Nadczynność tarczycy
Patofizjologia i mechanizm

Nadczynność tarczycy to stan charakteryzujący się nadmierną produkcją hormonów T3 i T4, prowadzącą do tyreotoksykozy i przyspieszenia metabolizmu. Najczęstszą przyczyną jest choroba Gravesa-Basedowa, w której przeciwciała TRAb (IgG1) stymulują receptor TSH, powodując wzrost produkcji hormonów, rozrost gruczołu i zwiększone wychwytywanie jodu. Inne etiologie to toksyczne wole guzkowe (TMNG) i toksyczny gruczolak, gdzie somatyczne mutacje receptora TSH prowadzą do autonomicznej produkcji hormonów. Nadczynność może być także indukowana jodem (np. amiodaronem), zapaleniem tarczycy, gruczolakiem przysadki wydzielającym TSH, ciążową nadczynnością, przerzutowym rakiem pęcherzykowym tarczycy czy jatrogenna nadczynnością po nadmiernym podawaniu hormonów tarczycy. W nadczynności obserwuje się zwykle większy wzrost T3 niż T4, co wiąże się z tyreotoksykozą T3. Objawy wynikają z nadmiaru hormonów, m.in. zwiększonej przemiany materii, pobudliwości układu nerwowego, drżeń, zaburzeń rytmu serca, biegunek, zaburzeń miesiączkowania i ginekomastii. Nieleczona nadczynność może prowadzić do poważnych powikłań, takich jak migotanie przedsionków, burza tarczycowa, oftalmopatia tarczycowa, osteoporoza i zaburzenia neurologiczne.

Nadczynność tarczycy (Hyperthyroidism) – Patogeneza i mechanizm

Nadczynność tarczycy (hyperthyroidism) to stan charakteryzujący się nadmierną produkcją i uwalnianiem hormonów tarczycy, co prowadzi do przyspieszenia metabolizmu i wielu objawów klinicznych. Jest to zaburzenie wynikające z różnych przyczyn, które prowadzą do podwyższonego stężenia hormonów tarczycy w tkankach.12

Autoimmunologiczna nadczynność tarczycy – choroba Gravesa-Basedowa

Choroba Gravesa-Basedowa jest najczęstszą przyczyną nadczynności tarczycy, stanowiącą około 60-80% wszystkich przypadków.34 Jest to autoimmunologiczne schorzenie, w którym układ odpornościowy tworzy przeciwciała przeciwko receptorom TSH (thyroid-stimulating hormone), prowadząc do zwiększonej produkcji hormonów tarczycy.5

W mechanizmie choroby Gravesa-Basedowa kluczową rolę odgrywają immunoglobuliny stymulujące tarczycę (TSI), które wiążą się z receptorami TSH (TSHR) i aktywują je, powodując ciągłą stymulację gruczołu tarczowego. Te przeciwciała (TRAb – thyroid-stimulating hormone receptor antibodies) należą głównie do podklasy IgG1.67 Wiązanie przeciwciał z receptorami TSH prowadzi do:

  • Zwiększonej produkcji i uwalniania hormonów tarczycy (T3 i T4)
  • Aktywacji wewnątrzkomórkowego cAMP, co powoduje rozrost i hiperplazję tyreocytów
  • Zwiększonego wychwytywania jodu przez tarczycę
  • Zwiększonej syntezy białek w gruczole tarczowym
  • Rozrostu gruczołu tarczowego (wole)89

W patogenezie choroby Gravesa-Basedowa istotną rolę odgrywają zarówno limfocyty B, jak i T skierowane przeciwko czterem głównym antygenom tarczycowym: tyreoglobulinie, peroksydazie tarczycowej, symporterowi sodowo-jodowemu i receptorowi TSH. Jednak to właśnie receptor TSH jest głównym autoantygenem odpowiedzialnym za hiperthyrozę.1011

Na rozwój choroby Gravesa-Basedowa wpływa interakcja między czynnikami genetycznymi a środowiskowymi. Wśród czynników genetycznych wymienia się geny: CD40, CTLA-4, gen tyreoglobuliny (TG), gen receptora TSH (TSHR), PTPN22, FOXP3, CD25 i VDR. Czynniki środowiskowe obejmują infekcje wirusowe, stres emocjonalny, palenie tytoniu i okres poporodowy.1213

Nadczynność tarczycy spowodowana autonomią gruczołu

Wole guzkowe toksyczne

Toksyczne wole guzkowe (multinodular toxic goiter, TMNG) jest drugą najczęstszą przyczyną nadczynności tarczycy, szczególnie u osób starszych i w obszarach niedoboru jodu.14 Patogeneza TMNG obejmuje długą fazę rozwoju choroby guzkowej, trwającej latami, zanim guzki rozwiną autonomię produkcji hormonów tarczycy. Mutacje somatyczne w obrębie receptora TSH prowadzą do konstytutywnej aktywacji szlaku sygnałowego cAMP, co skutkuje autonomią tarczycy.1516

W TMNG nodule powstają w wyniku częstej replikacji komórek klonogennych, co prowadzi do somatycznej mutacji aktywującej receptory TSH. Z czasem guzki stają się autonomiczne, wydzielając hormony tarczycy niezależnie od poziomu krążącego TSH.1718

Gruczolak toksyczny

Toksyczny gruczolak (choroba Plummera, toxic adenoma) to pojedynczy guzek autonomicznie produkujący hormony tarczycy z powodu somatycznych mutacji w receptorze TSH.19 Jest to monoklonalny, dobrze zdefiniowany otorebkowany łagodny guz wydzielający hormon tarczycy pod nieobecność bodźca TSH w poza tym normalnym gruczole.20

Charakteryzuje się zwiększonym transportem jodu i szybkością jodowania, ze zwiększoną ekspresją peroksydazy tarczycowej i mRNA symportera jodku sodu. W większości przypadków aktywująca mutacja receptora TSH ograniczona do tkanki gruczolaka (mutacja somatyczna) powoduje stymulację cyklazy adenylanowej i gromadzenie wewnątrzkomórkowego cAMP, co w konsekwencji zwiększa tempo replikacji komórek tarczycy.21

Nadczynność tarczycy indukowana jodem

Nadczynność tarczycy wywołana jodem jest zazwyczaj jatrogenna, wynikająca z nadmiernego spożycia jodu poprzez dietę lub podawanie leków zawierających jod, takich jak środki kontrastowe lub amiodaron.22

W przypadku nadczynności tarczycy wywołanej amiodaronem (AIT) wyróżnia się dwa podtypy:

  • Typ 1 AIT – prowadzi do zwiększonej produkcji hormonów tarczycy w następstwie nadmiernej ekspozycji na jod z amiodaronu w przypadku wcześniej istniejącej choroby tarczycy (jak w zjawisku Jod-Basedow).
  • Typ 2 AIT – jest destrukcyjnym zapaleniem tarczycy z powodu bezpośredniego toksycznego działania amiodaronu na komórki pęcherzykowe tarczycy.2324

Nadczynność tarczycy indukowana jodem może wystąpić u pacjentów po leczeniu wcześniejszych chorób tarczycy. Szczególnie pacjenci leczeni lekami przeciwtarczycowymi na chorobę Gravesa-Basedowa są podatni na rozwój nadczynności tarczycy wywołanej jodem.25

Zapalenie tarczycy

Różne etiologie zapalenia tarczycy mają wspólną patofizjologię, ale różnią się w prezentacji klinicznej. Zapalenie lub zniszczenie komórek pęcherzykowych tarczycy może wynikać z autoimmunizacji (zapalenie tarczycy Hashimoto, bezbolesne sporadyczne zapalenie tarczycy i bezbolesne poporodowe zapalenie tarczycy) lub być wynikiem czynników zewnętrznych (infekcje w bolesnym podostrym zapaleniu tarczycy, ropne zapalenie tarczycy, zapalenie tarczycy wywołane lekami).26

W przypadku zapalenia tarczycy, obecność stanu zapalnego powoduje uwolnienie zgromadzonych wcześniej hormonów tarczycy do krwiobiegu, co prowadzi do objawów nadczynności tarczycy. Po fazie nadczynności często następuje faza niedoczynności, zanim gruczoł tarczowy powróci do normy.2728

Inne przyczyny nadczynności tarczycy

Rzadziej występujące przyczyny nadczynności tarczycy obejmują:

  • Gruczolak przysadki wydzielający TSH – nadmierna produkcja TSH prowadzi do nadmiernej stymulacji tarczycy29
  • Ciążowa nadczynność tarczycy – rozwija się w pierwszym trymestrze ciąży w wyniku stymulującego działania łożyskowego beta ludzkiego choriongonadotropiny (β-hCG), który dzięki podobieństwu strukturalnemu do TSH, oddziałuje na gruczoł tarczowy30
  • Przerzutowy rak pęcherzykowy tarczycy – funkcjonujące komórki nowotworowe mogą nadal produkować hormony tarczycy31
  • Struma ovarii – guz jajnika produkujący hormony tarczycy3233
  • Jatrogenna nadczynność tarczycy – spowodowana nadmiernym przyjmowaniem syntetycznych hormonów tarczycy34

Zmiany biochemiczne i fizjologiczne w nadczynności tarczycy

W nadczynności tarczycy poziom T3 zazwyczaj wzrasta bardziej niż T4, prawdopodobnie z powodu zwiększonego wydzielania T3, a także konwersji T4 do T3 w tkankach obwodowych.35 Może to prowadzić do tzw. tyreotoksykozy T3, która może wystąpić w wielu powszechnych zaburzeniach powodujących nadczynność tarczycy, w tym w chorobie Gravesa-Basedowa, wolu wieloguzkowym i autonomicznie funkcjonującym pojedynczym guzku tarczycy.36

Nadmiar hormonów tarczycy we krwi (tyreotoksykoza) powoduje szereg zmian fizjologicznych:

  • Zwiększenie podstawowej przemiany materii
  • Zwiększenie pobudliwości neuronów w centralnym i obwodowym układzie nerwowym
  • Zwiększenie liczby kanałów wapniowych i receptorów beta-adrenergicznych
  • Wzrost zużycia tlenu przez tkanki
  • Przyspieszenie metabolizmu komórkowego3738

Na poziomie komórkowym, nadmiar hormonów tarczycy prowadzi do zwiększonej transkrypcji białek komórkowych, powodując wzrost podstawowej przemiany materii. W wielu aspektach objawy nadczynności tarczycy przypominają stan nadmiaru katecholamin, a blokada adrenergiczna może złagodzić te objawy.39

Wpływ nadczynności tarczycy na układ nerwowy

Nadczynność tarczycy istotnie wpływa na układ nerwowy, powodując zwiększoną pobudliwość nerwową. Może to prowadzić do drżenia, które jest częstym objawem nadczynności tarczycy. Mechanizm drżenia polega na zwiększeniu pobudliwości komórek nerwowych w pętlach oscylacyjnych centralnego i obwodowego układu nerwowego.40

Drżenie oscylacyjne jest spowodowane odruchami pochodzącymi z aferentnych dróg mięśniowych. To zwiększa amplitudę drżenia powyżej normalnej drobnej oscylacji, wytwarzając zsynchronizowane drżenie.41 Nadczynność tarczycy wiąże się również ze zwiększonym ryzykiem padaczki, co może wynikać ze zwiększonej pobudliwości mózgu obniżającej próg potrzebny do wystąpienia napadu.4243

