Materiały źródłowe

• #1 Primary Hyperparathyroidism – StatPearls – NCBI Bookshelf

  https://www.ncbi.nlm.nih.gov/books/NBK441895/

  Primary hyperparathyroidism is an endocrine disorder characterized by increased parathyroid hormone secretion, leading to hypercalcemia and renal and skeletal complications. […] Primary hyperparathyroidism involves excess parathyroid hormone (PTH) production by 1 of the 4 very small parathyroid glands normally located peripherally along the margins on the posterior aspect of the thyroid gland. […] A combination of increased clonal proliferation of parathyroid tissue with reduced CaSR usually causes primary hyperparathyroidism. […] PTH activates PTH receptors, increasing the resorption of calcium and phosphate from bone, enhancing the distal tubular calcium reabsorption, and decreasing renal phosphorus reabsorption. […] The primary regulator of PTH release is serum calcium, acting on the calcium-sensing receptors on the parathyroid surface.

• #2 Hyperparathyroidism: Background, Anatomy and Embryology, Primary Hyperparathyroidism

  https://emedicine.medscape.com/article/127351-overview

  Through their secretion of parathyroid hormone (PTH), an 84amino acid polypeptide hormone, the parathyroid glands are primarily responsible for maintaining extracellular calcium concentrations. Hyperparathyroidism is a disease characterized by excessive secretion of parathyroid hormone. The secretion of parathyroid hormone is regulated directly by the plasma concentration of ionized calcium. […] The main effects of parathyroid hormone are to increase the concentration of plasma calcium by increasing the release of calcium and phosphate from bone matrix, increasing calcium reabsorption by the kidney, and increasing renal production of 1,25-dihydroxyvitamin D-3 (calcitriol), which increases intestinal absorption of calcium. Thus, overproduction of parathyroid hormone results in elevated levels of plasma calcium. Parathyroid hormone also causes phosphaturia, thereby decreasing serum phosphate levels. Hyperparathyroidism is usually subdivided into primary, secondary, and tertiary hyperparathyroidism.

• #3 Primary Hyperparathyroidism – StatPearls – NCBI Bookshelf

  https://www.ncbi.nlm.nih.gov/books/NBK441895/

  PTH is a crucial hormone required to maintain calcium homeostasis, whose net effect is to increase serum calcium levels. […] PTH normally reduces urinary calcium excretion, but this effect can be overcome by significant hypercalcemia, which is why hypercalciuria can be found in primary hyperparathyroidism. […] The calcium-sensing receptor (CaSR) found on the parathyroid gland is also found in kidney tubules, especially the thick ascending loop of Henle, where about 25% of filtered calcium is reabsorbed. […] Chronic kidney disease causes a secondary increase in serum PTH levels due to hypocalcemia from decreased 1,25-VitD. […] The chronic stimulation of the parathyroid glands results in diffuse, multiglandular parathyroid hyperplasia. […] Parathyroid adenomas tend to be encapsulated and are typically composed primarily of chief cells.

• #4 Hyperparathyroidism – Wikipedia

  https://en.wikipedia.org/wiki/Hyperparathyroidism

  Rapid PTH regulation is controlled by the parathyroid G-protein coupled, calcium sensing receptors which responds to fluctuations in serum calcium levels. […] PTH stimulates the bones to release calcium through multiple mechanisms. […] PTH acts on the distal convoluted tubule and collecting duct to increase calcium reabsorption in the nephron. […] PTH stimulates the production of 1-alpha-hydroxylase in the proximal convoluted tubule. This enzyme activation hydroxylates inactive 25-hydroxycholecalciferol to active vitamin D (1, 25 dihydroxycholecalciferol). Active vitamin D allows for calcium absorption through transcellular and paracellular pathways.

• #5 Hyperparathyroidism – Endocrine and Metabolic Disorders – Merck Manual Professional Edition

  https://www.merckmanuals.com/professional/endocrine-and-metabolic-disorders/parathyroid-disorders/hyperparathyroidism

  Hyperparathyroidism occurs when one or more of the parathyroid glands become overactive, causing elevated serum levels of parathyroid hormone and leading to hypercalcemia. […] Parathyroid hormone (PTH) increases serum calcium by enhancing distal tubular calcium reabsorption, rapidly mobilizing calcium and phosphate from bone (bone resorption), and increasing intestinal absorption of calcium by stimulating conversion of vitamin D to its most active form, calcitriol. […] Hyperparathyroidism is characterized as Primary: Excessive secretion of PTH due to a disorder of the parathyroid glands, Secondary: Hypocalcemia due to non-parathyroid disorders leads to chronic PTH hypersecretion, Tertiary: Autonomous secretion of PTH unrelated to serum calcium concentration in patients with long-standing secondary hyperparathyroidism.

• #6 Hyperparathyroidism: Background, Anatomy and Embryology, Primary Hyperparathyroidism

  https://emedicine.medscape.com/article/127351-overview

  Through their secretion of parathyroid hormone (PTH), an 84amino acid polypeptide hormone, the parathyroid glands are primarily responsible for maintaining extracellular calcium concentrations. Hyperparathyroidism is a disease characterized by excessive secretion of parathyroid hormone. The secretion of parathyroid hormone is regulated directly by the plasma concentration of ionized calcium. […] The main effects of parathyroid hormone are to increase the concentration of plasma calcium by increasing the release of calcium and phosphate from bone matrix, increasing calcium reabsorption by the kidney, and increasing renal production of 1,25-dihydroxyvitamin D-3 (calcitriol), which increases intestinal absorption of calcium. Thus, overproduction of parathyroid hormone results in elevated levels of plasma calcium. Parathyroid hormone also causes phosphaturia, thereby decreasing serum phosphate levels. Hyperparathyroidism is usually subdivided into primary, secondary, and tertiary hyperparathyroidism.

• #7 Primary Hyperparathyroidism – StatPearls – NCBI Bookshelf

  https://www.ncbi.nlm.nih.gov/books/NBK441895/

  Primary hyperparathyroidism is an endocrine disorder characterized by increased parathyroid hormone secretion, leading to hypercalcemia and renal and skeletal complications. […] Primary hyperparathyroidism involves excess parathyroid hormone (PTH) production by 1 of the 4 very small parathyroid glands normally located peripherally along the margins on the posterior aspect of the thyroid gland. […] A combination of increased clonal proliferation of parathyroid tissue with reduced CaSR usually causes primary hyperparathyroidism. […] PTH activates PTH receptors, increasing the resorption of calcium and phosphate from bone, enhancing the distal tubular calcium reabsorption, and decreasing renal phosphorus reabsorption. […] The primary regulator of PTH release is serum calcium, acting on the calcium-sensing receptors on the parathyroid surface.

• #8 Hyperparathyroidism – Wikipedia

  https://en.wikipedia.org/wiki/Hyperparathyroidism

  Hyperparathyroidism is an increase in parathyroid hormone (PTH) levels in the blood. This occurs from a disorder either within the parathyroid glands (primary hyperparathyroidism) or as response to external stimuli (secondary hyperparathyroidism). […] Symptoms of hyperparathyroidism are caused by inappropriately normal or elevated blood calcium excreted from the bones and flowing into the blood stream in response to increased production of parathyroid hormone. […] Secondary hyperparathyroidism occurs if the calcium level is abnormally low. The normal glands respond by secreting parathyroid hormone at a persistently high rate. This typically occurs when the 1,25 dihydroxyvitamin D3 levels in the blood are low and hypocalcemia is present. […] Normal parathyroid glands measure the ionized calcium (Ca2+) concentration in the blood and secrete parathyroid hormone accordingly; if the ionized calcium rises above normal, the secretion of PTH is decreased, whereas when the Ca2+ level falls, parathyroid hormone secretion is increased.

