyperparathyroidism, the underlying cause is a non-cancerous tumor (called an adenoma) in one or more of the parathyroid glands. […] In the other 10 percent of people with this condition, the parathyroid glands become enlarged and produce too much hormone. […] Rarely, a cancerous tumor located on one or more of the parathyroid glands will cause hyperparathyroidism. […] Hyperparathyroidism occurs when too much parathyroid hormone is released, causing increased absorption of calcium in the digestive tract and release of stored calcium in the bones. […] Hyperparathyroidism risk factors include: Being a woman, since this condition is more common among women (especially post-menopausal women) than men. […] Having had radiation therapy in the neck, such as to treat cancer.
  • #78 Primary hyperparathyroidism and psychiatry: manifestations, causes and management | BJPsych Advances | Cambridge Core
    https://www.cambridge.org/core/journals/bjpsych-advances/article/primary-hyperparathyroidism-and-psychiatry-manifestations-causes-and-management/244AE2F2C49F37C671A725650E8BD8BF
    Primary hyperparathyroidism (PHPT) is a relatively common disorder, with an estimated overall prevalence of 0.840.86%. It is the most common cause of persistent hypercalcaemia and the third most common endocrine condition after diabetes and thyroid disease, although it tends to be underdiagnosed. […] PHPT can occur across all ages, but it usually manifests in later life, with a mean age at diagnosis of 65. It affects women three to four times more often than men. […] As awareness of the need to test for PHPT increases, so too will the numbers of people receiving mental health treatment who have PHPT. This underscores the importance of improving psychiatrists’ knowledge of this important topic. […] PHPT is usually sporadic, but it may be inherited as part of a genetic condition that may be syndromic or non-syndromic. Patients with genetic forms of PHPT may present differently and require different management. […] Lithium-associated hyperparathyroidism (LAH) is clinically indistinguishable from PHPT. While the exact mechanisms of LAH remain unclear, hypothetical mechanisms are discussed in greater detail below.
  • #79 Hyperparathyroidism | AAFP
    https://www.aafp.org/pubs/afp/issues/2004/0115/p333.html
    Primary hyperparathyroidism is caused by the inappropriate secretion of PTH, which results in hypercalcemia. The condition usually occurs sporadically, although familial forms are well recognized. In 85 percent of patients with primary hyperparathyroidism, the underlying cause is an adenoma in a single parathyroid gland. Hypertrophy of all four parathyroid glands and multiple adenomas within the parathyroid glands account for the remainder of cases. Fewer than 0.5 percent of cases are caused by parathyroid malignancies. Most patients with primary hyperparathyroidism are postmenopausal women. The incidence of the condition increases with age, and the average age at diagnosis is 55 years. A small percentage of patients presents years after external neck irradiation. Lithium therapy also can be responsible for overactive parathyroid glands, with the excess activity persisting even after discontinuation of the drug. In 10 to 20 percent of patients, primary hyperparathyroidism is caused by an inherited hyperfunction of multiple parathyroid glands. These patients tend to be diagnosed at a younger age. Although rare, familial disorders should be considered in patients diagnosed with primary hyperparathyroidism. With several of these familial disorders, patients should be evaluated for significant associated abnormalities. Familial forms of primary hyperparathyroidism include multiple endocrine neoplasia type I and type II, neonatal severe primary hyperparathyroidism, hyperparathyroidism-jaw tumor syndrome, familial hypocalciuric hypercalcemia, and familial isolated hyperparathyroidism. Approximately 95 percent of patients with multiple endocrine neoplasia type I, or Werner’s syndrome, have associated primary hyperparathyroidism. This syndrome is associated with various tumors, including pancreatic and pituitary adenomas. Patients with multiple endocrine neoplasia type II, or Sipple’s syndrome, may develop a milder form of primary hyperparathyroidism. This syndrome is characterized primarily by medullary thyroid carcinoma and pheochromocytoma. Genetic testing for both syndromes is available in some medical centers. Neonatal severe primary hyperparathyroidism presents with severe hypercalcemia during the newborn period. Hyperparathyroidism-jaw tumor syndrome is a rare condition that usually presents in adolescents or young adults as a solitary adenoma associated with bone lesions in the jaw and with Wilms’ tumor or renal cysts. Familial hypocalciuric hypercalcemia is caused by a single mutation in the calcium-sensing receptor, resulting in insensitivity to feedback inhibition of PTH secretion. In affected patients, the calcium/creatinine clearance ratio is less than 0.01, compared with a calcium/creatinine clearance ratio of greater than 0.02 in patients with primary hyperparathyroidism. Patients with familial hypocalciuric hypercalcemia are asymptomatic and require no treatment. Familial isolated hyperparathyroidism has no specific features. It is usually thought to be an expression of occult multiple endocrine neoplasia type I.
  • #80 Primary hyperparathyroidism and psychiatry: manifestations, causes and management | BJPsych Advances | Cambridge Core
    https://www.cambridge.org/core/journals/bjpsych-advances/article/primary-hyperparathyroidism-and-psychiatry-manifestations-causes-and-management/244AE2F2C49F37C671A725650E8BD8BF
    Primary hyperparathyroidism (PHPT) is a relatively common disorder, with an estimated overall prevalence of 0.840.86%. It is the most common cause of persistent hypercalcaemia and the third most common endocrine condition after diabetes and thyroid disease, although it tends to be underdiagnosed. […] PHPT can occur across all ages, but it usually manifests in later life, with a mean age at diagnosis of 65. It affects women three to four times more often than men. […] As awareness of the need to test for PHPT increases, so too will the numbers of people receiving mental health treatment who have PHPT. This underscores the importance of improving psychiatrists’ knowledge of this important topic. […] PHPT is usually sporadic, but it may be inherited as part of a genetic condition that may be syndromic or non-syndromic. Patients with genetic forms of PHPT may present differently and require different management. […] Lithium-associated hyperparathyroidism (LAH) is clinically indistinguishable from PHPT. While the exact mechanisms of LAH remain unclear, hypothetical mechanisms are discussed in greater detail below.
