Pediatric Hypoparathyroidism Treatment & Management

  • Author: Pisit (Duke) Pitukcheewanont, MD; Chief Editor: Stephen Kemp, MD, PhD  more...
Updated: Aug 05, 2015

Medical Care


Symptomatic hypocalcemia (eg, seizure, tetany, laryngospasm) in patients with hypoparathyroidism requires intravenous calcium and continuous monitoring for cardiac arrhythmias.

Oral calcium and active vitamin D (calcitriol) should be initiated as soon as possible (eg, when the patient is tolerating oral feeds).

Once serum calcium concentrations are in a safe range (>7.5 mg/dL), intravenous calcium can be stopped. Prolonged intravenous calcium therapy with existing high serum phosphate will increase further precipitation of calcium-phosphate compound. However, rebound hypocalcemia can occur and requires that a patient be monitored for therapeutic success on oral agents for at least 24 hours after intravenous calcium is withdrawn. In patients with hungry bone syndrome, prolonged intravenous calcium therapy may be needed.

The active form of vitamin D, 1,25-dihydroxyvitamin D (calcitriol), is preferred in the treatment of hypoparathyroidism because both the parathyroid hormone (PTH) deficiency/resistance and the hyperphosphatemia impair the activation of 25-hydroxyvitamin D by 1-alpha-hydroxylase.

General recent guidelines on chronic hypoparathyroidism by the European Society of Endocrinology are below:[5]

  • 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-Ca 2] <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-Ca 2+ 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 hypocalcaemia 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.


No special diet is required, but adequate calcium and vitamin D intake is recommended.

Contributor Information and Disclosures

Pisit (Duke) Pitukcheewanont, MD Associate Professor of Clinical Pediatrics, University of Southern California, Keck School of Medicine, Childrens Hospital Los Angeles

Pisit (Duke) Pitukcheewanont, MD is a member of the following medical societies: American Academy of Pediatrics, American Diabetes Association, American Medical Association, American Society for Bone and Mineral Research, Endocrine Society, Pediatric Endocrine Society

Disclosure: Nothing to disclose.

Specialty Editor Board

Mary L Windle, PharmD Adjunct Associate Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Nothing to disclose.

George P Chrousos, MD, FAAP, MACP, MACE, FRCP(London) Professor and Chair, First Department of Pediatrics, Athens University Medical School, Aghia Sophia Children's Hospital, Greece; UNESCO Chair on Adolescent Health Care, University of Athens, Greece

George P Chrousos, MD, FAAP, MACP, MACE, FRCP(London) is a member of the following medical societies: American Academy of Pediatrics, American College of Physicians, American Pediatric Society, American Society for Clinical Investigation, Association of American Physicians, Endocrine Society, Pediatric Endocrine Society, Society for Pediatric Research, American College of Endocrinology

Disclosure: Nothing to disclose.

Chief Editor

Stephen Kemp, MD, PhD Former Professor, Department of Pediatrics, Section of Pediatric Endocrinology, University of Arkansas for Medical Sciences College of Medicine, Arkansas Children's Hospital

Stephen Kemp, MD, PhD is a member of the following medical societies: American Academy of Pediatrics, American Association of Clinical Endocrinologists, American Pediatric Society, Endocrine Society, Phi Beta Kappa, Southern Medical Association, Southern Society for Pediatric Research

Disclosure: Nothing to disclose.

Additional Contributors

Thomas A Wilson, MD Professor of Clinical Pediatrics, Chief and Program Director, Division of Pediatric Endocrinology, Department of Pediatrics, The School of Medicine at Stony Brook University Medical Center

Thomas A Wilson, MD is a member of the following medical societies: Endocrine Society, Pediatric Endocrine Society, Phi Beta Kappa

Disclosure: Nothing to disclose.

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Electrocardiogram (ECG) findings in severe hypocalcemia.
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