Hypoparathyroidism is a condition of parathyroid hormone (PTH) deficiency. Primary hypoparathyroidism is a state of inadequate PTH activity. In the absence of adequate PTH activity, the ionized calcium concentration in the extracellular fluid falls below the reference range. Primary hypoparathyroidism, the subject of this article, is a syndrome resulting from iatrogenic causes or one of many rare diseases.[1]
Secondary hypoparathyroidism is a physiologic state in which PTH levels are low in response to a primary process that causes hypercalcemia. The primary processes that lead to hypercalcemia are discussed in other articles (see Hypercalcemia).
Treatment of patients with hypoparathyroidism involves correcting the hypocalcemia by administering calcium and vitamin D.[2] Recombinant human PTH (rhPTH[1-84], Natpara) is commercially available in the United States and is indicated as an adjunct to calcium and vitamin D to control hypocalcemia in patients with hypoparathyroidism.
The ionized calcium concentration in the extracellular fluid (ECF) remains nearly constant, at a level of approximately 1 mM. Ionized calcium in the ECF is in equilibrium with ionized calcium in storage pools such as bone, proteins in the circulation, and within the intracellular fluid. The intracellular fluid concentration of calcium is more than 10,000-fold lower than in the ECF. The maintenance of ionized calcium concentrations in the intracellular and extracellular fluids is highly regulated and modulates the functions of bone, renal tubular cells, clotting factors, adhesion molecules, excitable tissues, and a myriad of intracellular processes.
An extracellular calcium-sensing receptor has been isolated from parathyroid, kidney, and brain cells. The extracellular calcium-sensing receptor is G protein coupled. Mutations in the extracellular calcium-sensing receptor have been demonstrated to result in hypercalcemic or hypocalcemic states. Normally, the extracellular calcium-sensing receptor is extremely sensitive and responds to changes in the ECF calcium ion concentration of as small as 2%.
In parathyroid cells, the extracellular calcium-sensing receptor regulates the secretion of PTH. Inactivating mutations of the extracellular calcium-sensing receptor lead to hypercalcemia, as observed in familial hypocalciuric hypercalcemia (heterozygous mutation) and neonatal severe hyperparathyroidism (homozygous mutation). Conversely, activating mutations of the extracellular calcium-sensing receptor lead to hypocalcemia, as observed in some families with autosomal-dominant hypocalcemia.
The intracellular mechanism(s) whereby activation of the extracellular calcium-sensing receptor leads to inhibition of PTH exocytosis is unknown. Because pertussis toxin blocks the inhibition of cyclic adenosine monophosphate (cAMP), but not PTH, in response to a high ECF ionized calcium concentration, cAMP is probably not an important second messenger for the extracellular calcium-sensing receptor. Candidate second messengers include protein kinase C, phospholipase A2, and intracellular calcium.
Conversely, a fall in ECF ionized calcium concentration leads to exocytosis of PTH. PTH has the overall effect of returning the ECF ionized calcium concentration to the reference range by its effects on the kidneys and the skeleton.
PTH activates osteoclasts. Osteoclast activation results in bone resorption and a release of ionized calcium into the ECF. Evidence suggests that small pulse doses of PTH activate osteoblasts, with ensuing bone deposition. The effect of PTH on osteoclasts seems more important than the effect on osteoblasts.
PTH inhibits the proximal tubular transport of phosphate from the lumen to the interstitium. In conditions of primary PTH excess, hypophosphatemia tends to occur. Conversely, in hypoparathyroidism, the phosphate concentration in the plasma is within the reference range or slightly elevated.
PTH has a calcium-retaining effect on the distal tubule. The PTH-mediated calcium reabsorption is independent of any effects on sodium or water reabsorption. This effect of PTH is important in hypoparathyroidism because, in the absence of this distal tubular calcium reabsorption, the kidneys waste calcium. This depletes the ECF ionized calcium and increases the urinary calcium concentration.