  • #81 Patient education: Primary hyperparathyroidism (Beyond the Basics) – UpToDate
    https://www.uptodate.com/contents/primary-hyperparathyroidism-beyond-the-basics
    Primary hyperparathyroidism (PHPT) can be caused by several conditions, including: […] A noncancerous tumor (adenoma) due to overgrowth of normal cells in only one of the parathyroid glands. This is the most common cause, occurring in approximately 85 percent of cases. […] Enlargement of more than one parathyroid gland due to an overgrowth of normal cells in these glands, called hyperplasia. This occurs in approximately 15 percent of all cases. […] Parathyroid cancer; this is extremely rare and is due to abnormal (cancerous) overgrowth of cells usually in only one gland. This accounts for less than 1 percent of all cases. […] PHPT can occur at any age but is more common in females who have been through menopause (and no longer have monthly periods). At younger ages (eg, below 40 years), PHPT is more likely to be caused by a rare familial (inherited) hyperparathyroidism syndrome, which usually causes several of the parathyroid glands rather than a single gland to become enlarged. In some types of familial hyperparathyroidism, abnormalities are possible in other endocrine glands, including the pituitary, thyroid, pancreas, or adrenal glands.
  • #82 Primary Hyperparathyroidism – Parathyroid UK
    https://parathyroiduk.org/hyperparathyroidism/primary-hyperparathyroidism/
    In Primary Hyperparathyroidism (PHPT or Hyperpara), too much parathyroid hormone is produced by one or more of the parathyroid glands because they have become enlarged or overactive. This in turn causes the body to release calcium from the bones into the blood and results in high calcium levels (hypercalcaemia). […] The most common cause of PHPT is a parathyroid gland becoming enlarged due to the development of a benign (non-cancerous) tumour called an adenoma. This is more commonly diagnosed in women, particularly postmenopausal women, but can affect both men and women and all ages, including, less commonly, children. […] Sometimes all four parathyroid glands may become enlarged – this is called parathyroid hyperplasia. This may occur sporadically (without a family history) or as part of three familial (inherited) syndromes: multiple endocrine neoplasia 1 (MEN 1) and MEN 2A, and isolated familial hyperparathyroidism. In MEN 1, the problems in the parathyroid glands are associated with other tumours in the pituitary and the pancreas. In MEN 2A, overactivity of the parathyroid glands is associated with tumours in the adrenal gland or thyroid. […] Radiotherapy treatment to your head or neck may increase the risk of developing a parathyroid adenoma or carcinoma (cancer). Only in extremely rare cases indeed will the tumour be due to parathyroid cancer. If you have been diagnosed with parathyroid cancer please go to our Parathyroid Cancer.
  • #83 Patient education: Primary hyperparathyroidism (Beyond the Basics) – UpToDate
    https://www.uptodate.com/contents/primary-hyperparathyroidism-beyond-the-basics
    PHPT has been reported in people who have had past radiation to the head and neck (eg, to treat childhood cancer, to treat certain benign conditions, or after nuclear power plant accidents). People who have been exposed to radiation are more likely to have thyroid nodules (growths on the thyroid gland) as well as PHPT. If thyroid nodules are also present, they may impact the interpretation of some tests and the choice of treatment of PHPT.
  • #84 Causes of Parathyroid Disease, Tumors and Hyperparathyroidism
    https://www.parathyroid.com/causes.htm
    Radiation treatments to the neck and face as a youth or teenager, or as an adult for the treatment of certain cancers. […] These people are also at a much higher risk of developing a parathyroid tumor (always benign, not cancer). […] Long term use of Lithium. […] Many patients (as many as 40%) who have taken Lithium on a daily basis for 10 or more years will develop parathyroid problems. […] Familial (Hereditary) Forms of Hyperparathyroidism. This is just under 1% of all parathyroid patients. […] Hyperparathyroidism that occurs in families can occur in women and men, however, it can show up at any age. […] All four of the parathyroid glands grow big. […] These are not true tumors, but just bigger, juicy parathyroid glands. […] Multiple Endocrine Neoplasia Syndromes (MEN Syndromes). This is far less than 1% of all parathyroid patients. […] All of these patients have 4-gland hyperplasia. […] Kidney Disease. This is actually a different disease — Secondary Hyperparathyroidism. […] The term „Secondary” simply is a descriptive term, implying that the parathyroid glands grew big and juicy and are overproducing PTH in response to the kidney disease.
  • #85 Hyperparathyroidism Causes & Treatment Options | Dr. Babak Larian
    https://www.hyperparathyroidmd.com/hyperparathyroidism/
    Secondary hyperparathyroidism is caused by other medical problems causing the parathyroid glands to secondarily overwork. […] Furthermore, people may be more prone than others to primary or secondary hyperparathyroidism if they fall into any of the following categories: Have received radiation treatment for cancer that exposed the neck to radiation, or for Grave’s Disease. Or radiation exposure, such as living in the area close to Chernobyl or Fukushima, People who have used the medication lithium, Have multiple endocrine neoplasia, type 1 or other rare inherited disorder.
  • #86 Primary Hyperparathyroidism – StatPearls – NCBI Bookshelf
    https://www.ncbi.nlm.nih.gov/books/NBK441895/
    Malignancy-related hypercalcemia can be found in as many as 20% to 30% of all cancer patients. It can be confused with primary hyperparathyroidism, especially if hypercalcemia symptoms are the first clinical sign of the malignancy. The most common cause of malignancy-related hypercalcemia is the production and secretion of PTH-related protein, most often due to squamous cell carcinoma of the lung and renal cancers. […] […] Up to 10% of primary hyperparathyroidism cases have a genetic basis. Genetic mutations associated with hyperparathyroidism include multiple endocrine neoplasia types 1, 2A, and 4, hyperparathyroidism-jaw tumor syndrome, familial isolated hyperparathyroidism, neonatal severe hyperparathyroidism, and familial hypocalciuric hypercalcemia. A familial syndrome should be considered when primary hyperparathyroidism is diagnosed at an early age or there is a family history of hypercalcemia, pituitary adenomas, pancreatic islet cell tumors, pheochromocytomas, or medullary thyroid cancer.
  • #87 Familial hyperparathyroidism — Knowledge Hub
    https://www.genomicseducation.hee.nhs.uk/genotes/knowledge-hub/familial-hyperparathyroidism/
    Familial hyperparathyroidism is a genetic condition that predisposes affected individuals to parathyroid hormone-mediated hypercalcaemia, which presents in varying degrees. […] Familial hyperparathyroidism is a genetic predisposition to parathyroid hormone (PTH)-mediated hypercalcaemia. Primary hyperparathyroidism (PHPT) is a common condition and approximately 1-in-10 cases are caused by a hereditary syndrome. […] Hereditary forms of PHPT may occur as an isolated endocrinopathy or as part of one of several multiple-tumour syndromes. […] Variants in several genes have been associated with familial PHPT, including CDC73, CDKN1B, GCM2, MEN1, RET and CASR. […] Pathogenic variants in the CDKN1B gene are associated with a rare form of multiple endocrine neoplasia (MEN) known as MEN type 4 (MEN4), which results in PHPT.