• #9 Primary Hyperparathyroidism – StatPearls – NCBI Bookshelf

  https://www.ncbi.nlm.nih.gov/books/NBK441895/

  Primary hyperparathyroidism is an endocrine disorder characterized by increased parathyroid hormone secretion, leading to hypercalcemia and renal and skeletal complications. […] Primary hyperparathyroidism involves excess parathyroid hormone (PTH) production by 1 of the 4 very small parathyroid glands normally located peripherally along the margins on the posterior aspect of the thyroid gland. […] A combination of increased clonal proliferation of parathyroid tissue with reduced CaSR usually causes primary hyperparathyroidism. […] PTH activates PTH receptors, increasing the resorption of calcium and phosphate from bone, enhancing the distal tubular calcium reabsorption, and decreasing renal phosphorus reabsorption. […] The primary regulator of PTH release is serum calcium, acting on the calcium-sensing receptors on the parathyroid surface.

• #10 Primary hyperparathyroidism: Pathogenesis and etiology – UpToDate

  https://www.uptodate.com/contents/primary-hyperparathyroidism-pathogenesis-and-etiology

  Primary hyperparathyroidism is characterized by abnormal regulation of PTH secretion by calcium, resulting in hypersecretion of PTH relative to the serum calcium concentration. […] Experimental findings have advanced our understanding of the pathophysiology and causes of primary hyperparathyroidism. This topic will review these observations, beginning with a brief review of the basic aspects of PTH and calcium homeostasis.

• #11 Hyperparathyroidism | AAFP

  https://www.aafp.org/pubs/afp/issues/2004/0115/p333.html

  Primary hyperparathyroidism is caused by the inappropriate secretion of PTH, which results in hypercalcemia. The condition usually occurs sporadically, although familial forms are well recognized. […] In 85 percent of patients with primary hyperparathyroidism, the underlying cause is an adenoma in a single parathyroid gland. Hypertrophy of all four parathyroid glands and multiple adenomas within the parathyroid glands account for the remainder of cases. Fewer than 0.5 percent of cases are caused by parathyroid malignancies. […] Most patients with primary hyperparathyroidism are postmenopausal women. The incidence of the condition increases with age, and the average age at diagnosis is 55 years. A small percentage of patients presents years after external neck irradiation. Lithium therapy also can be responsible for overactive parathyroid glands, with the excess activity persisting even after discontinuation of the drug.

• #12 Hyperparathyroidism | AAFP

  https://www.aafp.org/pubs/afp/issues/1998/0415/p1795.html

  Hyperparathyroidism is a common cause of hypercalcemia. […] The parathyroid glands are located behind the thyroid gland. Although the number and position can vary, there are usually four parathyroid glands. Parathyroid hormone consists of 84 amino acids derived from a prohormone. The effects of parathyroid hormone on serum calcium are mediated by increasing renal tubular resorption of calcium, increasing calcium absorption from the intestines (via vitamin D) and increasing release of calcium from bone. A negative feedback mechanism normally decreases production of parathyroid hormone as the ionized serum calcium level increases. […] In 85 percent of the persons affected, hyperparathyroidism is the result of an adenoma in a single parathyroid gland. Hypertrophy of all four parathyroid glands causes hyperparathyroidism in 15 percent of patients. A very small number of cases of hyperparathyroidism result from parathyroid malignancies.

• #13 Etiology and Pathogenesis of Primary Hyperparathyroidism and Hypercalcemias | Oncohema Key

  https://oncohemakey.com/etiology-and-pathogenesis-of-primary-hyperparathyroidism-and-hypercalcemias/

  Recent studies indicate that adenomas represent clonal expansions. One of the earliest described molecular abnormalities leads to overexpression of cyclin D1 protein. […] Hyperplasia is sporadic in approximately 75% of cases, whereas 25% of cases are heritable. […] Familial HPT is a group of heterogeneous disorders including multiple endocrine neoplasia type 1 (MEN1), MEN2, FHH, neonatal severe hyper-parathyroidism, hyperparathyroidismjaw tumor (HPT-JT) syndrome, familial isolated hyperparathyroidism, and autosomal dominant mild hyperparathy-roidism or familial hypercalcemia with hypercalciuria. […] Parathyroid carcinoma is an uncommon tumor with the evidence of invasive growth. […] Atypical parathyroid adenomas show some of the features of parathyroid carcinomas without frank evidence of invasive growth.

• #14 Primary and secondary hyperparathyroidism present different expressions of calcium-sensing receptor | BMC Surgery | Full Text

  https://bmcsurg.biomedcentral.com/articles/10.1186/s12893-023-01928-5

  Decreased calcium-sensing receptor (CaSR) has been observed in hyperparathyroidism (HPT) without a known mechanism. The purpose of this study was to evaluate the expression of CaSR in primary (PHPT) and secondary (SHPT) subtypes. […] Depressed CaSR expression was a critical pathological hallmark of HPT. We found a differential decline of CaSR, in terms of both mRNA and protein levels, in PHPT and SHPT human samples. We think that CaSR dysregulation occurred at the very beginning of disease onset in PHPT, while a similar pathological scenario appeared at the later stage of SHPT. […] Our results showed that HPT, irrespective of its subtypes, significantly downregulated CaSR expression compared to that of the control parathyroid tissue samples. Furthermore, a direct disorder of the parathyroid glands, including PTA-related pathology, in PHPT showed a profound effect on the CaSR expression both at the mRNA and protein levels, as compared to that of the SHPT.

• #15 Hyperparathyroidism pathophysiology – wikidoc

  https://www.wikidoc.org/index.php/Hyperparathyroidism_pathophysiology

  Hyperparathyroidism is an increase in serum parathyroid hormone. Normally, parathyroid hormone increases serum calcium and magnesium concentration, and decreases serum phosphate concentration. Secretion of parathyroid hormone from parathyroid gland is stimulated by low serum calcium. Parathyroid glands have calcium-sensing receptors responsible for sensing extracellular ionized calcium. Calcium and magnesium provides a negative feedback for secretion of parathyroid hormone. Primary hyperparathyroidism is due to increase in secretion of parathyroid hormone from a primary process in parathyroid gland. Majority of times, increase in secretion of parathyroid hormone is the result of parathyroid adenoma (85%). Calcium-sensing receptor expression in reduced in parathyroid adenoma resulting in an increase in calcium sensing set point.

• #16 Hyperparathyroidism: Background, Anatomy and Embryology, Primary Hyperparathyroidism

  https://emedicine.medscape.com/article/127351-overview

  In primary hyperparathyroidism due to adenomas, the normal feedback on parathyroid hormone production by extracellular calcium seems to be lost, resulting in a change in the set point. However, this is not the case in primary hyperparathyroidism from parathyroid hyperplasia. An increase in the cell numbers is probably the cause. […] The chronic excessive resorption of calcium from bone caused by excessive parathyroid hormone can result in osteopenia. In severe cases, this may result in osteitis fibrosa cystica, which is characterized by subperiosteal resorption of the distal phalanges, tapering of the distal clavicles, salt-and-pepper appearance of the skull, and brown tumors of the long bones. This is not commonly seen now. In addition, the chronically increased excretion of calcium in the urine can predispose to the formation of renal stones.