Dokładny mechanizm, poprzez który hormony tarczycy wpływają na pobudliwość mózgu, nie jest w pełni poznany, ale badania sugerują, że nadmiar hormonów tarczycy może wpływać na aktywność pompy sodowo-potasowej (ATP-azy), prowadząc do istotnych zmian w stężeniach sodu w neuronach.44

Wpływ na układ pokarmowy

Nadczynność tarczycy może znacząco wpływać na układ pokarmowy poprzez pobudzenie układu współczulnego. Nadmierna ilość hormonów tarczycy prowadzi do nadmiernej stymulacji nerwów zarządzających przewodem pokarmowym, co powoduje zwiększoną motorykę jelit.45

Kiedy nerwy jelitowe są nadmiernie stymulowane, zwiększają motorykę jelit, co odnosi się do ruchu i skurczów mięśni w jelitach. Powoduje to szybsze niż zwykle kurczenie się mięśni jelit i przepychanie pokarmu, zanim zostanie w pełni strawiony. Zapobiega to również pełnemu wchłanianiu płynów z pokarmu podczas jego przechodzenia, prowadząc do wodnistej biegunki.4647

Gdy pokarm przechodzi przez przewód pokarmowy zbyt szybko, jelita nie mają wystarczająco dużo czasu na wchłonięcie składników odżywczych z pożywienia. Jest to tzw. zespół złego wchłaniania. Zapalenie, które może wynikać z nadczynności tarczycy, może również uniemożliwić jelitom wchłanianie składników odżywczych jak zwykle, prowadząc do niedożywienia.48

Wpływ na układ rozrodczy

Hormony tarczycy są niezbędne dla prawidłowego funkcjonowania układu rozrodczego. W nadczynności tarczycy miesiączkowanie może występować nieregularnie, a krwawienie miesiączkowe może być lżejsze. Może to powodować problemy z płodnością.49

Nadczynność tarczycy może powodować podwyższone stężenie białka wiążącego hormony płciowe (SHBG) we krwi, co może prowadzić do nieregularnych, lżejszych lub pominiętych okresów.50 Ponadto, w zaburzeniach tarczycy, takich jak nadczynność tarczycy, podwyższone poziomy hormonu prolaktyny we krwi mogą prowadzić do zaburzeń owulacji, co może powodować nieregularności i przerwy w miesiączkowaniu.51

Istnieją dwa różne mechanizmy przyczyniające się do rozwoju ginekomastii w tyreotoksykozie. Pierwszym i głównym czynnikiem przyczyniającym się do tej nierównowagi jest indukowna przez hormony tarczycy zwiększona produkcja białka osoczowego SHBG w wątrobie. Drugi mechanizm związany jest ze zwiększoną aktywnością aromatazy przez hormony tarczycy, która przekształca androgeny w estrogeny w tkankach obwodowych, zaburzając równowagę hormonalną poprzez zwiększenie poziomu estrogenów.52

Powikłania nadczynności tarczycy

Nieleczona lub źle leczona nadczynność tarczycy może prowadzić do różnych powikłań:

  • Powikłania sercowe – mogą być poważne i zagrażające życiu. Obejmują one szybką akcję serca i zmieniony rytm serca zwany migotaniem przedsionków, który może zwiększyć ryzyko udaru i niewydolności serca53
  • Burza tarczycowa (przełom tarczycowy) – nagłe zaostrzenie objawów, powodujące gorączkę, kołatanie serca i zmieniony stan psychiczny. Wymaga natychmiastowej pomocy medycznej5455
  • Oftalmopatia tarczycowa – w chorobie Gravesa-Basedowa może dojść do oftalmopatii naciekowej, która objawia się wytrzeszczem oczu. Patogeneza oftalmopatii nie jest w pełni zrozumiana, ale może wynikać z przeciwciał skierowanych na receptory TSH w fibroblastach oczodołu i tkance tłuszczowej, prowadzących do uwalniania cytokin prozapalnych, stanu zapalnego i gromadzenia glikozaminoglikanów56
  • Powikłania neurologiczne – nadczynność tarczycy wiąże się z wieloma różnymi powikłaniami neurologicznymi, takimi jak zaburzenia ruchu, drżenia, atypowe mimowolne ruchy mięśni, upośledzenie emocjonalne i poznawcze, zaburzenia psychiatryczne, bóle głowy, zaburzenia snu i uszkodzenia nerwów57

Nieleczona nadczynność tarczycy może również prowadzić do osłabienia mięśni, osteoporozy z powodu zwiększonej resorpcji kości, zaburzeń funkcji wątroby i niepłodności.5859

Rozpoznanie nadczynności tarczycy

Diagnoza nadczynności tarczycy opiera się na objawach klinicznych oraz badaniach laboratoryjnych:6061

  • Niskie stężenie hormonu tyreotropowego (TSH) i podwyższone stężenie hormonów tarczycy (T3 i/lub T4) w surowicy krwi
  • Obecność przeciwciał przeciwko receptorowi TSH w surowicy w chorobie Gravesa-Basedowa
  • Badania obrazowe, takie jak scyntygrafia tarczycy, badanie wychwytu radioaktywnego jodu lub ultrasonografia, pomagają zidentyfikować przyczynę nadczynności tarczycy

Opcje terapeutyczne

Leczenie nadczynności tarczycy zależy od przyczyny i nasilenia choroby. Główne opcje terapeutyczne to:626364

  • Leki przeciwtarczycowe (tionamidy) – metylotiouracyl (Metizol) i propylotiouracyl – działają poprzez hamowanie wytwarzania hormonów tarczycy
  • Jod radioaktywny – podawany doustnie w formie kapsułki lub płynu, stopniowo niszczy komórki gruczołu tarczowego, które produkują hormony tarczycy
  • Leczenie chirurgiczne – tyreoidektomia (usunięcie gruczołu tarczowego) może być stosowana jako leczenie definitywne, jeśli podejrzewa się nowotwór, występuje wole uciskowe lub radioaktywny jod/leki przeciwtarczycowe są nieodpowiednie
  • Leki blokujące receptory beta-adrenergiczne – stosowane do kontroli objawów, takich jak tachykardia

Po leczeniu definitywnym radioaktywnym jodem lub chirurgicznym, pacjenci często wymagają zastępczej terapii hormonalnej do końca życia z powodu rozwoju niedoczynności tarczycy.656667

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  1. 11.04.2026
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Materiały źródłowe