  • #88 Familial hyperparathyroidism — Knowledge Hub
    https://www.genomicseducation.hee.nhs.uk/genotes/knowledge-hub/familial-hyperparathyroidism/
    Familial hyperparathyroidism is a genetic condition that predisposes affected individuals to parathyroid hormone-mediated hypercalcaemia, which presents in varying degrees. […] Familial hyperparathyroidism is a genetic predisposition to parathyroid hormone (PTH)-mediated hypercalcaemia. Primary hyperparathyroidism (PHPT) is a common condition and approximately 1-in-10 cases are caused by a hereditary syndrome. […] Hereditary forms of PHPT may occur as an isolated endocrinopathy or as part of one of several multiple-tumour syndromes. […] Variants in several genes have been associated with familial PHPT, including CDC73, CDKN1B, GCM2, MEN1, RET and CASR. […] Pathogenic variants in the CDKN1B gene are associated with a rare form of multiple endocrine neoplasia (MEN) known as MEN type 4 (MEN4), which results in PHPT.
  • #89 Familial hyperparathyroidism — Knowledge Hub
    https://www.genomicseducation.hee.nhs.uk/genotes/knowledge-hub/familial-hyperparathyroidism/
    Familial hyperparathyroidism is a genetic condition that predisposes affected individuals to parathyroid hormone-mediated hypercalcaemia, which presents in varying degrees. […] Familial hyperparathyroidism is a genetic predisposition to parathyroid hormone (PTH)-mediated hypercalcaemia. Primary hyperparathyroidism (PHPT) is a common condition and approximately 1-in-10 cases are caused by a hereditary syndrome. […] Hereditary forms of PHPT may occur as an isolated endocrinopathy or as part of one of several multiple-tumour syndromes. […] Variants in several genes have been associated with familial PHPT, including CDC73, CDKN1B, GCM2, MEN1, RET and CASR. […] Pathogenic variants in the CDKN1B gene are associated with a rare form of multiple endocrine neoplasia (MEN) known as MEN type 4 (MEN4), which results in PHPT.
  • #90 So you have primary hyperparathyroidism – Harvard Health
    https://www.health.harvard.edu/newsletter_article/so_you_have_primary_hyperparathyroidism
    Primary hyperparathyroidism is a disorder of the parathyroids, four tiny pea-sized glands located behind the thyroid gland in the neck. […] The usual cause is an adenoma a noncancerous tumor. […] In primary hyperparathyroidism, one or more parathyroid glands produce more PTH than needed, raising calcium levels above the normal range. Usually, the cause is a benign (noncancerous) tumor, or adenoma, in a single parathyroid gland. […] Parathyroid glands may become overactive because of lithium therapy, past radiation to the neck, or certain gene defects. […] Roughly 3% to 5% of cases are linked to inherited syndromes. […] In some cases, the cause is simply unknown.
  • #91 Primary hyperparathyroidism and psychiatry: manifestations, causes and management | BJPsych Advances | Cambridge Core
    https://www.cambridge.org/core/journals/bjpsych-advances/article/primary-hyperparathyroidism-and-psychiatry-manifestations-causes-and-management/244AE2F2C49F37C671A725650E8BD8BF
    The mechanisms underlying the occurrence of hyperparathyroidism with lithium use are poorly understood. There are three theories currently in contention. According to the set-point theory, lithium disrupts calcium-sensing receptors (CaSR) on the parathyroid glands, increasing the calcium set point at which suppression of parathyroid hormone release occurs. […] Another theory suggests that lithium aggressively unmasks a parathyroid gland’s existing predisposition for disease. Finally, a third theory suggests that lithium directly stimulates increased parathyroid hormone secretion which, over time, results in gland hyperplasia. […] Studies have correlated lithium use with increased serum calcium and parathyroid hormone levels. […] The largest comprehensive review monitored 423 lithium users in two different locations. Of these, 18% were identified as suffering from LAH. Those with LAH had a median age of 65 years and the majority were women. […] The absolute risk of PHPT is 100 times greater with lithium use compared with risk in the general population.
  • #92 Secondary hyperparathyroidism: symptoms, causes & treatment | American Kidney Fund
    https://www.kidneyfund.org/living-kidney-disease/health-problems-caused-kidney-disease/secondary-hyperparathyroidism-symptoms-causes-treatment
    Secondary hyperparathyroidism (SHPT) is common in people who have kidney failure (stage 5 kidney disease). […] SHPT happens when another disease you have causes low levels of calcium in your blood. The most common cause of SHPT is end-stage renal disease (ESRD), also known as kidney failure. […] As your kidneys fail, they are no longer able to change inactive vitamin D to active vitamin D. This creates low levels of vitamin D in your body. When you have low levels of vitamin D, your body absorbs less calcium, and the level of calcium in your blood becomes low. This signals your parathyroid glands to make more PTH and grow larger, which causes SHPT. Your doctor may also call this „renal secondary hyperparathyroidism”.
  • #93 Hyperparathyroidism Causes, Symptoms and Natural Remedies – Dr. Axe
    https://draxe.com/health/hyperparathyroidism/
    Genetic inheritance or family history of hyperparathyroidism. […] Having a history of multiple endocrine neoplasia, which is a rare hereditary disorder. […] History of kidney disease or kidney failure. […] Severe calcium deficiency. […] Severe vitamin D deficiency, which affects calcium absorption. […] Taking the drug lithium, which is most often used to treat bipolar disorder.
  • #94 Hyperparathyroidism Causes, Symptoms and Natural Remedies – Dr. Axe
    https://draxe.com/health/hyperparathyroidism/
    Genetic inheritance or family history of hyperparathyroidism. […] Having a history of multiple endocrine neoplasia, which is a rare hereditary disorder. […] History of kidney disease or kidney failure. […] Severe calcium deficiency. […] Severe vitamin D deficiency, which affects calcium absorption. […] Taking the drug lithium, which is most often used to treat bipolar disorder.