• #17 Secondary Hyperparathyroidism – StatPearls – NCBI Bookshelf

  https://www.ncbi.nlm.nih.gov/books/NBK557822/

  Hyperparathyroidism secondary to chronic renal failure is a condition characterized by inappropriate secretion of parathyroid hormone (PTH), secondary to a phosphocalcic metabolic disorder. […] Secondary hyperparathyroidism (SHPT) is an increased secretion of PTH due to parathyroid hyperplasia caused by triggers such as hypocalcemia, hyperphosphatemia, or decreased active vitamin D. […] The increased PTH secretion, in turn, causes increased calcium in the blood by acting on bones, intestines, and kidneys. […] Hypocalcemia is the most important stimulus for increased secretion of PTH from parathyroid glands in SHPT. The increased stimulation also results in parathyroid hyperplasia. Increased PTH level results in increased calcium and phosphate absorption from the gut. PTH acts as a stimulus for increased osteoclast activity, which results in calcium and phosphorus resorption from the bone.

• #18 Hyperparathyroidism | AAFP

  https://www.aafp.org/pubs/afp/issues/2004/0115/p333.html

  Patients with multiple endocrine neoplasia type II, or Sipple’s syndrome, may develop a milder form of primary hyperparathyroidism. This syndrome is characterized primarily by medullary thyroid carcinoma and pheochromocytoma. […] Neonatal severe primary hyperparathyroidism presents with severe hypercalcemia during the newborn period. […] Familial hypocalciuric hypercalcemia is caused by a single mutation in the calcium-sensing receptor, resulting in insensitivity to feedback inhibition of PTH secretion. […] Secondary hyperparathyroidism is the result of a physiologic or pathophysiologic parathyroid response to hypocalcemia in an attempt to maintain calcium homeostasis. […] Tertiary hyperparathyroidism occurs because of prolonged hypocalcemia (usually secondary to chronic renal failure) that causes parathyroid gland hyperplasia. Autonomous oversecretion of PTH by the parathyroid glands results in hypercalcemia.

• #19 Secondary Hyperparathyroidism – StatPearls – NCBI Bookshelf

  https://www.ncbi.nlm.nih.gov/books/NBK557822/

  In chronic kidney disease, decreasing glomerular filtration rate (GFR) leads to increased secretion of PTH. Decreasing GFR leads to decreased phosphate clearance and hyperphosphatemia, which then stimulates the parathyroid glands to secrete PTH. […] In chronic renal failure, there is an increase in the ability of parathyroid cells to synthesize and secrete hormone, which is responsible for an increase in serum PTH concentration at first. This results in hyperplasia of the gland linked to both cell hypertrophy and increased cell proliferation, which is still potentially inhibited by therapeutic measures. […] As renal function deteriorates, the expression of calcium, vitamin D, and FGF23 receptors gradually decreases in the parathyroid gland, which leads to parathyroid gland hyperplasia.

• #20 Secondary hyperparathyroidism in chronic kidney disease: pathomechanism and current treatment possibilities | Rodzoń-Norwicz | Endokrynologia Polska

  https://journals.viamedica.pl/endokrynologia_polska/article/view/95820

  Secondary hyperparathyroidism (SHPT) is one of the most common metabolic complications resulting from chronic kidney disease (CKD). […] The aim of this study is to discuss the latest issues (in connection with the latest KDIGO guidelines) regarding the pathomechanism of secondary hyperparathyroidism and the current directions of the therapy in these disorders. […] It is believed that one of the first disorders in the development of SHPT in the course of CKD is the impairment of phosphate excretion by the kidneys. […] Elevated serum phosphate levels usually occur at the G4 stage of CKD, when GFR is less than 30 ml/min. […] Hyperphosphataemia with hypocalcaemia stimulates parathyroid cells to proliferate, leading to hypertrophy of these glands and excess secretion of PTH. […] It should be emphasized here that the results of recent studies indicate that fibroblast growth factor 23 (FGF-23) and Klotho protein are the factors whose concentrations changes appear the earliest in the development of SHPT.

• #21

  https://journals.lww.com/cjasn/fulltext/2011/04000/secondary_hyperparathyroidism__pathogenesis,.32.aspx

  Secondary hyperparathyroidism (SHPT) is a challenge frequently encountered in the management of patients with chronic kidney disease (CKD). Downregulation of the parathyroid vitamin D and calcium-sensing receptors represent critical steps that lead to abnormalities in mineral metabolism: high phosphate, low calcium, and vitamin D deficiency. […] These imbalances result in parathyroid hyperplasia and contribute to vascular calcification. New studies have established a central role for fibroblast growth factor 23 (FGF-23) in the regulation of phosphate-vitamin D homeostasis. FGF-23 concentration increases in CKD and contributes to SHPT. […] Treatment should include a combination of dietary phosphorus restriction, phosphate binders, vitamin D sterols, and calcimimetics. Parathyroidectomy is effective in suitable candidates refractory to medical therapy and the standard against which new approaches should be measured. Future strategies may focus on the stimulation of apoptotic activity of hyperplastic parathyroid cells.

• #22 Secondary hyperparathyroidism in chronic kidney disease: pathomechanism and current treatment possibilities | Rodzoń-Norwicz | Endokrynologia Polska

  https://journals.viamedica.pl/endokrynologia_polska/article/view/95820

  The main and most dangerous complications of SHPT involve the skeletal and cardiovascular systems. […] The last guidelines for the treatment of SHPT in the course of CKD were published by KDIGO in 2017 and have not been updated. […] As early as in the initial stage of CKD (stage G2), the concentration of calcitriol decreases, which is associated with a decrease in the activity of 1-alpha-hydroxylase in the kidney, as a result of increased concentration of inorganic phosphates in the serum. […] However, results of studies have shown that other factors are probably crucial in the development of SHPT, namely Klotho protein deficiency and an increase in the serum concentration of fibroblast growth factor 23 (FGF-23). […] The physiological role of FGF-23 is associated with the reduction of serum phosphate concentration by enhancing phosphaturia by PTH-independent inhibition of the expression of sodium-phosphate co-transporters in the renal tubules.

• #23 The treatment of renal hyperparathyroidism in: Endocrine-Related Cancer Volume 27 Issue 1 (2020)

  https://erc.bioscientifica.com/view/journals/erc/27/1/ERC-19-0284.xml

  Renal hyperparathyroidism (rHPT) is a complex and challenging disorder. It develops early in the course of renal failure and is associated with increased risks of fractures, cardiovascular disease and death. […] Renal hyperparathyroidism develops early in renal failure, mainly as a consequence of lower levels of vitamin D, hypocalcemia, diminished excretion of phosphate and inability to activate vitamin D. […] Renal hyperparathyroidism, rHPT, with increasing levels of parathyroid hormone (PTH) and parathyroid gland hyperplasia, is a major part of CKD-MBD and develops in all patients with CKD as renal function deteriorates. […] A central hormone in the rHPT process is fibroblast growth factor 23 (FGF23), produced by osteoblasts and osteocytes. It is the major phosphate regulatory hormone.

