Hyperparathyroidism overview: Difference between revisions
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==Pathophysiology== | ==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 gland]]<nowiki/>s 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 (genetics)|expression]] in reduced in [[parathyroid adenoma]] resulting in an increase in [[calcium]] sensing set point. In minority of cases, development of primary hyperparathyroidism is the result of multiple [[genetic mutations]]. [[Gene|Genes]] involved in the pathogenesis of primary hyperparathyroidism include calcium-sensing receptor gene, HRPT2 gene (CDC73 gene), [[Cyclin D1]] gene (CCND1)/PRAD1 gene, [[MEN1]] gene, and [[RET gene]]. Secondary hyperparathyroidism is due to increase in secretion of [[parathyroid hormone]] from a secondary process, most commonly due [[chronic renal failure]]. [[Fibroblast growth factor 23]] ([[Fibroblast growth factor 23|FGF-23]]) concentration increases in [[chronic renal failure]] which plays a central role in regulation of [[phosphate]] [[vitamin D]] [[homeostasis]] and pathogenesis of secondary hyperparathyroidism. Majority of times, tertiary hyperparathyroidism occurs in patients after [[renal transplantation]].Patients with secondary hyperparathyroidism continues to have elevated [[parathyroid hormone]] even after [[Kidney transplantation|renal transplantation]]. Classically, there is [[hyperplasia]] of all four of [[parathyroid gland]]. On gross pathology, [[parathyroid adenoma]] is a soft, tan nodule which is well-circumscribed by a delicate [[Capsule (anatomy)|capsule]]. Typically, cut surface of [[parathyroid adenoma]] is smooth, soft, and reddish brown in color. It should be differentiated from normal [[parathyroid gland]] tissue which is yellow-brown color. [[Parathyroid gland|Parathyroid]] [[hyperplasia]] usually involves multiple [[Gland|glands]]. [[Bones]] and [[kidney]] are also commonly involved in hyperparathyroidism. [[Hypercalcemia]] due to hyperparathyroidism may cause [[Metastasis|metastatic]] [[calcification]] in many organs including [[Lung|lungs]], [[heart]], [[blood vessels]], [[stomach]]. [[Chief cells]] are predominant in [[parathyroid adenoma]] on microcopy. [[Adenoma]] is seperated from a rim of non-neoplastic tissue on the edge by a fibrous [[capsule]]. [[Endocrine]] [[atypia]] (cells with bizarre and pleomorphic nuclei) is often seen in [[parathyroid adenoma]]. It should not be mistaken as a sign of [[malignancy]]. Majority of times, [[hyperplasia]] of [[Chief cell|chief cells]] is observed in [[Parathyroid gland|parathyroid]] [[hyperplasia]]. It may be diffuse or multinodular. Cytologic details are unreliable for diagnosis of [[parathyroid carcinoma]]. | |||
==Causes== | ==Causes== | ||
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1];Associate Editor(s)-in-Chief:
Overview
Hyperparathyroidism is overactivity of the parathyroid glands resulting in excess production of parathyroid hormone (PTH). The parathyroid hormone monitors calcium and phosphorus levels and helps to maintain these levels. Overactivity of one or more of the parathyroid glands causes high calcium levels (hypercalcemia) and low levels of phosphorus in the blood. Hyperparathyroidism was first described and treated in the 1930s by Fuller Albright of Massachusetts General Hospital, working at the Mallinckrodt General Clinical Research Center. The oldest known case was found in a cadaver from a Early Neolithic cemetery in southwest Germany.[1]
Historical Perspective
In 1880, Ivar Sandström, a Swedish anatomist, described parathyroids in human following 50 autopsies. In 1924, James Bertram Collip, a Canadian biochemist, discovered and extracted parathormone and treated tetany with the help of parathyroid extract along with Douglous B Leitch. In 1925, Felix Mandl, a viennese surgeon performed first parathyroidectomy to treat a patient suffering from suffering from osteitis fibrosa cystica. In 1959, Howard Rasmussen and Lyman C. Craig at the Rockefeller Institute for Medical Research purified parathyroid hormone. They also isolated the active polypeptide (parathormone B) from bovine parathyroid gland and gave its tentative formula in 1961.
Classification
Hyperparathyroidism can be classified into primary, secondary and tertiary. Primary hyperparathyroidism results from a hyperfunction of the parathyroid glands themselves. There is oversecretion of PTH due to adenoma, hyperplasia or, rarely, carcinoma of the parathyroid glands. Secondary hyperparathyroidism is due to increase in secretion of parathyroid hormone from a secondary process. Tertiary hyperparathyroidism is a state of excessive secretion of parathyroid hormone (PTH) after a long period of secondary hyperparathyroidism and resulting in hypercalcemia.
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. In minority of cases, development of primary hyperparathyroidism is the result of multiple genetic mutations. Genes involved in the pathogenesis of primary hyperparathyroidism include calcium-sensing receptor gene, HRPT2 gene (CDC73 gene), Cyclin D1 gene (CCND1)/PRAD1 gene, MEN1 gene, and RET gene. Secondary hyperparathyroidism is due to increase in secretion of parathyroid hormone from a secondary process, most commonly due chronic renal failure. Fibroblast growth factor 23 (FGF-23) concentration increases in chronic renal failure which plays a central role in regulation of phosphate vitamin D homeostasis and pathogenesis of secondary hyperparathyroidism. Majority of times, tertiary hyperparathyroidism occurs in patients after renal transplantation.Patients with secondary hyperparathyroidism continues to have elevated parathyroid hormone even after renal transplantation. Classically, there is hyperplasia of all four of parathyroid gland. On gross pathology, parathyroid adenoma is a soft, tan nodule which is well-circumscribed by a delicate capsule. Typically, cut surface of parathyroid adenoma is smooth, soft, and reddish brown in color. It should be differentiated from normal parathyroid gland tissue which is yellow-brown color. Parathyroid hyperplasia usually involves multiple glands. Bones and kidney are also commonly involved in hyperparathyroidism. Hypercalcemia due to hyperparathyroidism may cause metastatic calcification in many organs including lungs, heart, blood vessels, stomach. Chief cells are predominant in parathyroid adenoma on microcopy. Adenoma is seperated from a rim of non-neoplastic tissue on the edge by a fibrous capsule. Endocrine atypia (cells with bizarre and pleomorphic nuclei) is often seen in parathyroid adenoma. It should not be mistaken as a sign of malignancy. Majority of times, hyperplasia of chief cells is observed in parathyroid hyperplasia. It may be diffuse or multinodular. Cytologic details are unreliable for diagnosis of parathyroid carcinoma.
Causes
Differentiating ((Page name)) from Other Diseases
Epidemiology and Demographics
Risk Factors
Screening
Natural History, Complications, and Prognosis
Diagnosis
Diagnostic Criteria
History and Symptoms
Physical Examination
Laboratory Findings
Electrocardiogram
X-ray
CT scan
MRI
Ultrasound
Other Imaging Findings
Other Diagnostic Studies
Treatment
Medical Therapy
Surgery
Primary Prevention
Secondary Prevention
References
- ↑ Zink AR, Panzer S, Fesq-Martin M, Burger-Heinrich E, Wahl J, Nerlich AG (2005). "Evidence for a 7000-year-old case of primary hyperparathyroidism". JAMA. 293 (1): 40–2. doi:10.1001/jama.293.1.40-c. PMID 15632333.