  • #95 Hyperparathyroidism – Wikipedia
    https://en.wikipedia.org/wiki/Hyperparathyroidism
    Causes of primary hyperparathyroidism include parathyroid adenoma (80% of patients), multiglandular disease usually seen as hyperplasia of the 4 parathyroid glands (15-20% of patients), parathyroid carcinoma (less than 1% of patients). […] Primary hyperparathyroidism occurs sporadically and most patients do not have a family history. […] Radiation exposure increases the risk of primary hyperparathyroidism. […] Additional risk factors include lithium and thiazide diuretics exposure. […] A number of genetic conditions including multiple endocrine neoplasia syndromes, hyperparathyroidism-jaw tumor syndrome, familial hypocalciuric hypercalcemia, neonatal severe hyperparathyroidism also increase the risk. […] The most common causes for secondary hyperparathyroidism include vitamin D deficiency, chronic kidney disease, inadequate calcium intake, malabsorption. […] Tertiary hyperparathyroidism most commonly occurs from prolonged secondary hyperparathyroidism.
  • #96 Primary hyperparathyroidism: Pathogenesis and etiology – UpToDate
    https://www.uptodate.com/contents/primary-hyperparathyroidism-pathogenesis-and-etiology
    Primary hyperparathyroidism is characterized by abnormal regulation of PTH secretion by calcium, resulting in hypersecretion of PTH relative to the serum calcium concentration. […] Experimental findings have advanced our understanding of the pathophysiology and causes of primary hyperparathyroidism. […] ETIOLOGY […] Radiation exposure […] Environmental chemicals […] Calcium intake […] Genetic or chromosomal defects […] Cyclin D1/PRAD1 gene […] MEN1 gene […] CDKN1B and other CDKI genes […] CDC73/HRPT2 gene […] ZFX gene […] RET gene […] Vitamin D receptor gene […] Other candidate genes […] Ectopic PTH gene expression.
  • #97 Primary Hyperparathyroidism – StatPearls – NCBI Bookshelf
    https://www.ncbi.nlm.nih.gov/books/NBK441895/
    Primary hyperparathyroidism is a disorder characterized by excessive production of PTH. It is the third most common endocrine disorder after diabetes and thyroid disorders. Eighty percent of patients will present with a single adenoma, approximately 15% with hyperplasia of all 4 glands, 2% to 4% with multiple adenomas, and fewer than 1% with parathyroid carcinoma. A combination of increased clonal proliferation of parathyroid tissue with reduced CaSR usually causes primary hyperparathyroidism. Most of these adenomas will be located in the parathyroid glands, but in up to 10% of cases, they may be in an ectopic location. Potential ectopic locations include the thymus, thyroid, pericardium, retro-esophageal space, or superior mediastinum. More unusual locations to find ectopic parathyroid glands would be in the pharynx, lateral neck, or esophagus. […]
  • #98 Primary Hyperparathyroidism – StatPearls – NCBI Bookshelf
    https://www.ncbi.nlm.nih.gov/books/NBK441895/
    Normocalcemic primary hyperparathyroidism is the presence of persistently elevated PTH levels over at least 6 months despite normal corrected serum calcium and ionized calcium concentrations after excluding all causes of secondary hyperparathyroidism, including calcium and vitamin D deficiencies. Imaging studies to identify hyperfunctioning parathyroid glands are less likely to be positive than those with classical hypercalcemic primary hyperparathyroidism. Evaluation and treatment are similar to primary hyperparathyroidism. […] […] Lithium use can cause a degree of CaSR resistance, requiring higher serum calcium levels to suppress PTH secretion. The incidence of this effect is unknown, as PTH levels are not routinely checked in patients on lithium therapy, and cases are often asymptomatic. Lab values will generally show hypercalcemia, non-suppressed PTH, normal serum phosphorus, and hypocalciuria similar to familial hypocalciuric hypercalcemia. Lithium-related hyperparathyroidism is considered secondary hyperparathyroidism but can be associated with parathyroid gland hypertrophy requiring surgery and can present similarly to primary hyperparathyroidism. […]
  • #99 Primary Hyperparathyroidism – StatPearls – NCBI Bookshelf
    https://www.ncbi.nlm.nih.gov/books/NBK441895/
    Primary hyperparathyroidism is a disorder characterized by excessive production of PTH. It is the third most common endocrine disorder after diabetes and thyroid disorders. Eighty percent of patients will present with a single adenoma, approximately 15% with hyperplasia of all 4 glands, 2% to 4% with multiple adenomas, and fewer than 1% with parathyroid carcinoma. A combination of increased clonal proliferation of parathyroid tissue with reduced CaSR usually causes primary hyperparathyroidism. Most of these adenomas will be located in the parathyroid glands, but in up to 10% of cases, they may be in an ectopic location. Potential ectopic locations include the thymus, thyroid, pericardium, retro-esophageal space, or superior mediastinum. More unusual locations to find ectopic parathyroid glands would be in the pharynx, lateral neck, or esophagus. […]
  • #100 Pediatric Hyperparathyroidism: Practice Essentials, Pathophysiology, Etiology
    https://emedicine.medscape.com/article/921453-overview
    The main causes of hyperparathyroidism by age groups are detailed in Table 1. Homozygous inactivating CASR mutations lead to NSHPT, while heterozygous mutations are observed mainly in the milder form, familial hypocalciuric hypercalcemia (FHH), although cases of NSHPT with heterozygous mutations have been reported. FHH is inherited in an autosomal dominant manner, but may be sporadic. Additionally, mutations in the G protein subunit 1 and AP2S1 gene have recently been found to cause FHH. FHH manifests with mild hypercalcemia associated with hypocalciuria, most often not requiring specific treatment. […] In older children and adolescents primary hyperparathyroidism is most often caused by isolated sporadic parathyroid adenomas (80-92%). The remaining are due to multiglandular parathyroid hyperplasia observed in familial endocrine neoplastic syndromes, in which cases a family history of endocrine tumors with an autosomal dominant pattern of inheritance often exists. Multiple endocrine neoplasia type 1 is caused by a mutation in the gene MEN1 which encodes menin, a tumor suppressor protein. Hyperparathyroidism is the presenting sign in 95% of patients with MEN1, while pancreatic and pituitary tumors develop in 40 and 30% of cases respectively. MEN 2A is caused by mutations in the c-ret proto-oncogene (RET), which encodes a tyrosine kinase receptor. MEN 2A presents with medullary thyroid carcinoma associated with hyperparathyroidism (20%) and pheochromocytoma (50%). MEN 4 is caused by mutations in CDKN1B, a cyclin dependent kinase inhibitor, and has been diagnosed in a small percentage of patients with the tumors associated with MEN1 in addition to adrenal, gonadal and thyroid tumors. Hyperparathyroidism jaw tumor syndrome is caused by mutations in cell division cycle 73 gene (CDC73), which codes for parafibromin, a nuclear protein thought to be a tumor suppressor gene. In this syndrome, osseous fibromas of the jaw are associated with parathyroid adenomas or carcinomas, and renal and uterine tumors may also be found. In general, parathyroid carcinoma is very rare in children with 11 cases reported in the English literature in the past 41 years.