• #24 A new concept for the pathogenesis of secondary hyperparathyroidism: Pharmacological validation of the trade-off hypothesis and involvement of FGF23/Klotho

  https://www.jstage.jst.go.jp/article/jsdt/46/6/46_519/_article/-char/en

  The pathogenesis of secondary hyperparathyroidism (2HPT) is explained by the trade-off hypothesis: a reduction in renal function increases parathyroid hormone (PTH) secretion, which stimulates urinary phosphate (P) excretion and prevents hyperphosphatemia in compensation for metabolic bone disease. […] Dietary treatment with P binder can inhibit parathyroid hyper-function and prevent bone lesions, which indicates that P retention underlies the pathogenesis and pathophysiology of 2HPT. […] Moreover, eliminating the effect of fibroblast growth factor-23 (FGF23) with a neutralizing antibody increases blood P, Ca, and 1,25(OH)2 vitamin D3[1,25(OH)2D3] levels and decreases blood PTH levels in CKD rats with 2HPT. […] Therefore, FGF23 prevents the incidence of hyperphosphatemia in a coordinated manner with PTH and also lowers 1,25(OH)2D3 production, thereby increasing PTH secretion. […] Furthermore, the decreased expression of receptors for Ca, 1,25(OH)2D3, and FGF23 reported in the parathyroid gland and reduction in renal -klotho may contribute to the early pathogenesis and progression of 2HPT.

• #25 Secondary hyperparathyroidism in chronic kidney disease: pathomechanism and current treatment possibilities | Rodzoń-Norwicz | Endokrynologia Polska

  https://journals.viamedica.pl/endokrynologia_polska/article/view/95820

  It has been shown that the concentration of FGF-23 in the serum increases in the early stages of CKD, preceding the changes in the concentration of phosphates and calcaemia associated with this disease. […] Therefore, it is highly probable that the elevated concentration of FGF-23 in the serum is the result of reduced expression of the Klotho protein. […] The consequence of SHPT is mineral and bone disorders, which include renal osteodystrophy and calcifications in blood vessels leading to cardiovascular complications. […] Hyperphosphataemia, PTH hypersecretion, calcitriol deficiency, and high serum FGF-23 levels contribute to the deposition of calcium salts in the vascular wall and are risk factors for increased all-cause and cardiovascular mortality in patients with CKD. […] The second treatment strategy for SHPT is to lower serum PTH levels.

• #26 Secondary Hyperparathyroidism: Pathogenesis and Latest Treatment – SEARCH

  https://primo.qatar-weill.cornell.edu/discovery/fulldisplay/cdi_proquest_miscellaneous_2132267237/974WCMCIQ_INST:VU1

  AbstractThe classic pathogenesis of secondary hyperparathyroidism (SHPT) began with the trade-off hypothesis based on parathyroid hormone hypersecretion brought about by renal failure resulting from a physiological response to correct metabolic disorder of calcium, phosphorus, and vitamin D. In dialysis patients with failed renal function, physiological mineral balance control by parathyroid hormone through the kidney fails and hyperparathyroidism progresses. In this process, many significant genetic findings have been established. Abnormalities of Ca-sensing receptor and vitamin D receptor are associated with the pathogenesis of SHPT, and fibroblast growth factor 23 has also been shown to be involved in the pathogenesis. […] Hyperphosphatemia also affects progression of SHPT, and control of hyperphosphatemia is, therefore, thought to be fundamental for control of SHPT. Currently, a combination of a VDRA and a calcimimetic is recognized as the optimal strategy for SHPT, and for other outcomes such as reduced cardiovascular disease and improved survival. The latest findings on the pathogenesis and treatment of SHPT are summarized in this review.

• #27 Secondary Hyperparathyroidism – StatPearls – NCBI Bookshelf

  https://www.ncbi.nlm.nih.gov/books/NBK557822/

  Hyperparathyroidism secondary to chronic renal failure is a condition characterized by inappropriate secretion of parathyroid hormone (PTH), secondary to a phosphocalcic metabolic disorder. […] Secondary hyperparathyroidism (SHPT) is an increased secretion of PTH due to parathyroid hyperplasia caused by triggers such as hypocalcemia, hyperphosphatemia, or decreased active vitamin D. […] The increased PTH secretion, in turn, causes increased calcium in the blood by acting on bones, intestines, and kidneys. […] Hypocalcemia is the most important stimulus for increased secretion of PTH from parathyroid glands in SHPT. The increased stimulation also results in parathyroid hyperplasia. Increased PTH level results in increased calcium and phosphate absorption from the gut. PTH acts as a stimulus for increased osteoclast activity, which results in calcium and phosphorus resorption from the bone.

• #28 Hyperparathyroidism – Endocrine and Metabolic Disorders – Merck Manual Professional Edition

  https://www.merckmanuals.com/professional/endocrine-and-metabolic-disorders/parathyroid-disorders/hyperparathyroidism

  Primary hyperparathyroidism is a generalized disorder resulting from excessive secretion of parathyroid hormone by one or more parathyroid glands. […] Secondary hyperparathyroidism occurs most commonly in advanced chronic kidney disease when decreased formation of active vitamin D in the kidneys and other factors lead to hypocalcemia and chronic stimulation of PTH secretion. […] Tertiary hyperparathyroidism results when PTH secretion becomes autonomous of serum calcium concentration. […] Hyperparathyroidism in patients with renal failure is usually secondary. […] Secondary hyperparathyroidism can develop in patients with moderate chronic kidney disease. […] Tertiary hyperparathyroidism occurs when long-term stimulatory effects causing secondary hyperparathyroidism result in adenomatous transformation of parathyroid tissue.

• #29 Tertiary hyperparathyroidism | Endocrine Conditions

  https://www.yourhormones.info/endocrine-conditions/tertiary-hyperparathyroidism/

  Tertiary hyperparathyroidism means excess production of parathyroid hormone that has escaped all normal body feedback controls and so persists even in cases where the initial cause (low blood calcium) has been corrected. […] Tertiary hyperparathyroidism usually happens after long-term secondary hyperparathyroidism when the parathyroid glands have been producing high levels of parathyroid hormone for such a long time that they become overgrown and permanently overactive. This leads to high blood calcium levels. […] The most common cause of tertiary hyperparathyroidism is chronic kidney disease. It can continue even after a kidney transplant. High phosphate levels, low levels of active vitamin D and hypocalcaemia, all typical symptoms of kidney disease, cause long-term high parathyroid hormone and overgrowth of the parathyroid glands.

• #30 Tertiary hyperparathyroidism – Wikipedia

  https://en.wikipedia.org/wiki/Tertiary_hyperparathyroidism

  Tertiary hyperparathyroidism is a condition involving the overproduction of the hormone, parathyroid hormone, produced by the parathyroid glands. The parathyroid glands are involved in monitoring and regulating blood calcium levels and respond by either producing or ceasing to produce parathyroid hormone. […] Persistent low levels of circulating calcium are thought to be the catalyst in the progressive development of adenoma, in the parathyroid glands resulting in primary hyperparathyroidism. While primary hyperparathyroidism is the most common form of this condition, secondary and tertiary are thought to result due to chronic kidney disease (CKD). […] Tertiary hyperparathyroidism is defined by autonomous release of parathyroid hormone while in a hypercalcaemic state. Unlike primary hyperparathyroidism, hypercalcemia in the tertiary form is thought to be the result of resolution of secondary hyperparathyroidism rather than adenoma formation alone.

