In the kidneys, PTH acts to reduce calcium clearance and stimulates synthesis of 1,dihydroxyvitamin D, which stimulates calcium absorption in the gastrointestinal tract Figure 1. The glands synthesize and store the PTH, allowing it to respond within minutes of hypocalcemia. Sustained hypocalcemia leads to cellular replication and increased mass of the glands. Calcium and 1,dihydroxyvitamin D provide negative feedback at the parathyroid glands to inhibit PTH release.
One normal gland is sufficient for adequate secretion of PTH to maintain normal calcium levels. Control of mineral metabolism by parathyroid hormone PTH. Calcium-sensing receptors of parathyroid cells respond to serum calcium level and change with increased release hypocalcemia or suppression hypercalcemia of PTH.
PTH stimulates bone resorption, which increases serum calcium and phosphorus. In the kidney, PTH stimulates reabsorption of calcium and promotes phosphorus excretion. PTH also helps convert hydroxyvitamin D to 1,dihydroxyvitamin D in the kidneys, which then increases intestinal transport of calcium and phosphorus. Information from references 1 and 2. Parathyroid disorders most commonly present with serum calcium abnormalities. Rarely, patients can present with a neck mass or for evaluation of a family history of parathyroid or related disorders.
The estimated incidence of primary hyperparathyroidism is approximately 25 cases per , persons per year in outpatients of Western countries, 5 — 7 with a prevalence of one to four per 1, persons. Primary hyperparathyroidism, the most common cause of hypercalcemia in outpatients, is often discovered incidentally during evaluation of serum electrolyte levels.
Before the easily available measurement of serum calcium levels, patients presented with a spectrum of symptoms Table 1.
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Possible diagnoses: diastolic dysfunction, dysrhythmias, hypertension, left ventricular hypertrophy, vascular calcification. Anxiety, confusion, depression, fatigue, forgetfulness, impaired vision, insomnia, lethargy, weakness. Possible diagnoses: nephrocalcinosis, nephrolithiasis, nephrogenic diabetes insipidus.
Possible diagnoses: bone disease, insufficiency fractures, osteomalacia, osteoporosis. Information from references 4 , 12 , and Genetic disorders e. Parathyroid hormone—related protein dependent. Osteolytic metastases and multiple myeloma. Other humoral syndromes. Ingested or topical vitamin D analogues.
Granulomatous disease. Williams syndrome. Drugs: vitamin A intoxication, milk-alkali syndrome, thiazide diuretics, theophylline. Information from references 3 , 5 , 8 , 17 , and Risk factors for primary hyperparathyroidism include a history of neck radiation, age older than 50 years, and female sex; women are twice as likely as men to develop primary hyperparathyroidism.
There are also uncommon familial causes, such as MEN-1 and MEN-2A; persons with these conditions may have parathyroid adenomas or asymmetric hyperplasia. Secondary hyperparathyroidism most commonly occurs because of decreased levels of 1,dihydroxyvitamin D, hyperphosphatemia, and hypocalcemia in the setting of chronic kidney disease. Other causes include vitamin D deficiency secondary to low dietary intake, lack of sun exposure, malabsorption, liver disease, and other chronic illness.
In some patients with advanced renal failure, hypercalcemia is due to progression from appropriate parathyroid hyperplasia to autonomous overproduction of PTH, a disorder termed tertiary hyperparathyroidism. Patients with normocalcemic hyperparathyroidism may present with low bone density, osteoporosis, or a fragility fracture.
Many of these patients will probably evolve into having hyperparathyroidism, although the exact natural history is not known. It is important to exclude vitamin D deficiency and chronic kidney disease before making this diagnosis. Primary hyperparathyroidism is diagnosed when the serum calcium level is elevated, with an increased or inappropriately normal serum PTH level.