  • #101 Familial isolated hyperparathyroidism: MedlinePlus GeneticsLock
    https://medlineplus.gov/genetics/condition/familial-isolated-hyperparathyroidism/
    Familial isolated hyperparathyroidism can be caused by mutations in the MEN1, CDC73, or CASR gene. […] In familial isolated hyperparathyroidism, MEN1 gene mutations result in an altered menin protein that is no longer able to control cell growth and division. […] The CDC73 gene mutations that cause familial isolated hyperparathyroidism likely result in decreased activity of the parafibromin protein. […] CASR gene mutations associated with familial isolated hyperparathyroidism lead to the production of a less sensitive CaSR that requires an abnormally high concentration of calcium to trigger signaling. […] Mutations in the MEN1 gene and the CDC73 gene are involved in other conditions in which hyperparathyroidism is just one of many features. […] In many individuals with the signs and symptoms of familial isolated hyperparathyroidism, a mutation in the MEN1, CDC73, or CASR gene has not been identified, indicating that other genes may be involved in this condition.
  • #102 Pediatric Hyperparathyroidism: Practice Essentials, Pathophysiology, Etiology
    https://emedicine.medscape.com/article/921453-overview
    The main causes of hyperparathyroidism by age groups are detailed in Table 1. Homozygous inactivating CASR mutations lead to NSHPT, while heterozygous mutations are observed mainly in the milder form, familial hypocalciuric hypercalcemia (FHH), although cases of NSHPT with heterozygous mutations have been reported. FHH is inherited in an autosomal dominant manner, but may be sporadic. Additionally, mutations in the G protein subunit 1 and AP2S1 gene have recently been found to cause FHH. FHH manifests with mild hypercalcemia associated with hypocalciuria, most often not requiring specific treatment. […] In older children and adolescents primary hyperparathyroidism is most often caused by isolated sporadic parathyroid adenomas (80-92%). The remaining are due to multiglandular parathyroid hyperplasia observed in familial endocrine neoplastic syndromes, in which cases a family history of endocrine tumors with an autosomal dominant pattern of inheritance often exists. Multiple endocrine neoplasia type 1 is caused by a mutation in the gene MEN1 which encodes menin, a tumor suppressor protein. Hyperparathyroidism is the presenting sign in 95% of patients with MEN1, while pancreatic and pituitary tumors develop in 40 and 30% of cases respectively. MEN 2A is caused by mutations in the c-ret proto-oncogene (RET), which encodes a tyrosine kinase receptor. MEN 2A presents with medullary thyroid carcinoma associated with hyperparathyroidism (20%) and pheochromocytoma (50%). MEN 4 is caused by mutations in CDKN1B, a cyclin dependent kinase inhibitor, and has been diagnosed in a small percentage of patients with the tumors associated with MEN1 in addition to adrenal, gonadal and thyroid tumors. Hyperparathyroidism jaw tumor syndrome is caused by mutations in cell division cycle 73 gene (CDC73), which codes for parafibromin, a nuclear protein thought to be a tumor suppressor gene. In this syndrome, osseous fibromas of the jaw are associated with parathyroid adenomas or carcinomas, and renal and uterine tumors may also be found. In general, parathyroid carcinoma is very rare in children with 11 cases reported in the English literature in the past 41 years.
  • #103 Familial hyperparathyroidism — Knowledge Hub
    https://www.genomicseducation.hee.nhs.uk/genotes/knowledge-hub/familial-hyperparathyroidism/
    PHPT is the most common manifestation of multiple endocrine neoplasia type 1 (MEN1), which is an autosomal dominant endocrine neoplasia syndrome characterised by parathyroid, pituitary and gastropancreatic endocrine tumours. […] Activating pathogenic variants in the RET gene are associated with multiple endocrine neoplasia type 2a (MEN2A), which is characterised by medullary thyroid carcinoma, phaeochromocytoma and parathyroid tumours. […] Although the majority of patients with pathogenic loss-of-function variants in CASR are associated with FHH type 1, a small number of individuals with CASR variants have been reported to have features of primary hyperparathyroidism as part of apparent FIHP. […] The above conditions are inherited in an autosomal dominant manner and are typically associated with a high degree of penetrance (with the exception of activating GCM2 variants).
  • #104 Familial isolated hyperparathyroidism: MedlinePlus GeneticsLock
    https://medlineplus.gov/genetics/condition/familial-isolated-hyperparathyroidism/
    Familial isolated hyperparathyroidism can be caused by mutations in the MEN1, CDC73, or CASR gene. […] In familial isolated hyperparathyroidism, MEN1 gene mutations result in an altered menin protein that is no longer able to control cell growth and division. […] The CDC73 gene mutations that cause familial isolated hyperparathyroidism likely result in decreased activity of the parafibromin protein. […] CASR gene mutations associated with familial isolated hyperparathyroidism lead to the production of a less sensitive CaSR that requires an abnormally high concentration of calcium to trigger signaling. […] Mutations in the MEN1 gene and the CDC73 gene are involved in other conditions in which hyperparathyroidism is just one of many features. […] In many individuals with the signs and symptoms of familial isolated hyperparathyroidism, a mutation in the MEN1, CDC73, or CASR gene has not been identified, indicating that other genes may be involved in this condition.
  • #105 Familial hyperparathyroidism — Knowledge Hub
    https://www.genomicseducation.hee.nhs.uk/genotes/knowledge-hub/familial-hyperparathyroidism/
    Familial hyperparathyroidism is a genetic condition that predisposes affected individuals to parathyroid hormone-mediated hypercalcaemia, which presents in varying degrees. […] Familial hyperparathyroidism is a genetic predisposition to parathyroid hormone (PTH)-mediated hypercalcaemia. Primary hyperparathyroidism (PHPT) is a common condition and approximately 1-in-10 cases are caused by a hereditary syndrome. […] Hereditary forms of PHPT may occur as an isolated endocrinopathy or as part of one of several multiple-tumour syndromes. […] Variants in several genes have been associated with familial PHPT, including CDC73, CDKN1B, GCM2, MEN1, RET and CASR. […] Pathogenic variants in the CDKN1B gene are associated with a rare form of multiple endocrine neoplasia (MEN) known as MEN type 4 (MEN4), which results in PHPT.