  • #1 Hyperthyroidism – StatPearls – NCBI Bookshelf
    https://www.ncbi.nlm.nih.gov/books/NBK537053/
    Hyperthyroidism is a common thyroid disorder with multiple underlying etiologies. This disease is characterized by excess thyroid hormone production. Hyperthyroidism can be overt or subclinical. Overt hyperthyroidism is defined as low or suppressed thyroid stimulating hormone (TSH) levels with elevated triiodothyronine (T3) levels and/or elevated thyroxine (T4) levels. Hyperthyroidism is associated with significant short-term and long-term morbidity. Therefore, early recognition of this condition and timely instruction of appropriate therapy is critical. […] Hyperthyroidism has multiple etiologies, clinical manifestations, and treatment modalities. […] The pathophysiology of hyperthyroidism depends on the particular variant of hyperthyroidism. […] This is an autoimmune process with antibodies against the TSH receptor. An interplay between genetic and environmental factors influences this autoimmune process. The antibodies stimulate the TSH receptor (TSHR), leading to increased production and release of thyroid hormones. The trophic effects on the thyroid also lead to the growth of the thyroid gland. […] Pathogenesis of TMNG includes the initial phase of development of the nodular disease. This phase is prolonged and present for years before the nodules develop autonomy for thyroid hormone production. The somatic mutations involving the TSHR lead to constitutive activation of the cAMP signaling pathway, resulting in thyroid autonomy. […] These are solitary nodules with autonomous thyroid hormone production due to somatic mutations in the TSHR. […] This is typically iatrogenic, resulting from excessive iodine intake through diet or administration of iodine-containing medications such as contrast media or amiodarone. […] There are 2 subtypes of AIT: type 1 and type 2. Type 1 AIT leads to increased thyroid hormone production secondary to excess iodine exposure from amiodarone in the setting of pre-existing thyroid disease (as seen in the Jod-Basedow phenomenon). Type 2 AIT is destructive thyroiditis due to the direct toxic effects of amiodarone on the thyroid follicular cells. […] Various etiologies of thyroiditis have this common pathophysiology but vary in their clinical presentations. The inflammation or destruction of the thyroid follicular cells can result from autoimmunity (Hashimoto’s thyroiditis, painless sporadic thyroiditis, and painless, postpartum thyroiditis) or the result of external factors (infections in painful subacute thyroiditis, suppurative thyroiditis, drug-induced thyroiditis).
  • #2 Hyperthyroidism: Diagnosis and Treatment | AAFP
    https://www.aafp.org/pubs/afp/issues/2016/0301/p363.html
    Hyperthyroidism is an excessive concentration of thyroid hormones in tissues caused by increased synthesis of thyroid hormones, excessive release of preformed thyroid hormones, or an endogenous or exogenous extrathyroidal source. The most common causes of an excessive production of thyroid hormones are Graves disease, toxic multinodular goiter, and toxic adenoma. […] The common endogenous causes of hyperthyroidism are Graves disease, toxic multinodular goiter, toxic adenoma, and painless thyroiditis. Graves disease, the most common cause of hyperthyroidism in the United States, is an autoimmune disorder in which thyroid-stimulating antibodies activate thyroid-stimulating hormone (TSH) receptors, triggering thyroid hormone synthesis. Risk factors for Graves disease include female sex and personal or family history of an autoimmune disorder.
  • #3 Pulsenotes | Hyperthyroidism notes
    https://app.pulsenotes.com/medicine/endocrinology/notes/hyperthyroidism
    Hyperthyroidism is a common endocrine condition caused by an overactive thyroid gland causing an excess of thyroid hormone. […] Thyrotoxicosis with hyperthyroidism is an excess of thyroid hormone caused by overactivity of the thyroid gland. […] Graves disease is a common autoimmune condition and is the most common cause of hyperthyroidism (60-80% of cases) in the UK. […] It is caused by IgG antibodies to the TSH receptors found within the thyroid. Termed thyroid-stimulating hormone receptor antibodies (TSHR-Ab), these antibodies mimic the action of TSH causing excessive stimulation of the gland. […] Toxic multinodular goitre is the second most common cause of hyperthyroidism in the UK. […] In this condition, multiple autonomous nodules develop that are capable of producing and secreting thyroid hormones.
  • #4 Hyperthyroidism: Diagnosis and Treatment | AAFP
    https://www.aafp.org/pubs/afp/issues/2005/0815/p623.html
    The proper treatment of hyperthyroidism depends on recognition of the signs and symptoms of the disease and determination of the etiology. The most common cause of hyperthyroidism is Graves disease. Other common causes include thyroiditis, toxic multinodular goiter, toxic adenomas, and side effects of certain medications. […] Clinical hyperthyroidism, also called thyrotoxicosis, is caused by the effects of excess thyroid hormone and can be triggered by different disorders. Etiologic diagnosis influences prognosis and therapy. […] Graves disease is the most common cause of hyperthyroidism, accounting for 60 to 80 percent of all cases. It is an autoimmune disease caused by an antibody, active against the thyroid-stimulating hormone (TSH) receptor, which stimulates the gland to synthesize and secrete excess thyroid hormone.
  • #5 Graves’ disease – Wikipedia
    https://en.wikipedia.org/wiki/Graves%27_disease
    Graves’ disease, also known as toxic diffuse goiter or Basedow’s disease, is an autoimmune disease that affects the thyroid. It frequently results in and is the most common cause of hyperthyroidism. The exact cause of the disease is unclear, but symptoms are a result of antibodies binding to receptors on the thyroid causing over-expression of thyroid hormone. The disorder results from an antibody, called thyroid-stimulating immunoglobulin (TSI), that has a similar effect to thyroid stimulating hormone (TSH). These TSI antibodies cause the thyroid gland to produce excess thyroid hormones. Graves’ disease is an autoimmune disorder, in which the body produces antibodies that are specific to a self-protein – the receptor for thyroid-stimulating hormone. These antibodies cause hyperthyroidism because they bind to the TSH receptor and chronically stimulate it. The result of chronic stimulation is an abnormally high production of T3 and T4. This, in turn, causes the clinical symptoms of hyperthyroidism, and the enlargement of the thyroid gland visible as goiter. The three types of autoantibodies to the TSH receptor are thyroid stimulating immunoglobulins, thyroid growth immunoglobulins, and thyrotrophin binding-inhibiting immunoglobulins.
  • #6 Graves Disease: Practice Essentials, Pathophysiology, Epidemiology
    https://emedicine.medscape.com/article/120619-overview
    Graves disease is an autoimmune disorder characterized by hyperthyroidism due to circulating autoantibodies. Thyroid-stimulating immunoglobulins (TSIs) bind to and activate thyroid-stimulating hormone (TSH) receptors, causing the thyroid gland to grow and the thyroid follicles to increase synthesis of thyroid hormone. […] In Graves disease, B and T lymphocyte-mediated autoimmunity are known to be directed at 4 well-known thyroid antigens: thyroglobulin, thyroid peroxidase, sodium-iodide symporter and the TSH receptor. However, the TSH receptor itself is the primary autoantigen of Graves disease and is responsible for the manifestation of hyperthyroidism. […] The thyroid gland is under continuous stimulation by circulating autoantibodies against the TSH receptor, and pituitary TSH secretion is suppressed because of the increased production of thyroid hormones. The stimulating activity of TSH-receptor antibodies is found mostly in the immunoglobulin G1 subclass. These thyroid-stimulating antibodies cause release of thyroid hormone and thyroglobulin that is mediated by 3,’5′-cyclic adenosine monophosphate (cyclic AMP), and they also stimulate iodine uptake, protein synthesis, and thyroid gland growth.
  • #7 Pathogenesis of Graves’ disease – UpToDate
    https://www.uptodate.com/contents/pathogenesis-of-graves-disease
    Pathogenesis of Graves’ disease […] Graves’ disease is a syndrome that may consist of hyperthyroidism, goiter, thyroid eye disease (TED; Graves’ orbitopathy), and occasionally a dermopathy referred to as pretibial or localized myxedema (PTM). The terms Graves’ disease and hyperthyroidism are not synonymous, because some patients may have an orbitopathy but no hyperthyroidism, and there are other causes of hyperthyroidism in addition to Graves’ disease. […] Nevertheless, hyperthyroidism is the most common feature of Graves’ disease, affecting nearly all patients, and is caused by autoantibodies to the thyrotropin receptor (TRAb) that activate the receptor, thereby stimulating thyroid hormone synthesis and secretion as well as thyroid growth (causing a diffuse goiter). The presence of TRAb in serum and eye involvement on clinical examination immediately distinguishes the disorder from other causes of hyperthyroidism. […] This topic will review the immune pathogenesis of Graves’ thyroid disease, with emphasis on the role of B and T cells in the production of the TRAb that are responsible for the thyroid stimulation and growth.
  • #8 The Role of Nuclear Medicine in the Clinical Management of Benign Thyroid Disorders, Part 1: Hyperthyroidism | Journal of Nuclear Medicine
    https://jnm.snmjournals.org/content/62/3/304
    Benign thyroid disorders, especially hyper- and hypothyroidism, are the most prevalent endocrine disorders. The most common etiologies of hyperthyroidism are autoimmune hyperthyroidism (Graves disease, GD), toxic multinodular goiter (TMNG), and toxic thyroid adenoma (TA). […] GD is caused by autoantibodies against the thyroid-stimulating hormone (TSH) receptor. TMNG and TA are caused by a somatic activating gain-of-function mutation. […] Environmental factors such as dietary iodine, smoking, and emotional stress can precipitate GD in genetically predisposed individuals who harbor multiple susceptibility alleles (in particular at the MHC, CTLA4, and PTPN22 loci). […] As an organ-specific autoimmune disease, GD is caused by circulating autoantibodies (generally of the IgG1 isotype) directed against TSHR. In most patients, TSHR autoantibodies (TRAb) stimulate the thyroid after binding to TSHR, by increasing the production of intracellular cyclic adenosine monophosphate.
  • #9 Hyperthyroidism and Thyrotoxicosis: Practice Essentials, Background, Pathophysiology
    https://emedicine.medscape.com/article/121865-overview
    Hyperthyroidism is a set of disorders that involve excess synthesis and secretion of thyroid hormones by the thyroid gland, which leads to the hypermetabolic condition of thyrotoxicosis. […] The most common forms of hyperthyroidism include diffuse toxic goiter (Graves disease), toxic multinodular goiter, and toxic adenoma. […] In Graves disease, a circulating autoantibody against the thyrotropin receptor provides continuous stimulation of the thyroid gland. […] This stimulatory immunoglobulin is diagnostic for Graves disease and has been called thyroid-stimulating immunoglobulin (TSI), thyroid-stimulating antibody (TSab), and TSH-receptor antibody (TRab). […] These antibodies stimulate the production and release of thyroid hormones and thyroglobulin; they also stimulate iodine uptake, protein synthesis, and thyroid gland growth.
  • #10 Graves Disease: Practice Essentials, Pathophysiology, Epidemiology
    https://emedicine.medscape.com/article/120619-overview
    Graves disease is an autoimmune disorder characterized by hyperthyroidism due to circulating autoantibodies. Thyroid-stimulating immunoglobulins (TSIs) bind to and activate thyroid-stimulating hormone (TSH) receptors, causing the thyroid gland to grow and the thyroid follicles to increase synthesis of thyroid hormone. […] In Graves disease, B and T lymphocyte-mediated autoimmunity are known to be directed at 4 well-known thyroid antigens: thyroglobulin, thyroid peroxidase, sodium-iodide symporter and the TSH receptor. However, the TSH receptor itself is the primary autoantigen of Graves disease and is responsible for the manifestation of hyperthyroidism. […] The thyroid gland is under continuous stimulation by circulating autoantibodies against the TSH receptor, and pituitary TSH secretion is suppressed because of the increased production of thyroid hormones. The stimulating activity of TSH-receptor antibodies is found mostly in the immunoglobulin G1 subclass. These thyroid-stimulating antibodies cause release of thyroid hormone and thyroglobulin that is mediated by 3,’5′-cyclic adenosine monophosphate (cyclic AMP), and they also stimulate iodine uptake, protein synthesis, and thyroid gland growth.
  • #11 Pathogenesis of Graves’ disease – UpToDate
    https://www.uptodate.com/contents/pathogenesis-of-graves-disease/print