PTH stimulates renal 1-alpha-hydroxylase, the enzyme that synthesizes formation of 1,25-dihydroxy vitamin D; 1,25-dihydroxy vitamin D allows for better dietary calcium absorption. Thus, 1,25-dihydroxy vitamin D has a synergistic effect with PTH; both contribute to a rise in the ECF ionized calcium concentration.
In the absence of PTH, bone resorption, phosphaturic effect, renal distal tubular calcium reabsorption, and 1,25-dihydroxy vitamin D–mediated dietary calcium absorption cannot occur. Therefore, the consequence of PTH deficiency is hypocalcemia.
Hypoparathyroidism has an estimated prevalence in the United States of 37 per 100,000 person-years. In Denmark, it is estimated to be 22 per 100,000 person-years.[3]
Age-related demographics
A study by Powers et al found 74% of US hypoparathyroid patients to be aged 45 years or older.[4]
Sex-related demographics
In the United States, 75% of hypoparathyroidism cases are in females and 25% in males.[1] Similarly, in an Italian study, Cipriani et al found the rate of hospitalizations for hypoparathyroidism in women and men to be 72.2% and 27.8%, respectively.[5]
Hypoparathyroidism results in hypocalcemia, which may be variably symptomatic. The history should focus on eliciting signs and symptoms of neuromuscular irritability,[6] including the following:
Muscle cramps involving the lower back, legs, and feet are common in patients with hypoparathyroidism and hypocalcemia. Tetany develops if hypocalcemia is severe. In some patients, laryngospasm and bronchospasm may be life threatening.
Increased neuromuscular irritability from hypoparathyroidism-induced hypocalcemia may be demonstrated at the bedside by eliciting the following signs:
Chvostek sign: Facial twitching, especially around the mouth, is induced by gently tapping the ipsilateral facial nerve as it courses just anterior to the ear.
Trousseau sign: Carpal spasm is induced by inflating a blood pressure cuff around the arm to a pressure 20 mm Hg above obliteration of the radial pulse for 3-5 minutes.
Hypocalcemia of primary hypoparathyroidism may cause extrapyramidal choreoathetoid syndromes in patients with basal ganglia calcifications.[7]
Parkinsonism, dystonia, hemiballismus, and oculogyric crises may occur in approximately 5% of patients with idiopathic hypoparathyroidism.[8]
Spastic paraplegia, ataxia, dysphagia, and dysarthria have been documented in association with hypoparathyroidism-induced hypocalcemia. Severe hypocalcemia causes papilledema, which improves with treatment of the calcium derangement.
Emotional instability, anxiety, depression, confusion, hallucinations, and psychosis have been described in patients with hypoparathyroidism when the calcium level is low. Normocalcemia corrects these conditions.
Chronic hypocalcemia, as observed in primary hypoparathyroidism, is also associated with ocular cataracts; abnormal dentition; and dry, puffy, coarse skin. In severe hypocalcemia, a prolongation of the QT interval is observed on ECG, and congestive heart failure may develop. Correction of hypocalcemia reverses the cardiac effects of hypoparathyroidism.
In patients with autoimmune polyglandular syndrome, idiopathic hypoparathyroidism is associated with adrenal insufficiency and moniliasis. Moniliasis may affect the skin, nails, oral cavity, and vaginal cavity. It is frequently intractable. The underlying etiology is likely a defect in cellular immunity. Some authors advocate the term HAM syndrome, ie, hypoparathyroidism, Addison disease, and moniliasis (HAM), to denote these cases.
In a study of 33 patients with hypoparathyroidism, Rubin et al concluded that the disease causes bone to assume unusual structural and dynamic properties.[9] Examining biopsies of the iliac crest, the investigators found that, in comparison with biopsies from 33 patients with no known metabolic diseases, the individuals with hypoparathyroidism had greater cancellous bone volume, trabecular width, and cortical width. Moreover, the patients with hypoparathyroidism demonstrated profound suppression of dynamic skeletal indices, including mineralizing surface and bone formation rate.