  • #106 Primary hyperparathyroidism: Pathogenesis and etiology – UpToDate
    https://www.uptodate.com/contents/primary-hyperparathyroidism-pathogenesis-and-etiology
    Primary hyperparathyroidism is characterized by abnormal regulation of PTH secretion by calcium, resulting in hypersecretion of PTH relative to the serum calcium concentration. […] Experimental findings have advanced our understanding of the pathophysiology and causes of primary hyperparathyroidism. […] ETIOLOGY […] Radiation exposure […] Environmental chemicals […] Calcium intake […] Genetic or chromosomal defects […] Cyclin D1/PRAD1 gene […] MEN1 gene […] CDKN1B and other CDKI genes […] CDC73/HRPT2 gene […] ZFX gene […] RET gene […] Vitamin D receptor gene […] Other candidate genes […] Ectopic PTH gene expression.
  • #107 Pediatric Hyperparathyroidism: Practice Essentials, Pathophysiology, Etiology
    https://emedicine.medscape.com/article/921453-overview
    The main causes of hyperparathyroidism by age groups are detailed in Table 1. Homozygous inactivating CASR mutations lead to NSHPT, while heterozygous mutations are observed mainly in the milder form, familial hypocalciuric hypercalcemia (FHH), although cases of NSHPT with heterozygous mutations have been reported. FHH is inherited in an autosomal dominant manner, but may be sporadic. Additionally, mutations in the G protein subunit 1 and AP2S1 gene have recently been found to cause FHH. FHH manifests with mild hypercalcemia associated with hypocalciuria, most often not requiring specific treatment. […] In older children and adolescents primary hyperparathyroidism is most often caused by isolated sporadic parathyroid adenomas (80-92%). The remaining are due to multiglandular parathyroid hyperplasia observed in familial endocrine neoplastic syndromes, in which cases a family history of endocrine tumors with an autosomal dominant pattern of inheritance often exists. Multiple endocrine neoplasia type 1 is caused by a mutation in the gene MEN1 which encodes menin, a tumor suppressor protein. Hyperparathyroidism is the presenting sign in 95% of patients with MEN1, while pancreatic and pituitary tumors develop in 40 and 30% of cases respectively. MEN 2A is caused by mutations in the c-ret proto-oncogene (RET), which encodes a tyrosine kinase receptor. MEN 2A presents with medullary thyroid carcinoma associated with hyperparathyroidism (20%) and pheochromocytoma (50%). MEN 4 is caused by mutations in CDKN1B, a cyclin dependent kinase inhibitor, and has been diagnosed in a small percentage of patients with the tumors associated with MEN1 in addition to adrenal, gonadal and thyroid tumors. Hyperparathyroidism jaw tumor syndrome is caused by mutations in cell division cycle 73 gene (CDC73), which codes for parafibromin, a nuclear protein thought to be a tumor suppressor gene. In this syndrome, osseous fibromas of the jaw are associated with parathyroid adenomas or carcinomas, and renal and uterine tumors may also be found. In general, parathyroid carcinoma is very rare in children with 11 cases reported in the English literature in the past 41 years.
  • #108 Primary hyperparathyroidism: Pathogenesis and etiology – UpToDate
    https://www.uptodate.com/contents/primary-hyperparathyroidism-pathogenesis-and-etiology
    Primary hyperparathyroidism is characterized by abnormal regulation of PTH secretion by calcium, resulting in hypersecretion of PTH relative to the serum calcium concentration. […] Experimental findings have advanced our understanding of the pathophysiology and causes of primary hyperparathyroidism. […] ETIOLOGY […] Radiation exposure […] Environmental chemicals […] Calcium intake […] Genetic or chromosomal defects […] Cyclin D1/PRAD1 gene […] MEN1 gene […] CDKN1B and other CDKI genes […] CDC73/HRPT2 gene […] ZFX gene […] RET gene […] Vitamin D receptor gene […] Other candidate genes […] Ectopic PTH gene expression.
  • #109 Familial isolated hyperparathyroidism: MedlinePlus GeneticsLock
    https://medlineplus.gov/genetics/condition/familial-isolated-hyperparathyroidism/
    Familial isolated hyperparathyroidism can be caused by mutations in the MEN1, CDC73, or CASR gene. […] In familial isolated hyperparathyroidism, MEN1 gene mutations result in an altered menin protein that is no longer able to control cell growth and division. […] The CDC73 gene mutations that cause familial isolated hyperparathyroidism likely result in decreased activity of the parafibromin protein. […] CASR gene mutations associated with familial isolated hyperparathyroidism lead to the production of a less sensitive CaSR that requires an abnormally high concentration of calcium to trigger signaling. […] Mutations in the MEN1 gene and the CDC73 gene are involved in other conditions in which hyperparathyroidism is just one of many features. […] In many individuals with the signs and symptoms of familial isolated hyperparathyroidism, a mutation in the MEN1, CDC73, or CASR gene has not been identified, indicating that other genes may be involved in this condition.
  • #110 Secondary hyperparathyroidism: causes, symptoms and treatment
    https://www.kidneyresearchuk.org/conditions-symptoms/secondary-hyperparathyroidism/
    Secondary hyperparathyroidism occurs as a result of chronic kidney disease (CKD). […] Three things cause increased production of PTH: low blood calcium, low levels of activated vitamin D, and high phosphate levels. All three occur in chronic kidney disease. […] This triggers the parathyroid glands to overproduce PTH in an attempt to increase the amount of calcium in the blood. […] If left for too long, the parathyroid glands can remain overactive all the time. This is known as tertiary hyperparathyroidism. […] Treatment for secondary hyperparathyroidism includes: Changes to diet to control the intake of phosphate, Tablets including phosphate binders and vitamin D supplements, Surgery to remove the parathyroid glands, either completely or leaving a small amount of gland in place, A newer class of drugs called calcimimetics (cinacalcet, etelcalcitide) that mimic the action of calcium on tissues and suppress the production of PTH.