    Graves’ disease is a syndrome that may consist of hyperthyroidism, goiter, thyroid eye disease (TED; Graves’ orbitopathy), and occasionally a dermopathy referred to as pretibial or localized myxedema (PTM). […] Nevertheless, hyperthyroidism is the most common feature of Graves’ disease, affecting nearly all patients, and is caused by autoantibodies to the thyrotropin receptor (TRAb) that activate the receptor, thereby stimulating thyroid hormone synthesis and secretion as well as thyroid growth (causing a diffuse goiter). […] This topic will review the immune pathogenesis of Graves’ thyroid disease, with emphasis on the role of B and T cells in the production of the TRAb that are responsible for the thyroid stimulation and growth. […] The histology of the thyroid gland in patients with Graves’ hyperthyroidism is characterized by follicular hyperplasia, intracellular colloid droplets, cell scalloping, a reduction in follicular colloid, and a patchy (multifocal) lymphocytic infiltration.
  • #12 Graves Disease: Practice Essentials, Pathophysiology, Epidemiology
    https://emedicine.medscape.com/article/120619-overview
    Viral infection is an environmental factor linked to Graves disease. The prevalence of enteroviral proteins, the upregulation of human leukocyte antigen (HLA) class I expression, and co-localization with antiviral response proteins such as Stat1, VP1, and PKR all indicate an association between Graves disease and viral infection. […] Several autoimmune thyroid disease susceptibility genes are considered to be linked to Graves disease, including CD40, CTLA-4, the thyroglobulin gene (TG), the TSH-receptor gene (TSHR), PTPN22, FOXP3, CD25, and VDR. […] A genetic predisposition to thyroid autoimmunity may interact with environmental factors or events to precipitate the onset of Graves disease.
  • #13 Evaluating and managing patients with thyrotoxicosis
    https://www.racgp.org.au/afp/2012/august/evaluating-and-managing-patients-with-thyrotoxicos
    Graves disease is an autoimmune disorder characterised by the presence of thyroid stimulating hormone (TSH) receptor antibodies. It can occur at any age, but has a peak onset between 40 and 60 years. Women are 510 times more likely to be affected than men. It clusters in families and genetic associations have been found, but no single gene is known to be necessary or sufficient to cause Graves disease. Smoking, psychological stress and the postpartum period are associated with the development of Graves disease. Other autoimmune diseases, such as coeliac disease, occur more frequently in patients with Graves disease and this risk persists after treatment. […] Patients with Graves disease have thyrotoxicosis associated with a diffuse goitre. Clinical features that distinguish Graves disease from other causes of thyrotoxicosis include the presence of Graves ophthalmopathy (thyroid eye disease) and the presence of uncommon manifestations of Graves disease such as thyroid dermopathy (pretibial myxoedema, 12%) and thyroid acropachy (digital clubbing, 1%). Clinical features of Graves ophthalmopathy occur in about 50% of patients with Graves disease and a further 20% have evidence of ophthalmopathy on imaging. Eyelid lag or retraction and periorbital oedema are the most frequent signs and proptosis is common.
  • #14 Hyperthyroidism: Diagnosis and Treatment | AAFP
    https://www.aafp.org/pubs/afp/issues/2016/0301/p363.html
    Toxic multinodular goiter is the second most common cause of hyperthyroidism in the United States and the most common cause in older persons living in iodine-deficient areas. Over time, nodules arise from the frequent replication of clonogenic cells that leads to a somatic activating mutation of TSH receptors. A single nodule is called a toxic adenoma (Plummer disease). […] In contrast with these three disorders, painless or transient (silent) thyroiditis causes a destruction of thyroid follicles via an autoimmune mechanism and a release of preformed thyroid hormones into the circulation. […] Gestational hyperthyroidism develops in the first trimester of pregnancy as a result of the stimulatory action of placental beta human chorionic gonadotropin (-hCG), which shares structural features with TSH, on the thyroid gland. […] Other rare causes of hyperthyroidism are TSH-secreting pituitary adenoma, metastatic follicular thyroid cancer, and struma ovarii.
  • #15 Hyperthyroidism – StatPearls – NCBI Bookshelf
    https://www.ncbi.nlm.nih.gov/books/NBK537053/
    Hyperthyroidism is a common thyroid disorder with multiple underlying etiologies. This disease is characterized by excess thyroid hormone production. Hyperthyroidism can be overt or subclinical. Overt hyperthyroidism is defined as low or suppressed thyroid stimulating hormone (TSH) levels with elevated triiodothyronine (T3) levels and/or elevated thyroxine (T4) levels. Hyperthyroidism is associated with significant short-term and long-term morbidity. Therefore, early recognition of this condition and timely instruction of appropriate therapy is critical. […] Hyperthyroidism has multiple etiologies, clinical manifestations, and treatment modalities. […] The pathophysiology of hyperthyroidism depends on the particular variant of hyperthyroidism. […] This is an autoimmune process with antibodies against the TSH receptor. An interplay between genetic and environmental factors influences this autoimmune process. The antibodies stimulate the TSH receptor (TSHR), leading to increased production and release of thyroid hormones. The trophic effects on the thyroid also lead to the growth of the thyroid gland. […] Pathogenesis of TMNG includes the initial phase of development of the nodular disease. This phase is prolonged and present for years before the nodules develop autonomy for thyroid hormone production. The somatic mutations involving the TSHR lead to constitutive activation of the cAMP signaling pathway, resulting in thyroid autonomy. […] These are solitary nodules with autonomous thyroid hormone production due to somatic mutations in the TSHR. […] This is typically iatrogenic, resulting from excessive iodine intake through diet or administration of iodine-containing medications such as contrast media or amiodarone. […] There are 2 subtypes of AIT: type 1 and type 2. Type 1 AIT leads to increased thyroid hormone production secondary to excess iodine exposure from amiodarone in the setting of pre-existing thyroid disease (as seen in the Jod-Basedow phenomenon). Type 2 AIT is destructive thyroiditis due to the direct toxic effects of amiodarone on the thyroid follicular cells. […] Various etiologies of thyroiditis have this common pathophysiology but vary in their clinical presentations. The inflammation or destruction of the thyroid follicular cells can result from autoimmunity (Hashimoto’s thyroiditis, painless sporadic thyroiditis, and painless, postpartum thyroiditis) or the result of external factors (infections in painful subacute thyroiditis, suppurative thyroiditis, drug-induced thyroiditis).
  • #16 Hyperthyroidism: Diagnosis and Treatment | AAFP
    https://www.aafp.org/pubs/afp/issues/2005/0815/p623.html
    Toxic multinodular goiter causes 5 percent of the cases of hyperthyroidism in the United States and can be 10 times more common in iodine-deficient areas. […] Toxic adenomas are autonomously functioning nodules that are found most commonly in younger patients and in iodine-deficient areas. […] Subacute thyroiditis produces an abrupt onset of thyrotoxic symptoms as hormone leaks from an inflamed gland. […] Iodine-induced hyperthyroidism can occur after intake of excess iodine in the diet, exposure to radiographic contrast media, or medications. Excess iodine increases the synthesis and release of thyroid hormone in iodine-deficient patients and in older patients with preexisting multinodular goiters. […] Amiodarone- (Cordarone-) induced hyperthyroidism can be found in up to 12 percent of treated patients, especially those in iodine-deficient areas, and occurs by two mechanisms.
  • #17 Hyperthyroidism: Diagnosis and Treatment | AAFP
    https://www.aafp.org/pubs/afp/issues/2016/0301/p363.html
    Toxic multinodular goiter is the second most common cause of hyperthyroidism in the United States and the most common cause in older persons living in iodine-deficient areas. Over time, nodules arise from the frequent replication of clonogenic cells that leads to a somatic activating mutation of TSH receptors. A single nodule is called a toxic adenoma (Plummer disease). […] In contrast with these three disorders, painless or transient (silent) thyroiditis causes a destruction of thyroid follicles via an autoimmune mechanism and a release of preformed thyroid hormones into the circulation. […] Gestational hyperthyroidism develops in the first trimester of pregnancy as a result of the stimulatory action of placental beta human chorionic gonadotropin (-hCG), which shares structural features with TSH, on the thyroid gland. […] Other rare causes of hyperthyroidism are TSH-secreting pituitary adenoma, metastatic follicular thyroid cancer, and struma ovarii.
  • #18 The Role of Nuclear Medicine in the Clinical Management of Benign Thyroid Disorders, Part 1: Hyperthyroidism | Journal of Nuclear Medicine
    https://jnm.snmjournals.org/content/62/3/304
    TRAbs also interact with IGF1 receptors on the surface of thyroid cells and of orbital fibroblasts. The antibody-receptor complex promotes activation of intracellular cyclic adenosine monophosphate, with ensuing thyrocyte hyperplasia (causing gland enlargement), increased vascularity, and increased thyroid hormone production and secretion, resulting in hyperthyroidism. […] TMNG causes hyperthyroidism when nonfunctioning and functioning nodules coexist and, over time, become autonomous, secreting thyroid hormone independently of circulating levels of TSH. […] TA is a monoclonal well-defined encapsulated benign tumor secreting thyroid hormone in the absence of a TSH stimulus in an otherwise normal gland. It is characterized by increased iodine transport and iodination rate, with increased expression of thyroperoxidase and sodium iodide symporter messenger RNA. […] In most cases, an activating gain-of-function TSHR mutation confined to the adenomatous tissue (somatic mutation) results in stimulation of adenylyl cyclase and intracellular cyclic adenosine monophosphate accumulation, with a consequent increased replication rate of thyroid cells.
  • #19 Hyperthyroidism – StatPearls – NCBI Bookshelf
    https://www.ncbi.nlm.nih.gov/books/NBK537053/
    Hyperthyroidism is a common thyroid disorder with multiple underlying etiologies. This disease is characterized by excess thyroid hormone production. Hyperthyroidism can be overt or subclinical. Overt hyperthyroidism is defined as low or suppressed thyroid stimulating hormone (TSH) levels with elevated triiodothyronine (T3) levels and/or elevated thyroxine (T4) levels. Hyperthyroidism is associated with significant short-term and long-term morbidity. Therefore, early recognition of this condition and timely instruction of appropriate therapy is critical. […] Hyperthyroidism has multiple etiologies, clinical manifestations, and treatment modalities. […] The pathophysiology of hyperthyroidism depends on the particular variant of hyperthyroidism. […] This is an autoimmune process with antibodies against the TSH receptor. An interplay between genetic and environmental factors influences this autoimmune process. The antibodies stimulate the TSH receptor (TSHR), leading to increased production and release of thyroid hormones. The trophic effects on the thyroid also lead to the growth of the thyroid gland. […] Pathogenesis of TMNG includes the initial phase of development of the nodular disease. This phase is prolonged and present for years before the nodules develop autonomy for thyroid hormone production. The somatic mutations involving the TSHR lead to constitutive activation of the cAMP signaling pathway, resulting in thyroid autonomy. […] These are solitary nodules with autonomous thyroid hormone production due to somatic mutations in the TSHR. […] This is typically iatrogenic, resulting from excessive iodine intake through diet or administration of iodine-containing medications such as contrast media or amiodarone. […] There are 2 subtypes of AIT: type 1 and type 2. Type 1 AIT leads to increased thyroid hormone production secondary to excess iodine exposure from amiodarone in the setting of pre-existing thyroid disease (as seen in the Jod-Basedow phenomenon). Type 2 AIT is destructive thyroiditis due to the direct toxic effects of amiodarone on the thyroid follicular cells. […] Various etiologies of thyroiditis have this common pathophysiology but vary in their clinical presentations. The inflammation or destruction of the thyroid follicular cells can result from autoimmunity (Hashimoto’s thyroiditis, painless sporadic thyroiditis, and painless, postpartum thyroiditis) or the result of external factors (infections in painful subacute thyroiditis, suppurative thyroiditis, drug-induced thyroiditis).
  • #20 The Role of Nuclear Medicine in the Clinical Management of Benign Thyroid Disorders, Part 1: Hyperthyroidism | Journal of Nuclear Medicine
    https://jnm.snmjournals.org/content/62/3/304