Most people have 4 parathyroid glands; consequently, primary hypoparathyroidism is uncommon. Hypocalcemia from hypoparathyroidism requires all 4 parathyroid glands to be affected. Primary hypoparathyroidism may be permanent or reversible. Permanent primary hypoparathyroidism may be congenital or acquired.
Iatrogenic causes
The most common cause of primary hypoparathyroidism is excision of all parathyroid glands via surgery in the treatment of thyroid, laryngeal, or other neck malignancy.[10] Patients with parathyroid hyperplasia, as observed in the multiple endocrine neoplasia (MEN) syndromes, are treated by surgical removal of the parathyroid glands. Attempts at restoring normal PTH levels and normocalcemia by autotransplantation[11] of a fraction of one of the parathyroid glands sometimes are effective, but many patients become hypoparathyroid. Repeated neck explorations for primary hyperparathyroidism caused by parathyroid adenoma may also cause hypoparathyroidism.
A study by Dinc et al found the risk of permanent hypoparathyroidism to be greater in patients who underwent bilateral near-total thyroidectomy (BNTT) than in those who underwent bilateral total thyroidectomy (BTT), with hypocalcemia persisting in 2.4% of the BTT patients and in 7.5% of the BNTT patients in the report.[12]
Extensive irradiation to the face, neck, or mediastinum may cause destruction of all 4 parathyroid glands, with ensuing primary hypoparathyroidism and hypocalcemia.
The "hungry bone syndrome" develops after a parathyroidectomy for hyperparathyroidism. The body has been accustomed to high levels of PTH, causing hypercalcemia. Much of this hypercalcemic effect is because of resorption of bone. When the parathyroid gland or glands responsible for the hypersecretion of PTH are removed, the PTH level in the blood drops suddenly, and the patient experiences transient hypoparathyroidism. The bone, which has been starved of calcium, avidly retains it under the influence of osteoblasts. Without PTH and with bone now using calcium to remineralize, the ECF ionized calcium level falls. Postoperatively, patients require aggressive treatment with calcium for several hours to several days. Eventually, the hypoparathyroid state resolves, and calcium homeostasis is re-achieved.
Autoimmune causes
Type 1 autoimmune polyglandular syndrome (also referred to as HAM syndrome) includes primary hypoparathyroidism that is due to destruction of the parathyroid glands. On average, these patients develop primary hypoparathyroidism by age 10 years.
Autoimmune hypoparathyroidism may exist alone or in sporadic or familial forms. For patients with autoimmune primary hypoparathyroidism, the average age for development of hypocalcemia is 7 years, with a range of 6 months to 20 years.[13]
Congenital causes
Numerous conditions are described in the literature that result in congenital agenesis or hypoplasia and, therefore, can produce primary hypoparathyroidism with symptomatic hypocalcemia at birth or in the newborn period. These conditions, which are summarized from Goltzman and Cole (1996), are as follows:[14]
Velocardiofacial (Shprintzen) syndrome (CATCH 22 [for cardiac, abnormal facies, thymic aplasia, cleft palate, and hypocalcemia with 22q deletion] is a mnemonic for the features of this syndrome.)
Zellweger syndrome
Teratogenic effects
Diabetic embryopathy
Fetal alcohol syndrome
Retinoid embryopathy
Associational arhinencephalia and/or DiGeorge syndrome and the coloboma, heart disease, choanal atresia, retarded growth and development, genital anomalies, ear anomalies (CHARGE) syndrome and/or DiGeorge syndrome
Hypoparathyroidism with short stature, mental retardation, and seizures
In addition to the above list, several other genetic defects cause primary hypoparathyroidism. As opposed to the conditions listed above, no agenesis or hypoplasia of the parathyroid glands occurs in these other genetic defects. These mutations are functional, not anatomic, and are listed as follows:
Mutation of chromosome arm 3q has been demonstrated to cause primary hypoparathyroidism in several kindreds because of activation of the parathyroid extracellular calcium-sensing receptor. These patients have mild-to-moderate hypocalcemia, urinary calcium excretion that is high relative to serum calcium (presumably the extracellular calcium-sensing receptor in the kidney contributes to this), and serum PTH concentration that is within the reference range (but is inappropriately low).