• #31 Tertiary hyperparathyroidism – Wikipedia

  https://en.wikipedia.org/wiki/Tertiary_hyperparathyroidism

  Many of the mechanisms that drive the formation of tertiary hyperparathyroidism are due to outcomes of secondary hyperparathyroidism and so the tertiary form is said to be a continued progressive hyperparathyroidism. […] During prolonged secondary hyperparathyroidism increased blood phosphate levels drive hyperplasia of the parathyroid gland and this acts to reset calcium sensitivity at the calcium sensing receptors leading to tertiary hyperparathyroidism after resolution of the secondary form with the continued release of parathyroid hormone in the presence of hypercalcemia. […] Tertiary hyperparathyroidism is almost always related to end stage kidney disease and secondary hyperparathyroidism. Physiological changes due to the kidney damage adversely affect feedback loops that control secretion of parathyroid hormone.

• #32 The treatment of renal hyperparathyroidism in: Endocrine-Related Cancer Volume 27 Issue 1 (2020)

  https://erc.bioscientifica.com/view/journals/erc/27/1/ERC-19-0284.xml

  Long-standing CKD with rHPT leads to polyclonal and eventually monoclonal proliferation of parathyroid tissue with a loss of regulatory receptors. […] This condition is generally defined as tertiary hyperparathyroidism due to general hyperplasia of the parathyroid gland or autonomous adenoma. […] Tertiary HPT is a complication of long-term CKD most often after many years of dialysis treatment and can persist after successful renal transplantation. […] In summary, medical treatment is not the sine qua non for treatment of hyperparathyroidism in patients with CKD. […] However, in a small but important subset of patients, medical treatment cannot control rHPT. In these patients, surgical treatment with parathyroidectomy (PTX) is an option. […] Parathyroidectomy should likely not be too radical, especially if the patient is a candidate for future renal transplantation. […] Intraoperative measurement of PTH can be helpful; the value of preoperative imaging studies to localize parathyroid glands has not been definitely established for PTX in rHPT.

• #33 Tertiary hyperparathyroidism – Wikipedia

  https://en.wikipedia.org/wiki/Tertiary_hyperparathyroidism

  Primary hyperplasia of the parathyroid gland results from both hypocalcaemia and increased phosphate levels by decreasing expression of calcium sensing receptors and vitamin D receptors at the parathyroid gland. […] These decreases in receptor expression lead to hyperfunctioning of the parathyroid. Hyperfunction of the parathyroid gland is thought to exacerbate primary hyperplasia which evolves further to a secondary more aggressive hyperplasia. […] Secondary hyperplasia of the parathyroid gland is more often a nodular, monoclonal growth that sustains secondary hyperparathyroidism and is the catalyst in the progression to tertiary hyperparathyroidism.

• #34 Primary Hyperparathyroidism – StatPearls – NCBI Bookshelf

  https://www.ncbi.nlm.nih.gov/books/NBK441895/

  In patients with primary hyperparathyroidism, the chronic excess of PTH leads to increased proliferation and activity of osteoclasts with thinning and increased porosity of the bone cortex. […] The definitive treatment for primary hyperparathyroidism is surgery. […] Medical treatment with bisphosphonates or cinacalcet can be extremely useful in selected patients.

• #35 Hyperparathyroidism: Background, Anatomy and Embryology, Primary Hyperparathyroidism

  https://emedicine.medscape.com/article/127351-overview

  In primary hyperparathyroidism due to adenomas, the normal feedback on parathyroid hormone production by extracellular calcium seems to be lost, resulting in a change in the set point. However, this is not the case in primary hyperparathyroidism from parathyroid hyperplasia. An increase in the cell numbers is probably the cause. […] The chronic excessive resorption of calcium from bone caused by excessive parathyroid hormone can result in osteopenia. In severe cases, this may result in osteitis fibrosa cystica, which is characterized by subperiosteal resorption of the distal phalanges, tapering of the distal clavicles, salt-and-pepper appearance of the skull, and brown tumors of the long bones. This is not commonly seen now. In addition, the chronically increased excretion of calcium in the urine can predispose to the formation of renal stones.

• #36 Primary Hyperparathyroidism – StatPearls – NCBI Bookshelf

  https://www.ncbi.nlm.nih.gov/books/NBK441895/

  In patients with primary hyperparathyroidism, the chronic excess of PTH leads to increased proliferation and activity of osteoclasts with thinning and increased porosity of the bone cortex. […] The definitive treatment for primary hyperparathyroidism is surgery. […] Medical treatment with bisphosphonates or cinacalcet can be extremely useful in selected patients.

• #37 Skeletal Manifestations of Hyperparathyroidism | IntechOpen

  https://www.intechopen.com/chapters/59334

  The presentation of hyperparathyroidism changed over the last decades which gave rise to more variable presentations than before. Hyperparathyroidism has a catabolic effect on the skeleton whether the disease is symptomatic or asymptomatic or normocalcemic. […] It is now understood that the effect of parathyroid hormone (PTH) on the bone is mediated by complex interaction between different bone cells and cells of the immune system especially T lymphocytes. Protecting the skeletal system against bone loss and pathological fractures is among the important treatment goals of hyperparathyroidism. […] PTH acts on the bone cells through several mediators, and its action involves a variety of cells. It is now understood that parathyroid hormone has both catabolic and anabolic effects on bone metabolism.

• #38 Skeletal Manifestations of Hyperparathyroidism | IntechOpen

  https://www.intechopen.com/chapters/59334

  The main function of PTH is to maintain calcium levels within the normal range thorough its action on the bone, kidneys, and intestine. It also decreases serum phosphorous through inhibiting renal reabsorption. PTH can produce catabolic or anabolic effect on bone metabolism depending on the level of the hormone, periodicity, and duration of exposure. […] Primary hyperparathyroidism (PHPT), continuous PTH infusion (cPTH), and intermittent PTH treatment (iPTH) increase bone turnover in trabecular and cortical bone and elevate the markers for bone resorption and formation. […] PTH increases RANKL/OPG ratio with continuous exposure to high dose which produces catabolic effect as in hyperparathyroidism. This results in increased bone turnover, osteopenia, and bone loss in hyperparathyroidism.

• #39 Skeletal Manifestations of Hyperparathyroidism | IntechOpen

  https://www.intechopen.com/chapters/59334

  The OPG-RANK-RANKL pathway is the mechanism by which hyperparathyroidism induces bone catabolism. PTH regulates the production of RANKL and its soluble decoy receptor OPG by osteoblasts and osteocytes. […] In humans, the RANKL/osteoprotegerin (OPG) ratio is higher in patients with PHPT than controls. This ratio is decreased with parathyroidectomy (PTx) or medical treatment by alendronate. […] It is also noted that cPTH stimulates the production of TGF-, IL-6, and TNF- by bone cells and stromal cells. […] TNF- plays also an important role as a mediator of PTH catabolic action. PTH stimulates T cells to produce TNF-. […] Bone marrow macrophages also play a role in the action of PTH on the bone. Macrophages express PPR. Depletion of the precursors of macrophages decreases the anabolic effect of iPTH. […] The natural history of bone loss in normocalcemic hyperparathyroidism is not fully defined.