    TRAbs also interact with IGF1 receptors on the surface of thyroid cells and of orbital fibroblasts. The antibody-receptor complex promotes activation of intracellular cyclic adenosine monophosphate, with ensuing thyrocyte hyperplasia (causing gland enlargement), increased vascularity, and increased thyroid hormone production and secretion, resulting in hyperthyroidism. […] TMNG causes hyperthyroidism when nonfunctioning and functioning nodules coexist and, over time, become autonomous, secreting thyroid hormone independently of circulating levels of TSH. […] TA is a monoclonal well-defined encapsulated benign tumor secreting thyroid hormone in the absence of a TSH stimulus in an otherwise normal gland. It is characterized by increased iodine transport and iodination rate, with increased expression of thyroperoxidase and sodium iodide symporter messenger RNA. […] In most cases, an activating gain-of-function TSHR mutation confined to the adenomatous tissue (somatic mutation) results in stimulation of adenylyl cyclase and intracellular cyclic adenosine monophosphate accumulation, with a consequent increased replication rate of thyroid cells.
  • #21 The Role of Nuclear Medicine in the Clinical Management of Benign Thyroid Disorders, Part 1: Hyperthyroidism | Journal of Nuclear Medicine
    https://jnm.snmjournals.org/content/62/3/304
    TRAbs also interact with IGF1 receptors on the surface of thyroid cells and of orbital fibroblasts. The antibody-receptor complex promotes activation of intracellular cyclic adenosine monophosphate, with ensuing thyrocyte hyperplasia (causing gland enlargement), increased vascularity, and increased thyroid hormone production and secretion, resulting in hyperthyroidism. […] TMNG causes hyperthyroidism when nonfunctioning and functioning nodules coexist and, over time, become autonomous, secreting thyroid hormone independently of circulating levels of TSH. […] TA is a monoclonal well-defined encapsulated benign tumor secreting thyroid hormone in the absence of a TSH stimulus in an otherwise normal gland. It is characterized by increased iodine transport and iodination rate, with increased expression of thyroperoxidase and sodium iodide symporter messenger RNA. […] In most cases, an activating gain-of-function TSHR mutation confined to the adenomatous tissue (somatic mutation) results in stimulation of adenylyl cyclase and intracellular cyclic adenosine monophosphate accumulation, with a consequent increased replication rate of thyroid cells.
  • #22 Hyperthyroidism – StatPearls – NCBI Bookshelf
    https://www.ncbi.nlm.nih.gov/books/NBK537053/
    Hyperthyroidism is a common thyroid disorder with multiple underlying etiologies. This disease is characterized by excess thyroid hormone production. Hyperthyroidism can be overt or subclinical. Overt hyperthyroidism is defined as low or suppressed thyroid stimulating hormone (TSH) levels with elevated triiodothyronine (T3) levels and/or elevated thyroxine (T4) levels. Hyperthyroidism is associated with significant short-term and long-term morbidity. Therefore, early recognition of this condition and timely instruction of appropriate therapy is critical. […] Hyperthyroidism has multiple etiologies, clinical manifestations, and treatment modalities. […] The pathophysiology of hyperthyroidism depends on the particular variant of hyperthyroidism. […] This is an autoimmune process with antibodies against the TSH receptor. An interplay between genetic and environmental factors influences this autoimmune process. The antibodies stimulate the TSH receptor (TSHR), leading to increased production and release of thyroid hormones. The trophic effects on the thyroid also lead to the growth of the thyroid gland. […] Pathogenesis of TMNG includes the initial phase of development of the nodular disease. This phase is prolonged and present for years before the nodules develop autonomy for thyroid hormone production. The somatic mutations involving the TSHR lead to constitutive activation of the cAMP signaling pathway, resulting in thyroid autonomy. […] These are solitary nodules with autonomous thyroid hormone production due to somatic mutations in the TSHR. […] This is typically iatrogenic, resulting from excessive iodine intake through diet or administration of iodine-containing medications such as contrast media or amiodarone. […] There are 2 subtypes of AIT: type 1 and type 2. Type 1 AIT leads to increased thyroid hormone production secondary to excess iodine exposure from amiodarone in the setting of pre-existing thyroid disease (as seen in the Jod-Basedow phenomenon). Type 2 AIT is destructive thyroiditis due to the direct toxic effects of amiodarone on the thyroid follicular cells. […] Various etiologies of thyroiditis have this common pathophysiology but vary in their clinical presentations. The inflammation or destruction of the thyroid follicular cells can result from autoimmunity (Hashimoto’s thyroiditis, painless sporadic thyroiditis, and painless, postpartum thyroiditis) or the result of external factors (infections in painful subacute thyroiditis, suppurative thyroiditis, drug-induced thyroiditis).
  • #23 Hyperthyroidism – StatPearls – NCBI Bookshelf
    https://www.ncbi.nlm.nih.gov/books/NBK537053/
    Hyperthyroidism is a common thyroid disorder with multiple underlying etiologies. This disease is characterized by excess thyroid hormone production. Hyperthyroidism can be overt or subclinical. Overt hyperthyroidism is defined as low or suppressed thyroid stimulating hormone (TSH) levels with elevated triiodothyronine (T3) levels and/or elevated thyroxine (T4) levels. Hyperthyroidism is associated with significant short-term and long-term morbidity. Therefore, early recognition of this condition and timely instruction of appropriate therapy is critical. […] Hyperthyroidism has multiple etiologies, clinical manifestations, and treatment modalities. […] The pathophysiology of hyperthyroidism depends on the particular variant of hyperthyroidism. […] This is an autoimmune process with antibodies against the TSH receptor. An interplay between genetic and environmental factors influences this autoimmune process. The antibodies stimulate the TSH receptor (TSHR), leading to increased production and release of thyroid hormones. The trophic effects on the thyroid also lead to the growth of the thyroid gland. […] Pathogenesis of TMNG includes the initial phase of development of the nodular disease. This phase is prolonged and present for years before the nodules develop autonomy for thyroid hormone production. The somatic mutations involving the TSHR lead to constitutive activation of the cAMP signaling pathway, resulting in thyroid autonomy. […] These are solitary nodules with autonomous thyroid hormone production due to somatic mutations in the TSHR. […] This is typically iatrogenic, resulting from excessive iodine intake through diet or administration of iodine-containing medications such as contrast media or amiodarone. […] There are 2 subtypes of AIT: type 1 and type 2. Type 1 AIT leads to increased thyroid hormone production secondary to excess iodine exposure from amiodarone in the setting of pre-existing thyroid disease (as seen in the Jod-Basedow phenomenon). Type 2 AIT is destructive thyroiditis due to the direct toxic effects of amiodarone on the thyroid follicular cells. […] Various etiologies of thyroiditis have this common pathophysiology but vary in their clinical presentations. The inflammation or destruction of the thyroid follicular cells can result from autoimmunity (Hashimoto’s thyroiditis, painless sporadic thyroiditis, and painless, postpartum thyroiditis) or the result of external factors (infections in painful subacute thyroiditis, suppurative thyroiditis, drug-induced thyroiditis).
  • #24 Hyperthyroidism: Diagnosis and Treatment | AAFP
    https://www.aafp.org/pubs/afp/issues/2005/0815/p623.html
    Toxic multinodular goiter causes 5 percent of the cases of hyperthyroidism in the United States and can be 10 times more common in iodine-deficient areas. […] Toxic adenomas are autonomously functioning nodules that are found most commonly in younger patients and in iodine-deficient areas. […] Subacute thyroiditis produces an abrupt onset of thyrotoxic symptoms as hormone leaks from an inflamed gland. […] Iodine-induced hyperthyroidism can occur after intake of excess iodine in the diet, exposure to radiographic contrast media, or medications. Excess iodine increases the synthesis and release of thyroid hormone in iodine-deficient patients and in older patients with preexisting multinodular goiters. […] Amiodarone- (Cordarone-) induced hyperthyroidism can be found in up to 12 percent of treated patients, especially those in iodine-deficient areas, and occurs by two mechanisms.
  • #25 Hyperthyroidism | Nutrition Guide for Clinicians
    https://nutritionguide.pcrm.org/nutritionguide/view/Nutrition_Guide_for_Clinicians/1342005/all/Hyperthyroidism
    Thyroid storm is a rare and life-threatening form of hyperthyroidism. It can be precipitated by several factors in individuals with thyrotoxicosis and may be the first sign of this condition. […] Antithyroid drugs, such as methimazole and propylthiouracil, block thyroid hormone synthesis or conversion of active thyroid hormone. […] Radioactive iodine (I131) to ablate thyroid tissue is a definitive treatment with excellent success rates, and it is the most commonly used treatment in the US. […] Iodine-induced hyperthyroidism has been reported in patients after treatment for previous thyroid diseases. Specifically, patients treated with antithyroid drugs for Graves disease are prone to develop iodine-induced hyperthyroidism. […] Patients with celiac disease have an increased prevalence of autoimmune disease, including Graves disease.
  • #26 Hyperthyroidism – StatPearls – NCBI Bookshelf
    https://www.ncbi.nlm.nih.gov/books/NBK537053/
    Hyperthyroidism is a common thyroid disorder with multiple underlying etiologies. This disease is characterized by excess thyroid hormone production. Hyperthyroidism can be overt or subclinical. Overt hyperthyroidism is defined as low or suppressed thyroid stimulating hormone (TSH) levels with elevated triiodothyronine (T3) levels and/or elevated thyroxine (T4) levels. Hyperthyroidism is associated with significant short-term and long-term morbidity. Therefore, early recognition of this condition and timely instruction of appropriate therapy is critical. […] Hyperthyroidism has multiple etiologies, clinical manifestations, and treatment modalities. […] The pathophysiology of hyperthyroidism depends on the particular variant of hyperthyroidism. […] This is an autoimmune process with antibodies against the TSH receptor. An interplay between genetic and environmental factors influences this autoimmune process. The antibodies stimulate the TSH receptor (TSHR), leading to increased production and release of thyroid hormones. The trophic effects on the thyroid also lead to the growth of the thyroid gland. […] Pathogenesis of TMNG includes the initial phase of development of the nodular disease. This phase is prolonged and present for years before the nodules develop autonomy for thyroid hormone production. The somatic mutations involving the TSHR lead to constitutive activation of the cAMP signaling pathway, resulting in thyroid autonomy. […] These are solitary nodules with autonomous thyroid hormone production due to somatic mutations in the TSHR. […] This is typically iatrogenic, resulting from excessive iodine intake through diet or administration of iodine-containing medications such as contrast media or amiodarone. […] There are 2 subtypes of AIT: type 1 and type 2. Type 1 AIT leads to increased thyroid hormone production secondary to excess iodine exposure from amiodarone in the setting of pre-existing thyroid disease (as seen in the Jod-Basedow phenomenon). Type 2 AIT is destructive thyroiditis due to the direct toxic effects of amiodarone on the thyroid follicular cells. […] Various etiologies of thyroiditis have this common pathophysiology but vary in their clinical presentations. The inflammation or destruction of the thyroid follicular cells can result from autoimmunity (Hashimoto’s thyroiditis, painless sporadic thyroiditis, and painless, postpartum thyroiditis) or the result of external factors (infections in painful subacute thyroiditis, suppurative thyroiditis, drug-induced thyroiditis).
  • #27 Hyperthyroidism – Symptoms and causes – Mayo Clinic
    https://www.mayoclinic.org/diseases-conditions/hyperthyroidism/symptoms-causes/syc-20373659
    This condition happens when the thyroid gland becomes inflamed. In some cases, it’s due to an autoimmune disorder. In others, the reason for it is unclear. The inflammation can cause extra thyroid hormone stored in the thyroid gland to leak into the bloodstream and cause symptoms of hyperthyroidism.
  • #28 Hyperthyroidism – Endocrine and Metabolic Disorders – Merck Manual Professional Edition
    https://www.merckmanuals.com/professional/endocrine-and-metabolic-disorders/thyroid-disorders/hyperthyroidism