Familial isolated hypoparathyroidism is a heterogenous mix of disorders as follows: autosomal dominant abnormal prepro-PTH allele (C-to-T substitution in codon 18 of the prepeptide encoding region does not allow for cleavage to pro-PTH) and autosomal recessive abnormal prepro-PTH allele (C-to-G substitution in the first nucleotide position of prepro-PTH intron 2).
Causes related to metal overload (ion deficiency)
Hemochromatosis and thalassemia, both of which are associated with iron overload, may result in primary hypoparathyroidism.
Wilson disease, with copper overload, may also cause primary hypoparathyroidism.
Hypermagnesemia has been demonstrated to decrease PTH release. Correction of hypermagnesemia leads to correction of the primary hypoparathyroidism.
Aluminum deposition within the parathyroid glands may cause primary hypoparathyroidism in patients with end-stage renal disease who are on hemodialysis.
Causes related to infiltration of the parathyroid glands
In addition to hemochromatosis and Wilson disease, parathyroid gland destruction has been reported as a result of metastatic disease, granulomatous disease, amyloidosis, syphilis, and progressive systemic sclerosis.
Of note, clinically significant hypocalcemia is not always apparent in these patients.
Neonatal causes
The unborn baby of a mother with hypercalcemia has chronic suppression of parathyroid gland function. In the worst circumstances, the parathyroid glands may become atrophic.
At birth, the maternal calcium excess is eliminated, and newborns are at risk of hypocalcemia caused by primary hypoparathyroidism.
Clinically significant hypocalcemia may develop within the first 3 weeks of life but may occur as late as 1 year after birth. The primary hypoparathyroidism in these patients is self-limited.
Primary hypoparathyroidism is defined by a low concentration of PTH with a concomitant low calcium level.
In pseudohypoparathyroidism, the serum PTH concentration is elevated as a result of resistance to PTH caused by mutations in the PTH receptor system.
In secondary hypoparathyroidism, the serum PTH concentration is low and the serum calcium concentration is elevated.
Calcium
The calcium ion is highly bound to protein. A total calcium level cannot be interpreted without a total protein or albumin level.
Hypoalbuminemia causes a drop in total calcium concentration, but the ionized fraction may be within the reference range. Elevated protein states, such as multiple myeloma and paraproteinemias, may cause an elevation of the total calcium concentration, but the ionized fraction may be within the reference range.
Conversely, in the presence of albumin or protein excess, low ionized calcium levels with reference range levels of total calcium are possible. Likewise, if the patient is hypoalbuminemic, high ionized calcium levels with a reference range level of total calcium are possible.
Measurement of ionized calcium concentration in the plasma is ideal; however, it is not readily available in many places.
The relationship between total serum calcium and albumin is defined by the following simple rule: the serum total calcium concentration falls by 0.8 mg/dL for every 1-g/dL fall in serum albumin concentration. This rule assumes that normal albumin equals 4.0 g/dL and normal calcium is 10.0 mg/dL.
Alkalosis causes ionized calcium to bind to albumin more strongly. This causes a decrease in the ionized calcium and may trigger symptoms of hypocalcemia.
Measurement of 25-hydroxy vitamin D: This measurement is important to exclude vitamin D deficiency as a cause of hypocalcemia.
Serum magnesium: Hypomagnesemia may cause PTH deficiency and subsequent hypocalcemia. Exclude it in any patient with primary hypoparathyroidism.
Serum phosphorus: PTH is a phosphaturic hormone. In its absence, phosphorus levels in the blood rise.