An algorithm for the evaluation of patients with suggestive symptoms or asymptomatic hypercalcemia is shown in Figure 2. A physical examination is important to identify subtle features consistent with hyperparathyroidism and to assist in the differential diagnosis Table 3.
Algorithm for evaluating patients with hypercalcemia. Information from references 2 , 4 , 8 , 10 , and 21 through Congestive heart failure or systolic or diastolic dysfunction from hypo- or hypercalcemia. Information from references 1 , 4 , 8 , and Other tests listed in Figure 2 should identify patients with primary hyperparathyroidism.
In this situation, the calcimimetic cinacalcet Sensipar effectively lowers serum calcium levels, but does not affect bone density. The role of surgery in patients with asymptomatic primary hyperparathyroidism is not as clear. Younger patients and patients at risk of progression to symptomatic disease are the best candidates for parathyroidectomy.
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Recommendations from the Third International Workshop on the Management of Asymptomatic Primary Hyperparathyroidism include performing parathyroidectomy in asymptomatic persons with primary hyperparathyroidism and any one of the following 26 : Serum calcium level greater than 1. Creatinine clearance less than 60 mL per minute per 1. Asymptomatic persons with primary hyperparathyroidism and osteoporosis or osteopenia are candidates for parathyroidectomy because bone density and fracture risk improve after surgery.
Bone density, but not fracture risk, has also been shown to improve after bisphosphonate therapy and hormone therapy in these patients. If patients with primary hyperparathyroidism do not undergo parathyroidectomy, they should be closely monitored for the development of symptoms or other indications for surgery. These patients should have serum calcium and creatinine levels measured annually, and three-site i. The management of secondary hyperparathyroidism in chronic kidney disease usually involves consultation with a nephrologist.
Protein restriction and calcium supplementation have been shown to decrease the development of this complication, with a reduction in death from renal causes.
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Vitamin D supplements and calcimimetics, which inhibit PTH secretion, have been shown to improve biochemical markers without patient-oriented outcomes. There are several evidence-based reviews for managing chronic kidney disease-mineral and bone disorder; full discussion of these guidelines is beyond the scope of this article and is available from this referenced source.
Hypoparathyroidism most commonly occurs after inadvertent damage or removal of parathyroid glands during neck surgery. It can occur years after neck surgery. Rarely, there is tissue resistance to the actions of PTH, which results in a picture of hypoparathyroidism but with elevated PTH levels. This is termed pseudohypoparathyroidism, and it is a genetically heterogeneous condition.
Reversible impairment in parathyroid hormone secretion or action. NOTE : Causes are listed in order of clinical importance. Information from references 1 , 3 , and Most patients with hypoparathyroidism present with hypocalcemia. Figure 3 is an algorithm for evaluating patients with symptomatic or incidentally discovered hypocalcemia. Table 5 lists causes of hypocalcemia based on clinical clues. Serum levels of PTH, phosphorus, hydroxyvitamin D, and 1,dihydroxyvitamin D can help differentiate between disorders causing hypocalcemia Table 7.
Algorithm for evaluating patients with hypocalcemia. Information from references 1 through 4 , and Information from references 1 and Possible diagnoses: dysrhythmia, prolonged corrected QT interval, systolic dysfunction. Circumoral numbness and paresthesias; cramping, muscle twitching, spasms; seizures. Information from reference Figure 3 provides brief recommendations for the immediate treatment of severe hypocalcemia 1 — 4 , 24 ; a detailed discussion is beyond the scope of this article. Long-term management of hypoparathyroidism should include at least initial involvement of an endocrinologist.
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Vitamin D analogues are essential e. Food and Drug Administration for this purpose. Some patients present to their physician after a family member has been diagnosed with MEN. MEN-1 includes neoplasias of the parathyroid, pancreas, pituitary, and adrenal glands. MEN-2 includes neoplasias of the thyroid, adrenal, and parathyroid glands. MEN-2A involves medullary thyroid carcinoma, pheochromocytoma, and parathyroid tumors. The issue of screening family members for MEN-1 is controversial because presymptomatic detection has not been shown to reduce morbidity or mortality. Others advocate screening with measurement of calcium and PTH levels annually, starting at eight years of age.