    In hyperthyroidism, serum T3 usually increases more than does T4, probably because of increased secretion of T3 as well as conversion of T4 to T3 in peripheral tissues. […] T3 toxicosis may occur in any of the common disorders that cause hyperthyroidism, including Graves disease, multinodular goiter, and the autonomously functioning solitary thyroid nodule. […] The various forms of thyroiditis commonly have a hyperthyroid phase followed by a hypothyroid phase.
  • #29 Hyperthyroidism – Hormonal and Metabolic Disorders – Merck Manual Consumer Version
    https://www.merckmanuals.com/home/hormonal-and-metabolic-disorders/thyroid-gland-disorders/hyperthyroidism
    Hyperthyroidism is overactivity of the thyroid gland that leads to high levels of thyroid hormones and speeding up of vital body functions. […] Graves disease, the most common cause of hyperthyroidism, is an autoimmune disorder. In an autoimmune disorder, the person’s immune system produces antibodies that attack the body’s own tissues. However, in Graves disease, the antibodies stimulate the thyroid gland to produce and secrete excess thyroid hormones into the blood. […] A toxic (overactive) thyroid nodule (a benign tumor, or adenoma) is an area of abnormal local tissue growth within the thyroid gland. This abnormal tissue produces thyroid hormones even without stimulation by thyroid-stimulating hormone (TSH). […] An overactive pituitary gland can produce too much thyroid-stimulating hormone, which in turn leads to overproduction of thyroid hormones. However, this is an extremely rare cause of hyperthyroidism.
  • #30 Hyperthyroidism: Diagnosis and Treatment | AAFP
    https://www.aafp.org/pubs/afp/issues/2016/0301/p363.html
    Toxic multinodular goiter is the second most common cause of hyperthyroidism in the United States and the most common cause in older persons living in iodine-deficient areas. Over time, nodules arise from the frequent replication of clonogenic cells that leads to a somatic activating mutation of TSH receptors. A single nodule is called a toxic adenoma (Plummer disease). […] In contrast with these three disorders, painless or transient (silent) thyroiditis causes a destruction of thyroid follicles via an autoimmune mechanism and a release of preformed thyroid hormones into the circulation. […] Gestational hyperthyroidism develops in the first trimester of pregnancy as a result of the stimulatory action of placental beta human chorionic gonadotropin (-hCG), which shares structural features with TSH, on the thyroid gland. […] Other rare causes of hyperthyroidism are TSH-secreting pituitary adenoma, metastatic follicular thyroid cancer, and struma ovarii.
  • #31 Pulsenotes | Hyperthyroidism notes
    https://app.pulsenotes.com/medicine/endocrinology/notes/hyperthyroidism
    In metastatic follicular thyroid cancer, malignant tissue may remain functional. The increased amounts of tissue can lead to an overproduction of thyroid hormone. […] Hyperthyroidism may be asymptomatic or present with non-specific malaise or signs of thyroid hormone excess. […] The pathogenesis of Graves ophthalmopathy is not fully understood, it is known that TSHR-Abs are involved. Inflammation and accumulation of mucopolysaccharides occur in the retro-orbital adipose tissue and extra-ocular muscles. […] Measurement of TSH and fT4/fT3 are necessary to diagnose hyperthyroidism. […] TSH levels are the single most important diagnostic test. […] The vast majority of cases of hyperthyroidism are primary in nature. […] Anti-thyroid drugs (thioamides), radioactive iodine (RAI) and surgery are all viable management options.
  • #32 Hyperthyroidism: Diagnosis and Treatment | AAFP
    https://www.aafp.org/pubs/afp/issues/2016/0301/p363.html
    Toxic multinodular goiter is the second most common cause of hyperthyroidism in the United States and the most common cause in older persons living in iodine-deficient areas. Over time, nodules arise from the frequent replication of clonogenic cells that leads to a somatic activating mutation of TSH receptors. A single nodule is called a toxic adenoma (Plummer disease). […] In contrast with these three disorders, painless or transient (silent) thyroiditis causes a destruction of thyroid follicles via an autoimmune mechanism and a release of preformed thyroid hormones into the circulation. […] Gestational hyperthyroidism develops in the first trimester of pregnancy as a result of the stimulatory action of placental beta human chorionic gonadotropin (-hCG), which shares structural features with TSH, on the thyroid gland. […] Other rare causes of hyperthyroidism are TSH-secreting pituitary adenoma, metastatic follicular thyroid cancer, and struma ovarii.
  • #33 Hyperthyroidism: Diagnosis and Treatment | AAFP
    https://www.aafp.org/pubs/afp/issues/2005/0815/p623.html
    Factitial hyperthyroidism is caused by the intentional or accidental ingestion of excess amounts of thyroid hormone. […] Rare causes of hyperthyroidism include metastatic thyroid cancer, ovarian tumors that produce thyroid hormone (struma ovarii), trophoblastic tumors that produce human chorionic gonadotrophin and activate highly sensitive TSH receptors, and TSH-secreting pituitary tumors. […] The treatment of hyperthyroidism depends on the cause and severity of the disease, as well as on the patients age, goiter size, comorbid conditions, and treatment desires. […] Antithyroid drugs act principally by interfering with the organification of iodine, thereby suppressing thyroid hormone levels. Methimazole (Tapazole) and propylthiouracil (PTU) are the two agents available in the United States.
  • #34 Hyperthyroidism – Wikipedia
    https://en.wikipedia.org/wiki/Hyperthyroidism
    Hyperthyroidism is an endocrine disease in which the thyroid gland produces excessive amounts of thyroid hormones. Thyrotoxicosis is a condition that occurs due to elevated levels of thyroid hormones of any cause and therefore includes hyperthyroidism. Graves’ disease is the cause of about 50% to 80% of the cases of hyperthyroidism in the United States. Other causes include multinodular goiter, toxic adenoma, inflammation of the thyroid, eating too much iodine, and too much synthetic thyroid hormone. The diagnosis may be suspected based on signs and symptoms and then confirmed with blood tests. Typically blood tests show a low thyroid stimulating hormone (TSH) and raised T3 or T4. Treatment depends partly on the cause and severity of disease. There are three main treatment options: radioiodine therapy, medications, and thyroid surgery. Radioiodine therapy involves taking iodine-131 by mouth which is then concentrated in and destroys the thyroid over weeks to months. The resulting hypothyroidism is treated with synthetic thyroid hormone. Medications such as beta blockers may control the symptoms, and anti-thyroid medications such as methimazole may temporarily help people while other treatments are having an effect. Thyroid storm is a severe form of thyrotoxicosis characterized by rapid and often irregular heart beat, high temperature, vomiting, diarrhea, and mental agitation. Thyroid storm usually occurs due to untreated hyperthyroidism and can be provoked by infections.
  • #35 Hyperthyroidism – Endocrine and Metabolic Disorders – Merck Manual Professional Edition
    https://www.merckmanuals.com/professional/endocrine-and-metabolic-disorders/thyroid-disorders/hyperthyroidism
    In hyperthyroidism, serum T3 usually increases more than does T4, probably because of increased secretion of T3 as well as conversion of T4 to T3 in peripheral tissues. […] T3 toxicosis may occur in any of the common disorders that cause hyperthyroidism, including Graves disease, multinodular goiter, and the autonomously functioning solitary thyroid nodule. […] The various forms of thyroiditis commonly have a hyperthyroid phase followed by a hypothyroid phase.
  • #36 Hyperthyroidism – Endocrine and Metabolic Disorders – Merck Manual Professional Edition
    https://www.merckmanuals.com/professional/endocrine-and-metabolic-disorders/thyroid-disorders/hyperthyroidism
    In hyperthyroidism, serum T3 usually increases more than does T4, probably because of increased secretion of T3 as well as conversion of T4 to T3 in peripheral tissues. […] T3 toxicosis may occur in any of the common disorders that cause hyperthyroidism, including Graves disease, multinodular goiter, and the autonomously functioning solitary thyroid nodule. […] The various forms of thyroiditis commonly have a hyperthyroid phase followed by a hypothyroid phase.
  • #37 Azthena logo with the word Azthena
    https://www.news-medical.net/health/Overactive-Thyroid-and-Tremors.aspx
    An overactive thyroid results in the excessive production of thyroid hormone. This disorder is called hyperthyroidism. […] Hyperthyroidism is a condition in which the metabolic balance of the body is up regulated, resulting in increased energy production by every cell of the body. As a result, the nervous stimuli become excessive, resulting in hand tremor. […] The thyroid hormones (thyroxine and triiodothyronine) increase the excitability of the nerve cells in the oscillatory loops of the central and peripheral nervous systems. This is by increasing the number of calcium channels and beta-adrenergic receptors formed in response to calcium channels in all cells capable of excitation. […] Oscillatory tremor is caused by reflexes originating in the afferent muscle pathways. This increases the amplitude of the tremor above the normal fine oscillation, by producing a synchronized tremor.
  • #38 Hyperthyroidism and Thyrotoxicosis: Practice Essentials, Background, Pathophysiology
    https://emedicine.medscape.com/article/121865-overview
    Any process that causes an increase in the peripheral circulation of unbound thyroid hormone can cause thyrotoxicosis. […] Disturbances of the normal homeostatic mechanism can occur at the level of the pituitary gland, the thyroid gland, or in the periphery. […] Regardless of etiology, the result is an increase in transcription in cellular proteins, causing an increase in the basal metabolic rate. […] In many ways, signs and symptoms of hyperthyroidism resemble a state of catecholamine excess, and adrenergic blockade can improve these symptoms.
  • #39 Hyperthyroidism and Thyrotoxicosis: Practice Essentials, Background, Pathophysiology
    https://emedicine.medscape.com/article/121865-overview
    Any process that causes an increase in the peripheral circulation of unbound thyroid hormone can cause thyrotoxicosis. […] Disturbances of the normal homeostatic mechanism can occur at the level of the pituitary gland, the thyroid gland, or in the periphery. […] Regardless of etiology, the result is an increase in transcription in cellular proteins, causing an increase in the basal metabolic rate. […] In many ways, signs and symptoms of hyperthyroidism resemble a state of catecholamine excess, and adrenergic blockade can improve these symptoms.
  • #40 Azthena logo with the word Azthena
    https://www.news-medical.net/health/Overactive-Thyroid-and-Tremors.aspx
    An overactive thyroid results in the excessive production of thyroid hormone. This disorder is called hyperthyroidism. […] Hyperthyroidism is a condition in which the metabolic balance of the body is up regulated, resulting in increased energy production by every cell of the body. As a result, the nervous stimuli become excessive, resulting in hand tremor. […] The thyroid hormones (thyroxine and triiodothyronine) increase the excitability of the nerve cells in the oscillatory loops of the central and peripheral nervous systems. This is by increasing the number of calcium channels and beta-adrenergic receptors formed in response to calcium channels in all cells capable of excitation. […] Oscillatory tremor is caused by reflexes originating in the afferent muscle pathways. This increases the amplitude of the tremor above the normal fine oscillation, by producing a synchronized tremor.
  • #41 Azthena logo with the word Azthena
    https://www.news-medical.net/health/Overactive-Thyroid-and-Tremors.aspx
    An overactive thyroid results in the excessive production of thyroid hormone. This disorder is called hyperthyroidism. […] Hyperthyroidism is a condition in which the metabolic balance of the body is up regulated, resulting in increased energy production by every cell of the body. As a result, the nervous stimuli become excessive, resulting in hand tremor. […] The thyroid hormones (thyroxine and triiodothyronine) increase the excitability of the nerve cells in the oscillatory loops of the central and peripheral nervous systems. This is by increasing the number of calcium channels and beta-adrenergic receptors formed in response to calcium channels in all cells capable of excitation. […] Oscillatory tremor is caused by reflexes originating in the afferent muscle pathways. This increases the amplitude of the tremor above the normal fine oscillation, by producing a synchronized tremor.
  • #42 Hyperthyroidism and Seizures: Does One Lead to the Other?
    https://www.healthline.com/health/hyperthyroidism-seizures