Treatment of patients with hypoparathyroidism involves correcting the hypocalcemia by administering calcium and vitamin D.[2]
Recombinant human parathyroid hormone (rhPTH[1-84], Natpara) is commercially available in the United States and is indicated as an adjunct to calcium and vitamin D to control hypocalcemia in patients with hypoparathyroidism. Its approval was based on the REPLACE trial (n=134). The primary endpoint was patients who achieved a greater than 50% reduction of daily PO calcium and vitamin D from baseline while maintaining serum calcium above baseline concentrations and less than upper limits of normal at week 24. Results showed that 48 (53%) of patients in the rhPTH group achieved the primary endpoint compared with 1 (2%) patient in the placebo group (p< 0.0001).[15]
A prospective study by Rubin et al indicated that in patients with hypoparathyroidism, long-term, continuous therapy with rhPTH(1-84) has a good safety profile, reduces the need for supplemental calcium and calcitriol, leads to stable serum calcium concentration, and reduces urinary calcium excretion. The study included 33 patients, who underwent therapy with the hormone for up to 6 years.[16]
Guidelines on chronic hypoparathyroidism by the European Society of Endocrinology, released in 2015, are below:[17]
Consider a diagnosis of chronic hypoparathyroidism (HypoPT) in a patient with hypocalcemia and inappropriately low parathyroid hormone (PTH) levels.
Consider genetic testing and/or family screening in a patient with HypoPT of unknown etiology.
Treatment targeted to maintain serum calcium level (albumin adjusted total calcium or ionized calcium) in the lower part or slightly below the lower limit of the reference range (target range) is suggested, with patients being free of symptoms or signs of hypocalcemia.
Treat patients with chronic HypoPT with symptoms of hypocalcemia and/or an albumin adjusted serum calcium level < 2.0 mmol/L (< 8.0 mg/dL/ionized serum calcium levels [S-Ca2] < 1.00 mmol/L).
Offer treatment to asymptomatic patients with chronic HypoPT and an albumin adjusted calcium level between 2.0 mmol/L (8.0 mg/dL/S-Ca2+ 1.00 mmol/L) and the lower limit of the reference range in order to assess whether this may improve their well-being.
Use activated vitamin D analogues plus calcium supplements in divided doses as the primary therapy.
If activated vitamin D analogues are not available, treat with calciferol (preferentially cholecalciferol).
Titrate activated vitamin D analogues or cholecalciferol in such a manner that patients are without symptoms of hypocalcemia and serum calcium levels are maintained within the target range.
Provide vitamin D supplementations in a daily dose of 400–800 IU to patients treated with activated vitamin D analogues.
In a patient with hypercalciuria, consider a reduction in calcium intake, a sodium-restricted diet, and/or treatment with a thiazide diuretic.
In a patient with renal stones, evaluate renal stone risk factors and management according to relevant international guidelines.
In a patient with hyperphosphatemia and/or an elevated calcium-phosphate product, consider dietary interventions and/or adjustment of treatment with calcium and vitamin D analogues.
In a patient with hypomagnesemia, consider measures that may increase serum magnesium levels.
The routine use of replacement therapy with PTH or PTH analogues is not recommended.
Patients undergoing parathyroidectomy for parathyroid hyperplasia are at high risk of developing permanent primary hypoparathyroidism.
Patients may be treated with an autotransplant of a segment of parathyroid gland to prevent hypoparathyroidism.[11] This autotransplant is usually placed subcutaneously in the forearm or in the neck. A study by Teshima et al indicated that if the parathyroid glands cannot be preserved in situ during total thyroidectomy for thyroid cancer, hypoparathyroidism can best be avoided by autotransplantation of two or more parathyroid glands. The investigators found that 33% of the patients in whom one parathyroid gland was autotransplanted developed permanent hypoparathyroidism, while none of the patients in whom two or more parathyroid glands were autotransplanted developed this condition.[18]
If the autotransplantation fails, patients receive the same treatment that is administered to other patients with hypoparathyroidism.