• #40 Skeletal Manifestations of Hyperparathyroidism | IntechOpen

  https://www.intechopen.com/chapters/59334

  The OPG-RANK-RANKL pathway is the mechanism by which hyperparathyroidism induces bone catabolism. PTH regulates the production of RANKL and its soluble decoy receptor OPG by osteoblasts and osteocytes. […] In humans, the RANKL/osteoprotegerin (OPG) ratio is higher in patients with PHPT than controls. This ratio is decreased with parathyroidectomy (PTx) or medical treatment by alendronate. […] It is also noted that cPTH stimulates the production of TGF-, IL-6, and TNF- by bone cells and stromal cells. […] TNF- plays also an important role as a mediator of PTH catabolic action. PTH stimulates T cells to produce TNF-. […] Bone marrow macrophages also play a role in the action of PTH on the bone. Macrophages express PPR. Depletion of the precursors of macrophages decreases the anabolic effect of iPTH. […] The natural history of bone loss in normocalcemic hyperparathyroidism is not fully defined.

• #41 Hyperparathyroidism: Background, Anatomy and Embryology, Primary Hyperparathyroidism

  https://emedicine.medscape.com/article/127351-overview

  In primary hyperparathyroidism due to adenomas, the normal feedback on parathyroid hormone production by extracellular calcium seems to be lost, resulting in a change in the set point. However, this is not the case in primary hyperparathyroidism from parathyroid hyperplasia. An increase in the cell numbers is probably the cause. […] The chronic excessive resorption of calcium from bone caused by excessive parathyroid hormone can result in osteopenia. In severe cases, this may result in osteitis fibrosa cystica, which is characterized by subperiosteal resorption of the distal phalanges, tapering of the distal clavicles, salt-and-pepper appearance of the skull, and brown tumors of the long bones. This is not commonly seen now. In addition, the chronically increased excretion of calcium in the urine can predispose to the formation of renal stones.

• #42 Hyperparathyroidism – Rheumatology Advisor

  https://www.rheumatologyadvisor.com/ddi/hyperparathyroidism/

  Long-term secondary hyperparathyroidism can cause the parathyroid glands to enlarge in some patients. As a result, the parathyroid glands begin to release parathyroid hormone on their own and become unresponsive to medical treatment. This is known as tertiary hyperparathyroidism. […] The prognosis for hyperparathyroidism varies depending on the etiology, but the overall outlook is generally favorable. In the United States, most cases of primary hyperparathyroidism are diagnosed asymptomatically due to an elevated serum calcium level. Surgical parathyroidectomy typically resolves and permanently cures the disorder. […] The management of secondary hyperparathyroidism should focus on abnormal phosphocalcic metabolism, as maintaining serum calcium, phosphorus, parathyroid hormone, and vitamin D levels is key to long-term treatment. If pharmacotherapy is unsuccessful or refractory, parathyroidectomy is an option. […] Complications of hyperparathyroidism include fractures, bone pain, loss of bone mineral density, higher risk of urinary stones, gastrointestinal disturbances, psychological issues, and increased risk of cardiovascular disease.

• #43 Hyperparathyroidism: Background, Anatomy and Embryology, Primary Hyperparathyroidism

  https://emedicine.medscape.com/article/127351-overview

  In primary hyperparathyroidism due to adenomas, the normal feedback on parathyroid hormone production by extracellular calcium seems to be lost, resulting in a change in the set point. However, this is not the case in primary hyperparathyroidism from parathyroid hyperplasia. An increase in the cell numbers is probably the cause. […] The chronic excessive resorption of calcium from bone caused by excessive parathyroid hormone can result in osteopenia. In severe cases, this may result in osteitis fibrosa cystica, which is characterized by subperiosteal resorption of the distal phalanges, tapering of the distal clavicles, salt-and-pepper appearance of the skull, and brown tumors of the long bones. This is not commonly seen now. In addition, the chronically increased excretion of calcium in the urine can predispose to the formation of renal stones.

• #44 Primary Hyperparathyroidism – StatPearls – NCBI Bookshelf

  https://www.ncbi.nlm.nih.gov/books/NBK441895/

  PTH is a crucial hormone required to maintain calcium homeostasis, whose net effect is to increase serum calcium levels. […] PTH normally reduces urinary calcium excretion, but this effect can be overcome by significant hypercalcemia, which is why hypercalciuria can be found in primary hyperparathyroidism. […] The calcium-sensing receptor (CaSR) found on the parathyroid gland is also found in kidney tubules, especially the thick ascending loop of Henle, where about 25% of filtered calcium is reabsorbed. […] Chronic kidney disease causes a secondary increase in serum PTH levels due to hypocalcemia from decreased 1,25-VitD. […] The chronic stimulation of the parathyroid glands results in diffuse, multiglandular parathyroid hyperplasia. […] Parathyroid adenomas tend to be encapsulated and are typically composed primarily of chief cells.

• #45 Hyperparathyroidism, arterial hypertension and aortic stiffness: a possible bidirectional link between the adrenal cortex and the parathyroid glands that causes vascular damage? | Hypertension Research

  https://www.nature.com/articles/hr2010251

  Primary hyperparathyroidism (PPTH) is generally thought to be a common endocrine disorder. However, it represents an uncommon endocrine cause of arterial hypertension, with a likely prevalence among hypertensive patients of less than 0.01% an imprecise estimate because of the lack of prospective studies. […] Despite these findings, the mechanisms by which PPTH is associated with hypertension and increased cardiovascular risk remain poorly understood and somewhat intriguing. […] Therefore, that excess PTH per se has a major detrimental effect on the arterial wall, as shown by increased BP and induced stiffening of the aorta. […] Given the secretagogue effect of parathyroid hormone (PTH) on aldosterone, the excess secretion of PTH can cause absolute or relative hyperaldosteronism; the excess secretion may be either due to primary hyperparathyroidism (PPTH) or secondary to 25-OH vitamin D deficiency or to its impaired renal activation by 1 hydroxylase in patients with chronic renal insufficiency.

• #46 Secondary Hyperparathyroidism and Hypertension: An Intriguing Couple

  https://www.mdpi.com/2077-0383/9/3/629

  Secondary hyperparathyroidism (SHPTH) is a major complication in patients on maintenance hemodialysis burdened with high cardiovascular risk. […] A possible association between SHPTH and hypertension has been widely reported in the literature and several pathogenetic mechanisms have been described. […] The persistence of these triggers leads to a progressive reduction of calcium-sensing receptors (CaSR) and vitamin D receptors (VDR) expression in parathyroid glands preluding to irreversible parathyroid gland hyperplasia onset. […] In SHPTH, in fact, normal calcium deposition in bone tissue is diverted into vascular wall inducing atherosclerosis worsening. […] A possible pathophysiological cross-link between hypertension and hyperparathyroidism has been widely reported with evidence of BP normalization after parathyroidectomy.