    Hyperthyroidism has been linked to an increased risk of seizures. It may increase risk by creating excitability in your brain that lowers the threshold needed for one to occur. […] Its thought that hyperthyroidism might make you more prone to seizures by increasing the excitability in your brain. Seizures can also develop due to a serious complication of hyperthyroidism called a thyroid storm. […] Excessive thyroid hormone circulating through your bloodstream is called thyrotoxicosis. Thyrotoxicosis has been associated with seizures in people with no previous history of seizures or epilepsy. […] The results of animal research suggest that high levels of thyroid hormone might increase brain excitability and lower the seizure threshold. The exact mechanism by which thyroid hormone might influence seizure development is still largely unknown.
  • #43 Associations of hyperthyroidism with epilepsy: a Mendelian randomization study | Scientific Reports
    https://www.nature.com/articles/s41598-024-54933-w
    Hyperthyroidism, or thyrotoxicosis, is a common endocrine disorder with a rising incidence and a tendency for an earlier onset. […] Neurological complications are common in individuals with hyperthyroidism, and some present with symptoms like tremors when seeking medical attention. […] These complications mainly stem from direct stimulatory effects of thyroid hormones, a hypermetabolic state, autoimmune factors, thyroid tissue enlargement, and compression of surrounding nerves by the extraocular muscles. […] Hyperthyroidism was found to be causally related to all epilepsy but had no effect on other types of epilepsy. […] The precise relationship between thyroid hyperactivity and seizure risk remains enigmatic. […] The impact of elevated thyroid hormones on sodium-potassium adenosine triphosphatase activity, leading to significant alterations in neuronal sodium concentrations, has been acknowledged. […] A comprehensive grasp of the nuanced mechanisms through which thyroid hormones modulate brain excitability remains elusive. […] This study found evidence for a possible link between hyperthyroidism and an increased risk of epilepsy.
  • #44 Associations of hyperthyroidism with epilepsy: a Mendelian randomization study | Scientific Reports
    https://www.nature.com/articles/s41598-024-54933-w
    Hyperthyroidism, or thyrotoxicosis, is a common endocrine disorder with a rising incidence and a tendency for an earlier onset. […] Neurological complications are common in individuals with hyperthyroidism, and some present with symptoms like tremors when seeking medical attention. […] These complications mainly stem from direct stimulatory effects of thyroid hormones, a hypermetabolic state, autoimmune factors, thyroid tissue enlargement, and compression of surrounding nerves by the extraocular muscles. […] Hyperthyroidism was found to be causally related to all epilepsy but had no effect on other types of epilepsy. […] The precise relationship between thyroid hyperactivity and seizure risk remains enigmatic. […] The impact of elevated thyroid hormones on sodium-potassium adenosine triphosphatase activity, leading to significant alterations in neuronal sodium concentrations, has been acknowledged. […] A comprehensive grasp of the nuanced mechanisms through which thyroid hormones modulate brain excitability remains elusive. […] This study found evidence for a possible link between hyperthyroidism and an increased risk of epilepsy.
  • #45 Hyperthyroidism and Diarrhea: Causes and Treatment
    https://www.healthline.com/health/hyperthyroidism-and-diarrhea
    When you have hyperthyroidism, it can make your bodys fight or flight system work too much and cause diarrhea and other gastrointestinal (GI) tract symptoms. […] Hyperthyroidism happens when your thyroid produces too much of these hormones, speeding up your metabolism. Causes of hyperthyroidism include conditions like Graves disease, too much iodine consumption, or harmless nodules that grow on the thyroid. […] The thyroid has a close connection to these responses of sympathetic nervous system. With hyperthyroidism, the thyroid produces too many T4 and T3 hormones, overstimulating the nerves that manage your digestive tract. […] When your bowel nerves are overstimulated, they can increase your intestinal motility, which refers to the movement and contraction of muscles in the intestines. This causes your bowel muscles to contract more quickly than usual and push food through before its fully digested. This also prevents fluids from being fully absorbed from food as it passes through, leading to watery diarrhea.
  • #46 Hyperthyroidism and Diarrhea: Causes and Treatment
    https://www.healthline.com/health/hyperthyroidism-and-diarrhea
    When you have hyperthyroidism, it can make your bodys fight or flight system work too much and cause diarrhea and other gastrointestinal (GI) tract symptoms. […] Hyperthyroidism happens when your thyroid produces too much of these hormones, speeding up your metabolism. Causes of hyperthyroidism include conditions like Graves disease, too much iodine consumption, or harmless nodules that grow on the thyroid. […] The thyroid has a close connection to these responses of sympathetic nervous system. With hyperthyroidism, the thyroid produces too many T4 and T3 hormones, overstimulating the nerves that manage your digestive tract. […] When your bowel nerves are overstimulated, they can increase your intestinal motility, which refers to the movement and contraction of muscles in the intestines. This causes your bowel muscles to contract more quickly than usual and push food through before its fully digested. This also prevents fluids from being fully absorbed from food as it passes through, leading to watery diarrhea.
  • #47 Diarrhea as the only symptoms in hyperthyroidism-case report | ECE2022 | European Congress of Endocrinology 2022 | Endocrine Abstracts
    https://www.endocrine-abstracts.org/ea/0081/ea0081ep1107
    Hyperthyroidism (overactive thyroid) is a condition where thyroid makes and releases high levels of thyroid hormone (thyroxine) in the blood. This condition can speed up our body metabolism. Hyperthyroidism causes an overactivity of the sympathetic system. […] Unimazole control of such cases of hyperthyroidism with diarrhea can be explained by the effect of this drug in reducing intestinal hypermotility as the basis of physiopathology in hyperthyroidism. […] Thyroid hormone in excess, among its other possible effects in the organism, affect the gastrointestinal tract through sympathetic intestinal hyperstimulation and increased motility causing diarrhea. Antithyroid therapy act by blocking sympathetic hyperstimulation. Our case leads us to think that hyperthyroidism should be considered in the differential diagnosis of diarrhea of unknown cause.
  • #48 Hyperthyroidism and Diarrhea: Causes and Treatment
    https://www.healthline.com/health/hyperthyroidism-and-diarrhea
    Hyperthyroidism also has links to other GI tract problems that can result from increased metabolism. […] When food passes through your digestive tract too quickly, your intestines dont have enough time to absorb nutrients from your food. This is called malabsorption. Inflammation that may result from hyperthyroidism can also keep your intestines from absorbing nutrients as usual, leading to malnutrition. […] Hyperthyroidism can overstimulate the sympathetic nervous system and cause diarrhea and other gastrointestinal (GI) tract symptoms. These may include frequent bowel movements and malnutrition.
  • #49 Hyperthyroidism and menstrual cycle: Periods, fertility, and more
    https://www.medicalnewstoday.com/articles/hyperthyroidism-and-menstrual-cycle
    Hyperthyroidism is when the thyroid gland, a small, butterfly-shaped gland at the front of the neck, produces more thyroid hormones than the body needs. […] Thyroid hormones are essential to most bodily functions, systems, and organs, including the menstrual cycle and reproductive system. […] In people with hyperthyroidism, menstruation may occur irregularly, and menstrual flow may be lighter. This may cause fertility problems. […] Hyperthyroidism can cause low levels of a protein called sex hormone binding globulin (SHBG). This protein attaches itself to both male and female sex hormones. […] A person with abnormal SHBG levels may experience fertility problems. […] An irregular menstrual cycle is a potential complication of hyperthyroidism. […] People with hyperthyroidism are more likely to experience abnormally low bleeding during periods. This is known as hypomenorrhea.
  • #50 Hyperthyroidism and menstrual cycle: Periods, fertility, and more
    https://www.medicalnewstoday.com/articles/hyperthyroidism-and-menstrual-cycle
    Hyperthyroidism can also cause a person to have fewer periods. […] In thyroid disorders, such as hyperthyroidism, elevated levels of the hormone prolactin in the blood may lead to impaired ovulation, which can cause irregularities and stoppages in menstruation. […] Because hyperthyroidism can affect ovulation, which is the release of an egg from the ovary, it can affect fertility. […] Increased prolactin levels can prevent the egg, or ovum, from releasing and traveling down the fallopian tube in preparation for fertilization. […] If the immune system is the cause of a persons hyperthyroidism for example, in Graves disease it may affect other glands, including the ovaries. […] When this occurs, the condition can lead to premature menopause before the age of 40. […] Hyperthyroidism can cause menstrual problems because it leads to higher production of the protein sex hormone-binding globulin (SHBG), which can lead to irregular, lighter, or missed periods.
  • #51 Hyperthyroidism and menstrual cycle: Periods, fertility, and more
    https://www.medicalnewstoday.com/articles/hyperthyroidism-and-menstrual-cycle
    Hyperthyroidism can also cause a person to have fewer periods. […] In thyroid disorders, such as hyperthyroidism, elevated levels of the hormone prolactin in the blood may lead to impaired ovulation, which can cause irregularities and stoppages in menstruation. […] Because hyperthyroidism can affect ovulation, which is the release of an egg from the ovary, it can affect fertility. […] Increased prolactin levels can prevent the egg, or ovum, from releasing and traveling down the fallopian tube in preparation for fertilization. […] If the immune system is the cause of a persons hyperthyroidism for example, in Graves disease it may affect other glands, including the ovaries. […] When this occurs, the condition can lead to premature menopause before the age of 40. […] Hyperthyroidism can cause menstrual problems because it leads to higher production of the protein sex hormone-binding globulin (SHBG), which can lead to irregular, lighter, or missed periods.
  • #52 Gynecomastia as a presenting symptom of Graves’ disease in a 49-year-old man in: Endocrinology, Diabetes & Metabolism Case Reports Volume 2021 Issue 1 (2021)
    https://edm.bioscientifica.com/view/journals/edm/2021/1/EDM20-0181.xml
    The underlying mechanism of an increased expression of SHBG is not well understood. However, in vitro and in vivo research in mice suggests that thyrotoxicosis causes an increased expression of HNF4A in liver cells. Thus, upregulating the expression of SHBG. […] Two different mechanisms contribute to the development of gynecomastia in thyrotoxicosis. The first and major contributing factor to this disbalance is a thyroid hormone-induced increased production of the plasma protein SHBG in the liver. […] The exact pathway behind thyroid hormone increased SHBG levels remains unclear, but hepatocyte nuclear factor-4 (HNF4A) seems to play an essential role. […] Interestingly, this gene also seems to play an important role in diabetes and specifically in maturity-onset diabetes of the young (MODY) in pancreatic -cells. […] The second underlying pathophysiological cause is due to an increased activity of aromatase by thyroid hormones, that converts androgens into estrogens in peripheral tissue. Thus, dysregulating the hormonal balance by increasing estrogen levels.
  • #53 Thyroid Disorders: Types, Signs, Symptoms, Treatment & Causes
    https://www.medicinenet.com/thyroid_disorders/article.htm
    Hyperthyroidism describes excessive production of thyroid hormone, a less common condition than hypothyroidism. Symptoms of hypothyroidism usually relate to increased metabolism. In mild cases, there may not be apparent symptoms. […] Some of the most common causes of hyperthyroidism include: Graves’ disease, Toxic multinodular goiter, Thyroid nodules that overexpress thyroid hormone (known as „hot” nodules), Excessive iodine consumption. […] If untreated, hyperthyroidism can lead to various complications, such as: Cardiac (heart) complications: Cardiac complications of hyperthyroidism can be serious and life-threatening. Cardiac complications include a rapid heart rate and altered heart rhythm called atrial fibrillation which can increase the risk of stroke and heart failure. […] Thyrotoxic crisis: Thyrotoxic crisis is a sudden intensification of symptoms, causing fever, palpitations, and altered mental status. This requires emergency medical attention.
  • #54 Graves’ Disease: What It Is, Causes, Symptoms & Treatment
    https://my.clevelandclinic.org/health/diseases/15244-graves-disease