Guidelines on chronic hypoparathyroidism by the European Society of Endocrinology, released in 2015, are below:[17]
Consider a diagnosis of chronic hypoparathyroidism (HypoPT) in a patient with hypocalcemia and inappropriately low parathyroid hormone (PTH) levels.
Consider genetic testing and/or family screening in a patient with HypoPT of unknown etiology.
Treatment targeted to maintain serum calcium level (albumin adjusted total calcium or ionized calcium) in the lower part or slightly below the lower limit of the reference range (target range) is suggested, with patients being free of symptoms or signs of hypocalcemia.
Treat patients with chronic HypoPT with symptoms of hypocalcemia and/or an albumin adjusted serum calcium level < 2.0 mmol/L (< 8.0 mg/dL/ionized serum calcium levels [S-Ca2] < 1.00 mmol/L).
Offer treatment to asymptomatic patients with chronic HypoPT and an albumin adjusted calcium level between 2.0 mmol/L (8.0 mg/dL/S-Ca2+ 1.00 mmol/L) and the lower limit of the reference range in order to assess whether this may improve their well-being.
Use activated vitamin D analogues plus calcium supplements in divided doses as the primary therapy.
If activated vitamin D analogues are not available, treat with calciferol (preferentially cholecalciferol).
Titrate activated vitamin D analogues or cholecalciferol in such a manner that patients are without symptoms of hypocalcemia and serum calcium levels are maintained within the target range.
Provide vitamin D supplementations in a daily dose of 400–800 IU to patients treated with activated vitamin D analogues.
In a patient with hypercalciuria, consider a reduction in calcium intake, a sodium-restricted diet, and/or treatment with a thiazide diuretic.
In a patient with renal stones, evaluate renal stone risk factors and management according to relevant international guidelines.
In a patient with hyperphosphatemia and/or an elevated calcium-phosphate product, consider dietary interventions and/or adjustment of treatment with calcium and vitamin D analogues.
In a patient with hypomagnesemia, consider measures that may increase serum magnesium levels.
The routine use of replacement therapy with PTH or PTH analogues is not recommended.
Clinical Context:
Moderates nerve and muscle performance and facilitates normal cardiac function. Many commercially available preparations exist. Titrate total daily dose of elemental calcium to minimize the daily dose of vitamin D and to keep patients asymptomatic. Ionized calcium is absorbed best in an acidic environment; 400 mg elemental calcium equals 1 g calcium carbonate.
Clinical Context:
Moderates nerve and muscle performance and facilitates normal cardiac function; 210 mg of elemental calcium equals 1 g calcium citrate.
Clinical Context:
Moderates nerve and muscle performance and facilitates normal cardiac function. Available for IV use. Infuse slowly over 5-10 min; 10 mL calcium gluconate contains approximately 90 mg elemental calcium; 1000 mg of calcium gluconate equals 90 mg elemental calcium.
Without PTH, the ionized calcium levels in the plasma drop. Bone becomes an inefficient source of calcium for plasma, and kidneys waste calcium. Calcium helps maintain the ionized calcium level close to the reference range.
Clinical Context:
Synthetic analog of vitamin D. Stimulates calcium and phosphate absorption from small intestine and promotes secretion of calcium from bone to blood. Promotes renal tubule resorption of phosphate.
Clinical Context:
Promotes absorption of calcium and phosphorus in the small intestine. Promotes renal tubule resorption of phosphate. Increases rate of accretion and resorption in bone minerals.
Clinical Context:
Promotes absorption of calcium in intestines and retention at kidneys to increase calcium levels in serum. Decreases excessive serum phosphatase levels and parathyroid levels. Decreases bone resorption.
Vitamin D is synthesized by the kidneys, and the synthesis of 1,25-dihydroxy vitamin D is PTH dependent. In most patients with chronic hypoparathyroidism, treatment with the active vitamin D form is necessary.[2]
Clinical Context:
Parathyroid hormone raises serum calcium by increasing renal tubular calcium reabsorption, increasing intestinal calcium absorption, and increasing bone turnover. rhPTH is indicated as an adjunct to calcium and vitamin D to control hypocalcemia in patients with hypoparathyroidism.