• #47 Primary hyperparathyroidism and hypertension – Fisher – Gland Surgery

  https://gs.amegroups.org/article/view/32624/html

  First recognized as a cardiovascular hormone by Collip and Clark in 1925, parathyroid hormone (PTH) has far-reaching effects, although exact cellular mechanisms are not clearly understood and are outside the scope of this article. In brief, PTH activates protein kinase C, augments cellular calcium influx, and indirectly inhibits the contractile effect of beta-adrenergic stimulation in the adult cardiomyocyte. PTH also acts as a vasodilator on vascular smooth muscle cells. Although in vitro studies support this vasodilatory mechanism, in vivo studies are paradoxical, with hypertension (as well as hypercalcemia) resulting from the infusion of physiologic doses of PTH in otherwise healthy adults. Others have described increased levels of, and enhanced cardiovascular reactivity to, norepinephrine in patients with both hyperparathyroidism and hypertension, and shown resolution of the noradrenergic excess after parathyroidectomy. Other potential mechanisms to explain hypertension as a result of PTH include mediation by the resulting hypercalcemia, amplified effects of the renin-angiotensin system, increased endothelin levels, and production of reactive-oxygen species. Finally, clinically observed end-organ effects include lack of arterial distensibility, which appears to be independent of endothelial signals and related to reactivity within the arterial media, increased end diastolic volume, and left ventricular hypertrophy.

• #48 Hyperparathyroidism, arterial hypertension and aortic stiffness: a possible bidirectional link between the adrenal cortex and the parathyroid glands that causes vascular damage? | Hypertension Research

  https://www.nature.com/articles/hr2010251

  The hyperaldosteronism could consequently contribute to increases in PTH, thus instituting a feed-forward mechanism. […] Therefore, the functional link between PTH and aldosterone might have an amplification role in inducing the vascular changes that are associated with cardiovascular events. […] In summary, the finding that PPTH is associated with increased stiffness of large elastic arteries, in both hypertensive and normotensive patients, along with the observation that aortic PWV is normalized after correction of the PPTH, strongly supports a cause-effect relationship between excess PTH and changes in the mechanical properties of the walls of large elastic arteries.

• #49 Primary hyperparathyroidism and hypertension – Fisher – Gland Surgery

  https://gs.amegroups.org/article/view/32624/html

  First recognized as a cardiovascular hormone by Collip and Clark in 1925, parathyroid hormone (PTH) has far-reaching effects, although exact cellular mechanisms are not clearly understood and are outside the scope of this article. In brief, PTH activates protein kinase C, augments cellular calcium influx, and indirectly inhibits the contractile effect of beta-adrenergic stimulation in the adult cardiomyocyte. PTH also acts as a vasodilator on vascular smooth muscle cells. Although in vitro studies support this vasodilatory mechanism, in vivo studies are paradoxical, with hypertension (as well as hypercalcemia) resulting from the infusion of physiologic doses of PTH in otherwise healthy adults. Others have described increased levels of, and enhanced cardiovascular reactivity to, norepinephrine in patients with both hyperparathyroidism and hypertension, and shown resolution of the noradrenergic excess after parathyroidectomy. Other potential mechanisms to explain hypertension as a result of PTH include mediation by the resulting hypercalcemia, amplified effects of the renin-angiotensin system, increased endothelin levels, and production of reactive-oxygen species. Finally, clinically observed end-organ effects include lack of arterial distensibility, which appears to be independent of endothelial signals and related to reactivity within the arterial media, increased end diastolic volume, and left ventricular hypertrophy.

• #50 Hyperparathyroidism: Background, Anatomy and Embryology, Primary Hyperparathyroidism

  https://emedicine.medscape.com/article/127351-overview

  The other symptoms of hyperparathyroidism are due to the hypercalcemia itself and are not specific to hyperparathyroidism. These can include muscle weakness, fatigue, volume depletion, nausea and vomiting, and in severe cases, coma and death. Neuropsychiatric manifestations are particularly common and may include depression, confusion, or subtle deficits that are often characterized poorly and may not be noted by the patient (or may be attributed to aging). Increased calcium can increase gastric acid secretion, and persons with hyperparathyroidism may have a higher prevalence of peptic ulcer disease. Rare cases of pancreatitis have also been attributed to hypercalcemia. […] A prospective cohort study by Ejlsmark-Svensson et al reported that in patients with primary hyperparathyroidism, quality-of-life questionnaire scores were significantly lower in association with moderate-to-severe hypercalcemia than in relation to mild hypercalcemia. However, quality of life did not seem to be related to the presence of organ-associated manifestations of primary hyperparathyroidism, such as osteoporosis, renal calcifications, and renal function impairment. This suggests that hypercalcemia is the primary driver of an impaired quality of life.

• #51 Reversible Neuropsychiatric Symptoms of Primary Hyperparathyroidism after Parathyroidectomy

  https://www.kjfp.or.kr/journal/view.html?uid=1143&vmd=Full&

  Hyperparathyroidism is a generalized disease associated with calcium metabolism due to excessive secretion of parathyroid hormone (PTH). […] Primary hyperparathyroidism, which is mainly caused by parathyroid adenoma, is the most common cause of hypercalcemia. […] The mechanism of hypercalcemia-induced neuropsychiatric symptoms remains unclear; however, it may be explained by dopaminergic and serotonergic dysfunction in the central nervous system and glutaminergic excitotoxicity via N-methyl-D-aspartate receptors. […] There is no doubt about the benefits of parathyroidectomy in symptomatic patients; however, the impact of parathyroidectomy in neuropsychiatric symptoms remains controversial. […] Neuropsychiatric symptoms improved after parathyroidectomy in many cases; however, the irreversibility of neuropsychiatric symptoms has been reported.

• #52 Reversible Neuropsychiatric Symptoms of Primary Hyperparathyroidism after Parathyroidectomy

  https://www.kjfp.or.kr/journal/view.html?uid=1143&vmd=Full&

  Irreversible neuropsychiatric symptoms were not clearly explained; however, they could possibly be due to prolonged exposure to hypercalcemia leading to irreversible neuronal damage. […] This report describes a case of primary hyperparathyroidism caused by a parathyroid adenoma that might have been misdiagnosed as somatization disorder, fibromyalgia, or affective disorder with cognitive dysfunction. […] The patient’s symptoms, chronic musculoskeletal pain, and neuropsychiatric symptoms improved after surgery, and the number of hospital visits decreased.

• #53 Reversible Neuropsychiatric Symptoms of Primary Hyperparathyroidism after Parathyroidectomy

  https://www.kjfp.or.kr/journal/view.html?uid=1143&vmd=Full&

  Hyperparathyroidism is a generalized disease associated with calcium metabolism due to excessive secretion of parathyroid hormone (PTH). […] Primary hyperparathyroidism, which is mainly caused by parathyroid adenoma, is the most common cause of hypercalcemia. […] The mechanism of hypercalcemia-induced neuropsychiatric symptoms remains unclear; however, it may be explained by dopaminergic and serotonergic dysfunction in the central nervous system and glutaminergic excitotoxicity via N-methyl-D-aspartate receptors. […] There is no doubt about the benefits of parathyroidectomy in symptomatic patients; however, the impact of parathyroidectomy in neuropsychiatric symptoms remains controversial. […] Neuropsychiatric symptoms improved after parathyroidectomy in many cases; however, the irreversibility of neuropsychiatric symptoms has been reported.

