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Hypoparathyroidism Treatment & Management

  • Author: Joseph Michael Gonzalez-Campoy, MD, PhD, FACE; Chief Editor: George T Griffing, MD  more...
 
Updated: Aug 04, 2015
 

Medical Care

Treatment of patients with hypoparathyroidism involves correcting the hypocalcemia by administering calcium and vitamin D.[8]

Recombinant human parathyroid hormone (rhPTH, 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).[9]

More recent guidelines on chronic hypoparathyroidism by the European Society of Endocrinology are below:[10]

  • 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.
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Surgical Care

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.[5] This autotransplant is usually placed subcutaneously in the forearm or in the neck.

If the autotransplantation fails, patients receive the same treatment that is administered to other patients with hypoparathyroidism.

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Consultations

An endocrinologist should be involved in the care of all patients who have primary hypoparathyroidism or who are at risk of developing it.

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Diet

A diet rich in calcium content (ie, emphasizing dairy products) is recommended for patients with primary hypoparathyroidism.

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Activity

Patients with symptomatic hypocalcemia develop tetany. Otherwise, no restriction in activity for these patients is necessary.

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Contributor Information and Disclosures
Author

Joseph Michael Gonzalez-Campoy, MD, PhD, FACE Medical Director and CEO, Minnesota Center for Obesity, Metabolism, and Endocrinology

Joseph Michael Gonzalez-Campoy, MD, PhD, FACE is a member of the following medical societies: American Association of Clinical Endocrinologists, Association of Clinical Researchers and Educators, Minnesota Medical Association

Disclosure: Nothing to disclose.

Specialty Editor Board

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

Yoram Shenker, MD is a member of the following medical societies: American Heart Association, Central Society for Clinical and Translational Research, Endocrine Society

Disclosure: Nothing to disclose.

Chief Editor

George T Griffing, MD Professor Emeritus of Medicine, St Louis University School of Medicine

George T Griffing, MD is a member of the following medical societies: American Association for the Advancement of Science, International Society for Clinical Densitometry, Southern Society for Clinical Investigation, American College of Medical Practice Executives, American Association for Physician Leadership, American College of Physicians, American Diabetes Association, American Federation for Medical Research, American Heart Association, Central Society for Clinical and Translational Research, Endocrine Society

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

David S Schade, MD is a member of the following medical societies: American College of Physicians, American Diabetes Association, American Federation for Medical Research, Endocrine Society, New Mexico Medical Society, New York Academy of Sciences, Society for Experimental Biology and Medicine

Disclosure: Nothing to disclose.

References
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  2. Assfaw Z, Assefa G. Basal ganglia calcification with hypoparathyroidism: a case report. Ethiop Med J. 2011 Jul. 49(3):273-7. [Medline].

  3. Goswami R, Goel S, Tomar N, et al. Prevalence of clinical remission in patients with sporadic idiopathic hypoparathyroidism. Clin Endocrinol (Oxf). 2009 Jun 22. [Medline].

  4. Rubin MR, Dempster DW, Zhou H, et al. Dynamic and structural properties of the skeleton in hypoparathyroidism. J Bone Miner Res. 2008 Dec. 23(12):2018-24. [Medline]. [Full Text].

  5. Ebrahimi H, Edhouse P, Lundgren CI, et al. Does autoimmune thyroid disease affect parathyroid autotransplantation and survival?. ANZ J Surg. 2009 May. 79(5):383-5. [Medline].

  6. Brown EM. Anti-parathyroid and anti-calcium sensing receptor antibodies in autoimmune hypoparathyroidism. Endocrinol Metab Clin North Am. 2009 Jun. 38(2):437-45, x. [Medline]. [Full Text].

  7. 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.

  8. Cheung M. Drugs used in paediatric bone and calcium disorders. Endocr Dev. 2009. 16:218-232. [Medline].

  9. Mannstadt M, Clarke BL, Vokes T, Brandi ML, Ranganath L, Fraser WD, et al. Efficacy and safety of recombinant human parathyroid hormone (1-84) in hypoparathyroidism (REPLACE): a double-blind, placebo-controlled, randomised, phase 3 study. Lancet Diabetes Endocrinol. 2013 Dec. 1(4):275-83. [Medline].

  10. Bollerslev J, Rejnmark L, Marcocci C, Shoback DM, Sitges-Serra A, van Biesen W, et al. European Society of Endocrinology Clinical Guideline: Treatment of chronic hypoparathyroidism in adults. Eur J Endocrinol. 2015 Aug. 173 (2):G1-G20. [Medline].

  11. Brown EM, Harris HW, Vassilev PM. The biology of the extracellular Ca2+-sensing receptor. Bilezikian JP, ed. Principles of Bone Biology. San Diego, Calif: Academic Press; 1996. 243-62.

  12. Cole DEC, Hendy GN. Hypoparathyroidism and pseudohypoparathyroidism. Endotext.com. 2005, Available at. [Full Text].

  13. Marx SJ. Hyperparathyroid and hypoparathyroid disorders. N Engl J Med. 2000 Dec 21. 343(25):1863-75. [Medline].

  14. Thakker RV. Molecular basis of PTH underexpression. Bilezikian JP, et al, eds. Principles of Bone Biology. San Diego, Calif: Academic Press; 1996. 837-51.

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