Diuretic use: The use of any diuretic medication may alter calcium homeostasis. Patients must know this and should remind their practitioner whenever new medications are prescribed.
Pregnancy: Medications that alter the synthesis of proteins and albumin in the liver and/or hyperestrogenic states, such as pregnancy, may lead to alterations in calcium homeostasis. Instruct patients to consult their doctor prior to any changes in any medications.
What is hypoparathyroidism?What is the pathophysiology of hypoparathyroidism?What is the prevalence of hypoparathyroidism?Which age groups have the highest prevalence of hypoparathyroidism?What are the sexual predilections of hypoparathyroidism?Which clinical history findings are characteristic of hypoparathyroidism?Which physical findings are characteristic of hypoparathyroidism?What are the iatrogenic causes of hypoparathyroidism?What are the autoimmune causes of hypoparathyroidism?What are the congenital causes of hypoparathyroidism?What other genetic defects can cause hypoparathyroidism?What are the metal overload causes of hypoparathyroidism?What causes parathyroid gland destruction in hypoparathyroidism?What are neonatal causes of hypoparathyroidism?What are the differential diagnoses for Hypoparathyroidism?What is the role of parathyroid hormone (PTH) measurement in the diagnosis of hypoparathyroidism?What is the role of calcium measurement in the diagnosis of hypoparathyroidism?What is the role of 25-hydroxy vitamin D measurement in the diagnosis of hypoparathyroidism?What is the role of serum magnesium measurement in the diagnosis of hypoparathyroidism?What is the role of serum phosphorus measurement in the diagnosis of hypoparathyroidism?How is hypoparathyroidism treated?What are the ESE guidelines on the diagnosis and treatment of chronic hypoparathyroidism?What is the role of surgery in the treatment of hypoparathyroidism?Which specialist consultations are beneficial to patients with hypoparathyroidism?Which dietary modifications are used in the treatment of hypoparathyroidism?Which activity modifications are used in the treatment of hypoparathyroidism?What are the ESE guidelines on the diagnosis and treatment of chronic hypoparathyroidism?Which medications are used in the treatment of hypoparathyroidism?Which medications in the drug class Parathyroid Hormone Analogs are used in the treatment of Hypoparathyroidism?Which medications in the drug class Vitamin D preparations are used in the treatment of Hypoparathyroidism?Which medications in the drug class Calcium salts are used in the treatment of Hypoparathyroidism?What is included in the long-term monitoring of hypoparathyroidism?What are the possible complications of hypoparathyroidism?What is included in patient education about hypoparathyroidism?
Joseph Michael Gonzalez-Campoy, MD, PhD, FACE, Medical Director and CEO, Minnesota Center for Obesity, Metabolism, and Endocrinology
Disclosure: Nothing to disclose.
Specialty Editors
Francisco Talavera, PharmD, PhD, Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference
Disclosure: Received salary from Medscape for employment. for: Medscape.
Yoram Shenker, MD, Chief of Endocrinology Section, Veterans Affairs Medical Center of Madison; Interim Chief, Associate Professor, Department of Internal Medicine, Section of Endocrinology, Diabetes and Metabolism, University of Wisconsin at Madison
Disclosure: Nothing to disclose.
Chief Editor
George T Griffing, MD, Professor Emeritus of Medicine, St Louis University School of Medicine
Disclosure: Nothing to disclose.
Additional Contributors
David S Schade, MD, Chief, Division of Endocrinology and Metabolism, Professor, Department of Internal Medicine, University of New Mexico School of Medicine and Health Sciences Center
Goltzman D, Cole DEC. Hypoparathyroidism. Favus MJ, ed. Primer on the Metabolic Bone Diseases and Disorders of Mineral Metabolism. Philadelphia, Pa: Lippincott-Raven; 1996. 220-3.