  • #111 Secondary hyperparathyroidism: causes, symptoms and treatment
    https://www.kidneyresearchuk.org/conditions-symptoms/secondary-hyperparathyroidism/
    Secondary hyperparathyroidism occurs as a result of chronic kidney disease (CKD). […] Three things cause increased production of PTH: low blood calcium, low levels of activated vitamin D, and high phosphate levels. All three occur in chronic kidney disease. […] This triggers the parathyroid glands to overproduce PTH in an attempt to increase the amount of calcium in the blood. […] If left for too long, the parathyroid glands can remain overactive all the time. This is known as tertiary hyperparathyroidism. […] Treatment for secondary hyperparathyroidism includes: Changes to diet to control the intake of phosphate, Tablets including phosphate binders and vitamin D supplements, Surgery to remove the parathyroid glands, either completely or leaving a small amount of gland in place, A newer class of drugs called calcimimetics (cinacalcet, etelcalcitide) that mimic the action of calcium on tissues and suppress the production of PTH.
  • #112 Secondary hyperparathyroidism: causes, symptoms and treatment
    https://www.kidneyresearchuk.org/conditions-symptoms/secondary-hyperparathyroidism/
    Secondary hyperparathyroidism occurs as a result of chronic kidney disease (CKD). […] Three things cause increased production of PTH: low blood calcium, low levels of activated vitamin D, and high phosphate levels. All three occur in chronic kidney disease. […] This triggers the parathyroid glands to overproduce PTH in an attempt to increase the amount of calcium in the blood. […] If left for too long, the parathyroid glands can remain overactive all the time. This is known as tertiary hyperparathyroidism. […] Treatment for secondary hyperparathyroidism includes: Changes to diet to control the intake of phosphate, Tablets including phosphate binders and vitamin D supplements, Surgery to remove the parathyroid glands, either completely or leaving a small amount of gland in place, A newer class of drugs called calcimimetics (cinacalcet, etelcalcitide) that mimic the action of calcium on tissues and suppress the production of PTH.
  • #113 Hyperparathyroidism: Background, Anatomy and Embryology, Primary Hyperparathyroidism
    https://emedicine.medscape.com/article/127351-overview
    Secondary hyperparathyroidism results from a chronic stimulus of the parathyroid gland to release parathyroid hormone. Parathyroid hormone release is increased in the setting of hypocalcemia and hyperphosphatemia and is decreased by fibroblast growth factor 23 (FGF-23). […] Tertiary disease is characterized by the development of autonomous hypersecretion of parathyroid hormone, causing hypercalcemia. The etiology is unknown but may be due to monoclonal expansion of parathyroid cells (nodule formation within hyperplastic glands). A change may occur in the set point of the calcium-sensing mechanism to hypercalcemic levels. Four-gland involvement occurs in most patients.
  • #114 Hyperparathyroidism | AAFP
    https://www.aafp.org/pubs/afp/issues/1998/0415/p1795.html
    Hyperparathyroidism is a common cause of hypercalcemia. […] In 85 percent of the persons affected, hyperparathyroidism is the result of an adenoma in a single parathyroid gland. Hypertrophy of all four parathyroid glands causes hyperparathyroidism in 15 percent of patients. A very small number of cases of hyperparathyroidism result from parathyroid malignancies. […] In addition, the incidence of hyperparathyroidism is higher in patients with type I and type II multiple endocrine neoplasia syndromes, in patients with familial hyperparathyroidism and in patients who received radiation therapy to the head and neck area for benign diseases during childhood. […] Secondary hyperparathyroidism occurs when the parathyroid glands are chronically stimulated to release parathyroid hormone. A decrease in circulating calcium is the stimulus for this release. Chronic renal failure, rickets and malabsorption syndromes are the most frequent conditions leading to secondary hyperparathyroidism. […] In some cases of prolonged secondary hyperparathyroidism, the glands take on an autonomous function manifested by continued high levels of parathyroid hormone despite resolution of the original stimulus. This state is referred to as tertiary hyperparathyroidism.
  • #115 Hyperparathyroidism: Symptoms, Causes, & Treatment
    https://patient.info/hormones/thyroid-and-parathyroid-glands/hyperparathyroidism
    Tertiary hyperparathyroidism occurs as a result of long-standing secondary hyperparathyroidism. In tertiary hyperparathyroidism, the condition that was causing your low blood calcium level and the secondary hyperparathyroidism, has been treated (or your blood calcium level has been brought back to normal). […] However, your parathyroid glands continue to produce large amounts of parathyroid hormone. This is because they start to act by themselves (autonomously) and are no longer sensitive to your blood calcium level. They are not 'switched off’ when your blood calcium level rises. This results in a high calcium level in your blood.
  • #116 Hyperparathyroidism: Background, Anatomy and Embryology, Primary Hyperparathyroidism
    https://emedicine.medscape.com/article/127351-overview
    Secondary hyperparathyroidism results from a chronic stimulus of the parathyroid gland to release parathyroid hormone. Parathyroid hormone release is increased in the setting of hypocalcemia and hyperphosphatemia and is decreased by fibroblast growth factor 23 (FGF-23). […] Tertiary disease is characterized by the development of autonomous hypersecretion of parathyroid hormone, causing hypercalcemia. The etiology is unknown but may be due to monoclonal expansion of parathyroid cells (nodule formation within hyperplastic glands). A change may occur in the set point of the calcium-sensing mechanism to hypercalcemic levels. Four-gland involvement occurs in most patients.
  • #117 Hyperparathyroidism (Types, Causes, Symptoms and Treatment)
    https://patient.info/doctor/hyperparathyroidism-pro
    Hyperparathyroidism causes4 […] Excess PTH is produced by one or more of the parathyroid glands, due to: […] A single parathyroid gland adenoma (85% of cases). […] Parathyroid hyperplasia (10-12%). […] Double adenomas (4-5%). […] Parathyroid carcinoma (less than 1%). […] The aetiology of adenomas or hyperplasia is largely unknown. […] There may be an association with ionising radiation. […] Familial cases can occur as part of the multiple endocrine neoplasia syndromes (MEN 1 or MEN 2a), hyperparathyroid-jaw tumour (HPT-JT) syndrome, or familial isolated hyperparathyroidism (FIHPT). […] […] […] Secondary hyperparathyroidism causes […] Secondary hyperparathyroidism (SHPT) is most commonly seen in the setting of chronic kidney disease (CKD). […] The parathyroid glands become hyperplastic after long-term stimulation in response to chronic hypocalcaemia.