In a family with a history of MEN-2, a sample from one patient already affected should be tested to determine the specific genetic mutation for that family.
When a mutation is found, all persons of unknown status in that family should then be definitively genotyped. Rarely, patients with parathyroid disorders may present with a neck mass, either self-reported or as an incidental finding on examination. Parathyroid cancer, hyperplasia, adenomas, and cysts could all present in this way. Other neck tumors, including primary or metastatic cancers, are more common than parathyroid causes.
Ultrasonography, computed tomography, and biopsy are typically required to determine the diagnosis. The search included meta-analyses, randomized controlled trials, clinical trials, and reviews. Search dates: June 5 through December 22, Already a member or subscriber?
Log in. Address correspondence to Thomas C. Reprints are not available from the authors. The opinions and assertions contained herein are the private views of the authors and are not to be construed as official or as reflecting the views of the U. Army Medical Department or the U.
Shoback D. Clinical practice. N Engl J Med. Stack BC, Randolph G. Chichester, UK: Wiley-Blackwell; — Hormones and disorders of mineral metabolism. Williams Textbook of Endocrinology. Philadelphia, Pa. Stearns M, Cox J. Primary hyperparathyroidism. The natural history of treated and untreated primary hyperparathyroidism: the parathyroid epidemiology and audit research study. The rise and fall of primary hyperparathyroidism: a population-based study in Rochester, Minnesota, — Ann Intern Med.
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Pallan S, Khan A. Primary hyperparathyroidism: Update on presentation, diagnosis, and management in primary care. Can Fam Physician. McGinn JD. Otolaryngol Clin North Am. Guidelines for diagnosis and therapy of MEN type 1 and type 2. J Clin Endocrinol Metab. Parathyroid cancer. Semin Oncol. Taniegra ED.
Am Fam Physician. The diagnosis and management of asymptomatic primary hyperparathyroidism. Nat Clin Pract Endocrinol Metab. Lendel I, Horwith M. An update from the latest workshop on asymptomatic primary hyperparathyroidism. Marcocci C, Cetani F. Primary hyperparathyroidism [published correction appears in N Engl J Med. Mikhail N. Clinical significance of vitamin D deficiency in primary hyperparathyroidism, and safety of vitamin D therapy. South Med J. Diagnosis of asymptomatic primary hyperparathyroidism: proceedings of the third international workshop.
Clinical inquiries. How should you evaluate elevated calcium in an asymptomatic patient? J Fam Pract. Hyperparathyroidism and multiple endocrine neoplasia. Larson, Jorge A. Lesnik, Miriam A. Pieter Noordzij, Gregory W. Patel, Bhuvanesh Singh. Ground breaking content includes chapters dedicated to advances in molecular biology, the latest in radiological assessment, cytology and advances in surgical technique such as endoscopic and robotic assisted modalities. Accessible and practical with key points, case scenarios, colour photographs and diagrams throughout.
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Practical Manual of Thyroid and Parathyroid Disease. Selected type: Hardcover. Added to Your Shopping Cart. View on Wiley Online Library. This is a dummy description. Edited and authored by international experts, A Practical Manual of Thyroid and Parathyroid Disease presents concise, evidence-based, multi-disciplinary guidance relevant for a global audience.
Where appropriate, chapters include an evidence appraisal section which critically assesses the level of the evidence available for different treatment options. Reflecting the latest in clinical research and showcasing techniques pioneered by the contributors, the book includes chapters dedicated to advances in: cytology radiological assessment molecular biology and treatment rationale in thyroid cancer surgical technique including minimally invasive modalities Designed to be user-friendly, the book contains key points, case studies, color photographs and diagrams throughout.
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