• #54 Normocalcemic Primary Hyperparathyroidism – Endocrine Surgery | UCLA Health

  https://www.uclahealth.org/medical-services/surgery/endocrine-surgery/conditions-treated/parathyroid/normocalcemic-primary-hyperparathyroidism

  Normocalcemic primary hyperparathyroidism (nPHPT) is suspected when patients calcium level is within the normal range, but parathyroid hormone level is too high. […] Normocalcemic primary hyperparathyroidism (nPHPT) is hypothesized to be an early type of primary hyperparathyroidism. Primary hyperparathyroidism is when one or more of the parathyroid glands makes too much parathyroid hormone, which draws calcium from the bones into the blood, weakening bone density and raising blood calcium level. In normocalcemic PHPT, the parathyroid glands are releasing too much hormone, but the blood calcium level has not risen yet. […] Proper diagnosis of normocalcemic primary hyperparathyroidism is challenging, because there are several other causes of high parathyroid hormone levels and normal calcium levels. Because several other conditions may mimic normocalcemic primary hyperparathyroidism, detailed blood and sometimes urine testing is required to establish the definitive diagnosis.

• #55 Normocalcemic Primary Hyperparathyroidism – Endocrine Surgery | UCLA Health

  https://www.uclahealth.org/medical-services/surgery/endocrine-surgery/conditions-treated/parathyroid/normocalcemic-primary-hyperparathyroidism

  Normocalcemic primary hyperparathyroidism (nPHPT) is suspected when patients calcium level is within the normal range, but parathyroid hormone level is too high. […] Normocalcemic primary hyperparathyroidism (nPHPT) is hypothesized to be an early type of primary hyperparathyroidism. Primary hyperparathyroidism is when one or more of the parathyroid glands makes too much parathyroid hormone, which draws calcium from the bones into the blood, weakening bone density and raising blood calcium level. In normocalcemic PHPT, the parathyroid glands are releasing too much hormone, but the blood calcium level has not risen yet. […] Proper diagnosis of normocalcemic primary hyperparathyroidism is challenging, because there are several other causes of high parathyroid hormone levels and normal calcium levels. Because several other conditions may mimic normocalcemic primary hyperparathyroidism, detailed blood and sometimes urine testing is required to establish the definitive diagnosis.

• #56 Normocalcemic Primary Hyperparathyroidism – Endocrine Surgery | UCLA Health

  https://www.uclahealth.org/medical-services/surgery/endocrine-surgery/conditions-treated/parathyroid/normocalcemic-primary-hyperparathyroidism

  Nearly half of patients diagnosed with normocalcemic primary hyperparathyroidism have been found to have osteoporosis. […] Therefore, normocalcemic primary hyperparathyroidism may cause bone loss. […] In secondary hyperparathyroidism, the parathyroid gland is functioning normally and is only producing high levels of parathyroid hormone because the body is signaling that it needs more calcium in the blood. […] One major cause of secondary hyperparathyroidism is vitamin D deficiency. […] After vitamin D supplementation, the patients PTH level should return to normal. If calcium levels become high and PTH remains high after Vitamin D supplementation, this establishes the diagnosis of primary hyperparathyroidism. […] Kidney failure, or an eGFR of less than 60, causes a problem with vitamin D metabolism. This also leads to the parathyroid glands appropriately compensating the loss of blood calcium by increasing PTH levels.

• #57 Hyperparathyroidism pathophysiology – wikidoc

  https://www.wikidoc.org/index.php/Hyperparathyroidism_pathophysiology

  Hyperparathyroidism is an increase in serum parathyroid hormone. Normally, parathyroid hormone increases serum calcium and magnesium concentration, and decreases serum phosphate concentration. Secretion of parathyroid hormone from parathyroid gland is stimulated by low serum calcium. Parathyroid glands have calcium-sensing receptors responsible for sensing extracellular ionized calcium. Calcium and magnesium provides a negative feedback for secretion of parathyroid hormone. Primary hyperparathyroidism is due to increase in secretion of parathyroid hormone from a primary process in parathyroid gland. Majority of times, increase in secretion of parathyroid hormone is the result of parathyroid adenoma (85%). Calcium-sensing receptor expression in reduced in parathyroid adenoma resulting in an increase in calcium sensing set point.

• #58 Hyperparathyroidism – Knowledge @ AMBOSS

  https://www.amboss.com/us/knowledge/hyperparathyroidism/

  Hyperparathyroidism (HPT) is characterized by abnormally high parathyroid hormone (PTH) levels in the blood due to parathyroid gland overactivity. […] pHPT develops as a result of hyperplasia of the parathyroid glands. sHPT develops as a result of decreased levels of calcium in the blood (reactive HPT). […] Overproduction of PTH by parathyroid chief cells. […] Effect of PTH on bone bone resorption release of calcium phosphate calcium levels. […] Induces RANKL expression in osteoblasts binding of RANKL to RANK on osteoclasts activation of osteoclasts. […] Induces IL-1 expression in osteoblasts activation of osteoclasts. […] Secondary hyperparathyroidism: calcium and/or phosphate blood levels reactive hyperplasia of the parathyroid glands PTH secretion. […] Tertiary hyperparathyroidism: chronic renal disease refractory and autonomous secretion of PTH hypercalcemia. […] Renal disease: secondary or tertiary hyperparathyroidism renal osteodystrophy bone lesions.

• #59 Hyperparathyroidism pathophysiology – wikidoc

  https://www.wikidoc.org/index.php/Hyperparathyroidism_pathophysiology

  Primary hyperparathyroidism is due to increase in secretion of parathyroid hormone from a primary process in parathyroid gland. Majority of times, increase in secretion of parathyroid hormone is the result of parathyroid adenoma (85%). Other causes of increase in secretion of parathyroid hormone includes parathyroid hyperplasia (15%) and parathyroid carcinoma (5%). […] Secondary hyperparathyroidism is due to increase in secretion of parathyroid hormone from a secondary process, most commonly due chronic renal failure. Other causes include vitamin D deficiency, severe calcium deficiency. […] FGF-23 fails to activate mitogen-activated protein kinase pathway in hyperplastic parathyroid gland secondary to chronic renal failure.

• #60 Primary Hyperparathyroidism – StatPearls – NCBI Bookshelf

  https://www.ncbi.nlm.nih.gov/books/NBK441895/

  In patients with primary hyperparathyroidism, the chronic excess of PTH leads to increased proliferation and activity of osteoclasts with thinning and increased porosity of the bone cortex. […] The definitive treatment for primary hyperparathyroidism is surgery. […] Medical treatment with bisphosphonates or cinacalcet can be extremely useful in selected patients.

• #61 Hyperparathyroidism – Rheumatology Advisor

  https://www.rheumatologyadvisor.com/ddi/hyperparathyroidism/

  Long-term secondary hyperparathyroidism can cause the parathyroid glands to enlarge in some patients. As a result, the parathyroid glands begin to release parathyroid hormone on their own and become unresponsive to medical treatment. This is known as tertiary hyperparathyroidism. […] The prognosis for hyperparathyroidism varies depending on the etiology, but the overall outlook is generally favorable. In the United States, most cases of primary hyperparathyroidism are diagnosed asymptomatically due to an elevated serum calcium level. Surgical parathyroidectomy typically resolves and permanently cures the disorder. […] The management of secondary hyperparathyroidism should focus on abnormal phosphocalcic metabolism, as maintaining serum calcium, phosphorus, parathyroid hormone, and vitamin D levels is key to long-term treatment. If pharmacotherapy is unsuccessful or refractory, parathyroidectomy is an option. […] Complications of hyperparathyroidism include fractures, bone pain, loss of bone mineral density, higher risk of urinary stones, gastrointestinal disturbances, psychological issues, and increased risk of cardiovascular disease.

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