  • #118 Primary hyperparathyroidism and psychiatry: manifestations, causes and management | BJPsych Advances | Cambridge Core
    https://www.cambridge.org/core/journals/bjpsych-advances/article/primary-hyperparathyroidism-and-psychiatry-manifestations-causes-and-management/244AE2F2C49F37C671A725650E8BD8BF
    The mechanisms underlying the occurrence of hyperparathyroidism with lithium use are poorly understood. There are three theories currently in contention. According to the set-point theory, lithium disrupts calcium-sensing receptors (CaSR) on the parathyroid glands, increasing the calcium set point at which suppression of parathyroid hormone release occurs. […] Another theory suggests that lithium aggressively unmasks a parathyroid gland’s existing predisposition for disease. Finally, a third theory suggests that lithium directly stimulates increased parathyroid hormone secretion which, over time, results in gland hyperplasia. […] Studies have correlated lithium use with increased serum calcium and parathyroid hormone levels. […] The largest comprehensive review monitored 423 lithium users in two different locations. Of these, 18% were identified as suffering from LAH. Those with LAH had a median age of 65 years and the majority were women. […] The absolute risk of PHPT is 100 times greater with lithium use compared with risk in the general population.
  • #119 Primary hyperparathyroidism: Pathogenesis and etiology – UpToDate
    https://www.uptodate.com/contents/primary-hyperparathyroidism-pathogenesis-and-etiology
    Primary hyperparathyroidism is characterized by abnormal regulation of PTH secretion by calcium, resulting in hypersecretion of PTH relative to the serum calcium concentration. […] Experimental findings have advanced our understanding of the pathophysiology and causes of primary hyperparathyroidism. […] ETIOLOGY […] Radiation exposure […] Environmental chemicals […] Calcium intake […] Genetic or chromosomal defects […] Cyclin D1/PRAD1 gene […] MEN1 gene […] CDKN1B and other CDKI genes […] CDC73/HRPT2 gene […] ZFX gene […] RET gene […] Vitamin D receptor gene […] Other candidate genes […] Ectopic PTH gene expression.
  • #120 Hyperparathyroidism, arterial hypertension and aortic stiffness: a possible bidirectional link between the adrenal cortex and the parathyroid glands that causes vascular damage? | Hypertension Research
    https://www.nature.com/articles/hr2010251
    Primary hyperparathyroidism (PPTH) is generally thought to be a common endocrine disorder. However, it represents an uncommon endocrine cause of arterial hypertension, with a likely prevalence among hypertensive patients of less than 0.01% an imprecise estimate because of the lack of prospective studies. […] Despite these findings, the mechanisms by which PPTH is associated with hypertension and increased cardiovascular risk remain poorly understood and somewhat intriguing. […] Therefore, that excess PTH per se has a major detrimental effect on the arterial wall, as shown by increased BP and induced stiffening of the aorta. […] Given the secretagogue effect of parathyroid hormone (PTH) on aldosterone, the excess secretion of PTH can cause absolute or relative hyperaldosteronism; the excess secretion may be either due to primary hyperparathyroidism (PPTH) or secondary to 25-OH vitamin D deficiency or to its impaired renal activation by 1 hydroxylase in patients with chronic renal insufficiency.
  • #121 Hyperparathyroidism, arterial hypertension and aortic stiffness: a possible bidirectional link between the adrenal cortex and the parathyroid glands that causes vascular damage? | Hypertension Research
    https://www.nature.com/articles/hr2010251
    Primary hyperparathyroidism (PPTH) is generally thought to be a common endocrine disorder. However, it represents an uncommon endocrine cause of arterial hypertension, with a likely prevalence among hypertensive patients of less than 0.01% an imprecise estimate because of the lack of prospective studies. […] Despite these findings, the mechanisms by which PPTH is associated with hypertension and increased cardiovascular risk remain poorly understood and somewhat intriguing. […] Therefore, that excess PTH per se has a major detrimental effect on the arterial wall, as shown by increased BP and induced stiffening of the aorta. […] Given the secretagogue effect of parathyroid hormone (PTH) on aldosterone, the excess secretion of PTH can cause absolute or relative hyperaldosteronism; the excess secretion may be either due to primary hyperparathyroidism (PPTH) or secondary to 25-OH vitamin D deficiency or to its impaired renal activation by 1 hydroxylase in patients with chronic renal insufficiency.
  • #122 Hyperparathyroidism: Understanding Parathyroid Disease and Treatment Options
    https://www.parathyroid.com/parathyroid-disease.htm
    The high calcium increases your risk of stroke, heart attack, and heart failure due to the aggressive buildup of calcium in the arteries. The high calcium increases the risk of developing several cancers by 2 to 3 times, including breast cancer, colon cancer, kidney cancer and prostate cancer. […] The good news is that hyperparathyroidism is a disease that is easily cured. We don’t „treat” hyperparathyroidism like you would „treat” diabetes. Parathyroid problems are cured by simply taking out the parathyroid tumor that is causing all the troubles.
  • #123 Hyperparathyroidism: Causes, Types, Treatment
    https://www.healthline.com/health/endocrine-health/hyperparathyroidism
    Most cases of secondary hyperparathyroidism are due to vitamin D deficiency and chronic kidney failure that results in low active vitamin D and calcium levels. […] This type occurs after longstanding secondary hyperparathyroidism. The parathyroid glands keep making too much PTH after your calcium levels return to typical levels. This type usually occurs in people with kidney problems. […] Hyperparathyroidism can occur with other conditions that may include: low vitamin D levels, kidney issues, osteoporosis, or bone weakening. […] Primary hyperparathyroidism leads to osteoporosis because high levels of PTH cause the release of calcium from the bones, thereby weakening them.
  • #124 Normocalcemic Primary Hyperparathyroidism – Endocrine Surgery | UCLA Health
    https://www.uclahealth.org/medical-services/surgery/endocrine-surgery/conditions-treated/parathyroid/normocalcemic-primary-hyperparathyroidism
    To diagnose normocalcemic primary hyperparathyroidism, other conditions that may cause high parathyroid hormone levels need to be ruled out. […] One major cause of secondary hyperparathyroidism is vitamin D deficiency. […] Another possible cause of secondary hyperparathyroidism is not eating enough calcium or the intestines not absorbing calcium. […] Kidney failure, or an eGFR of less than 60, causes a problem with vitamin D metabolism. […] Not everyone with normocalcemic primary hyperparathyroidism needs treatment. […] Bone loss related to nPHPT may also be treated with medications used to treat osteopenia and osteoporosis.