    If Graves disease is properly treated, the prognosis (outlook) is generally good. […] Untreated or poorly managed Graves disease increases your risk for these complications: […] Thyroid storm (also called thyroid crisis and thyrotoxic crisis) happens when your thyroid gland releases a large amount of thyroid hormone in a short amount of time. Its a rare complication of hyperthyroidism and Graves disease and can happen if you suddenly stop taking your antithyroid medication or experience trauma or an infection. Thyroid storm is a medical emergency and is life-threatening. Symptoms include high fever and a rapid heart rate.
  • #55 Thyroid Disorders: Types, Signs, Symptoms, Treatment & Causes
    https://www.medicinenet.com/thyroid_disorders/article.htm
    Hyperthyroidism describes excessive production of thyroid hormone, a less common condition than hypothyroidism. Symptoms of hypothyroidism usually relate to increased metabolism. In mild cases, there may not be apparent symptoms. […] Some of the most common causes of hyperthyroidism include: Graves’ disease, Toxic multinodular goiter, Thyroid nodules that overexpress thyroid hormone (known as „hot” nodules), Excessive iodine consumption. […] If untreated, hyperthyroidism can lead to various complications, such as: Cardiac (heart) complications: Cardiac complications of hyperthyroidism can be serious and life-threatening. Cardiac complications include a rapid heart rate and altered heart rhythm called atrial fibrillation which can increase the risk of stroke and heart failure. […] Thyrotoxic crisis: Thyrotoxic crisis is a sudden intensification of symptoms, causing fever, palpitations, and altered mental status. This requires emergency medical attention.
  • #56 Hyperthyroidism – Endocrine and Metabolic Disorders – Merck Manual Professional Edition
    https://www.merckmanuals.com/professional/endocrine-and-metabolic-disorders/thyroid-disorders/hyperthyroidism
    Hyperthyroidism may result from increased synthesis and secretion of thyroid hormones (thyroxine [T4] and triiodothyronine [T3]) from the thyroid, caused by thyroid-stimulating immunoglobulin (TSI) or by autonomous thyroid hyperfunction. […] Graves disease is caused by an autoantibody (TSI) against the thyroid receptor for thyroid-stimulating hormone (TSH); unlike most autoantibodies, which are inhibitory, this autoantibody is stimulatory, thus causing continuous synthesis and secretion of excess T4 and T3. […] The pathogenesis of infiltrative ophthalmopathy (responsible for the exophthalmos in Graves disease) is poorly understood but may result from immunoglobulins directed to the TSH receptors in the orbital fibroblasts and fat that result in release of proinflammatory cytokines, inflammation, and accumulation of glycosaminoglycans.
  • #57 Hyperthyroidism and Seizures: Does One Lead to the Other?
    https://www.healthline.com/health/hyperthyroidism-seizures
    Hyperthyroidism has been linked to many different neurological complications, such as movement disorders, tremors, atypical involuntary muscle movements, emotional and cognitive impairment, psychiatric disorders, headaches, sleep disorders, and nerve damage. […] Hyperthyroidism has been linked to an increased risk of seizures. Additionally, seizures are also associated with a complication of hyperthyroidism called a thyroid storm.
  • #58 Hyperthyroidism and menstrual cycle: Periods, fertility, and more
    https://www.medicalnewstoday.com/articles/hyperthyroidism-and-menstrual-cycle
    Elevated levels of the hormone prolactin in the blood, which can affect menstruation, ovulation, and fertility. […] High levels of prolactin and the protein SHBG can interfere with the functioning of the ovaries, causing periods to become irregular, infrequent, or lighter than usual. It can also cause periods to stop. […] Because hyperthyroidism may directly affect ovulation, it can lead to infertility or difficulty conceiving. […] If a person does not receive treatment, hyperthyroidism can lead to serious health problems.
  • #59 Hyperthyroidism in Cats | Cornell University College of Veterinary Medicine
    https://www.vet.cornell.edu/departments-centers-and-institutes/cornell-feline-health-center/health-information/feline-health-topics/hyperthyroidism-cats
    Because of the important role the thyroid gland plays in the body, some cats with hyperthyroidism develop secondary problems, including heart disease and high blood pressure. […] Elevated thyroid hormones stimulate an increased heart rate and a stronger contraction of the heart muscle, and can cause thickening of the left ventricle of the heart over time. […] Hypertension, or high blood pressure, is another potential complication of hyperthyroidism, and can cause additional damage to several organs, including the eyes, kidneys, heart, and brain. […] The prognosis for cats with hyperthyroidism is generally good with appropriate therapy.
  • #60 Graves’ Disease Testing – Testing.com
    https://www.testing.com/graves-disease-testing/
    Graves’ disease is an autoimmune disease which most commonly causes hyperthyroidism, or an overactive thyroid. When you have Graves’ disease, your immune system makes thyroid antibodies which cause your thyroid gland to produce more thyroid hormones than needed by the body. […] Hyperthyroidism increases a person’s metabolism and causes symptoms such as anxiety, weight loss, intolerance to heat, and sleep problems. […] Although most cases of hyperthyroidism are due to Graves’ disease, an overactive thyroid gland can also be caused by other medical problems, such as certain medications, too much iodine in the diet, and thyroid tumors. […] Patients being evaluated for Graves’ disease may have tests that measure thyroid hormone levels, tests that detect the presence of thyroid antibodies, and imaging tests. […] The following imaging tests may be ordered: Radioactive Iodine Uptake, Thyroid Scan, Ultrasound.
  • #61 Graves’ Disease
    https://www.thyroid.org/graves-disease/
    Graves disease is an autoimmune disease that leads to a generalized overactivity of the entire thyroid gland (hyperthyroidism). […] In Graves disease these antibodies (called the thyrotropin receptor antibodies (TRAb) or thyroid stimulating immunoglobulins (TSI) do the opposite they cause the cells to work overtime. The antibodies in Graves disease bind to receptors on the surface of thyroid cells and stimulate those cells to overproduce and release thyroid hormones. This results in an overactive thyroid (hyperthyroidism). […] The diagnosis of hyperthyroidism is made on the basis of your symptoms and findings during a physical exam and it is confirmed by laboratory tests that measure the amount of thyroid hormones (thyroxine, or T4, and triiodothyronine, or T3) and thyroid-stimulating hormone (TSH) in your blood.
  • #62 Hyperthyroidism | Graves’ Disease | Overactive Thyroid | MedlinePlus
    https://medlineplus.gov/hyperthyroidism.html
    Hyperthyroidism, or overactive thyroid, happens when your thyroid gland makes more thyroid hormones than your body needs. […] Hyperthyroidism has several causes. They include: Graves’ disease, an autoimmune disorder in which your immune system attacks your thyroid and causes it to make too much hormone. This is the most common cause. […] Thyroiditis, inflammation of the thyroid. It causes stored thyroid hormone to leak out of your thyroid gland. […] If hyperthyroidism isn’t treated, it can cause some serious health problems, including: An irregular heartbeat that can lead to blood clots, stroke, heart failure, and other heart problems. […] Radioiodine therapy is a common and effective treatment for hyperthyroidism. It involves taking radioactive iodine by mouth as a capsule or liquid. This slowly destroys the cells of the thyroid gland that produce thyroid hormone.
  • #63 Hyperthyroidism | American Thyroid Association
    https://www.thyroid.org/hyperthyroidism/
    Hyperthyroidism can be caused by an autoimmune condition (Graves disease), inflammation of the thyroid (thyroiditis), or due to thyroid nodules making too much thyroid hormone (hot nodule or toxic multinodular goiter). […] Graves disease is the most common cause of hyperthyroidism. It is an autoimmune thyroid condition caused by antibodies that stimulate all the cells in the thyroid gland to make too much thyroid hormone. […] Thyroiditis is due to inflammation of your thyroid gland. This can cause the thyroid hormones inside the thyroid gland to leak out into the blood stream, resulting in too much thyroid hormone in the body. […] Hyperthyroidism due to thyroiditis is usually self-limited, meaning that it goes away on its own after a few weeks to months. In some cases, hypothyroidism (underactive thyroid) can occur after the hyperthyroidism stage of thyroiditis. […] Radioactive iodine works by destroying the thyroid cells that are making thyroid hormones. This treatment works for Graves disease and toxic nodules but is not effective in thyroiditis. […] Hyperthyroidism can be cured by surgical removal of the overactive thyroid gland or nodules.
  • #64 Hyperthyroidism – Hormonal and Metabolic Disorders – Merck Manual Consumer Version
    https://www.merckmanuals.com/home/hormonal-and-metabolic-disorders/thyroid-gland-disorders/hyperthyroidism
    Thyroid storm, which is sudden extreme overactivity of the thyroid gland, is a life-threatening emergency. All body functions are accelerated to dangerously high levels. […] Treatment of hyperthyroidism depends on the cause. In most cases, the problem causing hyperthyroidism can be cured or the symptoms can be eliminated or greatly reduced. […] Radioactive iodine may be given by mouth to destroy part of the thyroid gland. This is the most common treatment for hyperthyroidism. […] Methimazole and propylthiouracil are the medications most commonly used to treat hyperthyroidism. They work by decreasing the gland’s production of thyroid hormones. […] In Graves disease, additional treatment may be needed for the eye and skin symptoms.
  • #65 Hyperthyroidism – Life Extension
    https://www.lifeextension.com/protocols/metabolic-health/hyperthyroidism?srsltid=AfmBOorhGBSztUHNekvX-jwByu6ut5w6Vxfd89hJN8TcL1Cc_9JPQMTp
    In most cases of hyperthyroidism, the thyroid gland is overactive even though it is not being stimulated by TSH. This is known as primary hyperthyroidism. […] Risk factors for hyperthyroidism include family history, female gender, and having certain medical conditions such as type 1 diabetes and adrenal insufficiency. […] Anti-thyroid drugs (thionamides), such as methimazole (Tapazole) and propylthiouracil, prevent the thyroid gland from making too much T3 and T4. […] Radioactive iodine therapy involves orally consuming sodium iodide (I-131). I-131 is absorbed into the thyroid gland where it emits local radiation and damages thyroid cells over a period of 12 to 18 weeks. […] Patients who undergo thyroid-ablative treatment like radioactive iodine or surgery typically experience overt or subclinical hypothyroidism after treatment.
  • #66 Become a member
    https://www.btf-thyroid.org/older-patients-and-thyroid-disease
    Symptoms of hyperthyroidism may be brought under control with other medications alongside the antithyroid drugs such as beta-blockers, which are often given to slow a rapid heart rate. Definitive treatment with radioactive iodine is considered once thyroid function is maintained in the normal range with oral medication.
  • #67 Radioactive Iodine (I-131) Therapy for Hyperthyroidism
    https://www.radiologyinfo.org/en/info/radioiodine
    Radioactive Iodine I-131 (also called Radioiodine I-131) therapy is a nuclear medicine treatment. Doctors use it to treat an overactive thyroid, a condition called hyperthyroidism. Hyperthyroidism can be caused by Graves’ disease, in which the entire thyroid gland is overactive, or by nodules within the gland which are locally overactive in producing too much thyroid hormone. […] The thyroid is a gland in the neck that produces two hormones. These hormones regulate all aspects of the body’s metabolism, the chemical process of converting food into energy. When a thyroid gland is overactive, it produces too much of these hormones, accelerating the metabolism. […] The radioiodine I-131 is swallowed in a single capsule or liquid dose and is quickly absorbed into the bloodstream in the gastrointestinal (GI) tract. It is concentrated from the blood by the thyroid gland, where it begins destroying the gland’s cells. Although the radioactivity remains in the thyroid for some time, it is greatly diminished within a few days. The effect of this treatment on the thyroid gland usually takes between one and three months to develop. Maximum benefit occurs three to six months after treatment. Usually, a single dose is successful in treating hyperthyroidism. However, rarely, a second treatment is necessary. A third treatment is very rarely necessary. […] It is highly likely that this procedure will destroy some or most of your thyroid gland. Since hormones produced by the thyroid are essential for metabolism, most patients will need to take thyroid pills for the rest of their life following the procedure.