eMedicine Specialties > Pediatrics: General Medicine > Endocrinology

Hypoparathyroidism: Treatment & Medication

Author: James CM Chan, MD, Professor of Pediatrics, University of Vermont College of Medicine; Director of Research, The Barbara Bush Children's Hospital, Maine Medical Center
Contributor Information and Disclosures

Updated: Sep 17, 2009

Treatment

Medical Care

  • Symptomatic hypocalcemia (eg, seizure, tetany, laryngospasm) in patients with hypoparathyroidism requires intravenous calcium and continuous monitoring for cardiac arrhythmias.
  • Oral calcium and vitamin D 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. 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that a patient be monitored for therapeutic success on oral agents for at least 24 hours after intravenous calcium is withdrawn.
  • The active form of vitamin D, 1,25-dihydroxyvitamin D, 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.

Diet

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

Medication

Calcium and vitamin D are the mainstays of treatment for hypoparathyroidism and pseudohypoparathyroidism (PHP). To relieve immediate severe symptoms of hypocalcemia, an intravenous bolus of 9-15 mg elemental calcium/kg (1 g calcium gluconate = 90 mg elemental calcium = 4.5 mEq elemental calcium) is administered over 10-30 min. Then, either intermittent boluses or a continuous IV infusion is initiated (£ 60 mg elemental calcium/kg/d). Oral calcium is initiated for a total of 100 mg elemental calcium/kg/d divided 4 times daily. Once serum calcium concentrations range from 8-9 mg/dL, the calcium dose is weaned to the minimum dose necessary to maintain a low-normal serum calcium concentration.

Calcium supplements

Numerous calcium preparations are available. An intravenous dose quickly but transiently corrects the serum calcium concentration and relieves hypocalcemic symptoms. Severe hypocalcemia can be treated with a continuous calcium infusion; a transition to the oral form can be made when the serum calcium concentration is within a safe range. Tailoring of calcium dosing to each patient's needs is essential. In fact, once adequate amounts of active vitamin D are present, some patients can absorb all the calcium they need through the diet and oral calcium preparations can be discontinued.


Calcium gluconate

Used to correct serum calcium concentration and relieve hypocalcemic symptoms. Moderates nerve and muscle performance and facilitates normal cardiac function (1 g = 90 mg elemental = 4.5 mEq elemental calcium).

Adult

100-300 mg elemental calcium IV diluted in 150 mL D5W over 10 min; initial rate of infusion should be 0.3-2 mg of elemental calcium/kg/h

Pediatric

10% calcium gluconate solution (contains 9 mg/mL elemental calcium), 9-15 mg elemental/kg IV over 30 - 120 min initially; then 100 mg elemental/kg/d PO/IV (initially maximum IV dose of 60 mg elemental/kg/d should be administered for severe hypocalcemia until transition to PO dosing is safe)

May decrease effects of tetracyclines, atenolol, salicylates, iron salts, and fluoroquinolones; antagonizes effects of verapamil; large intakes of dietary fiber may decrease calcium absorption and levels

Renal calculi; hypercalcemia; hypophosphatemia; renal or cardiac disease; digitalis toxicity

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Rapid IV bolus may affect cardiac conduction, careful cardiac monitoring is necessary when IV calcium is administered; use extravasation precautions; caution in digitalized patients, respiratory failure, acidosis, or severe hyperphosphatemia


Calcium glubionate (Neo-Calglucon)

PO calcium can be used to correct mild hypocalcemia and for maintenance therapy. Moderates nerve and muscle performance and facilitates normal cardiac function (1 g = 64 mg elemental = 3.3 mEq elemental calcium).

Adult

1-2 g/d elemental calcium PO divided tid/qid

Pediatric

100 mg elemental calcium/kg/d PO initially, then wean as necessary
Infants: 60 mg/kg/d PO elemental calcium
Older children: Require less per kg than infants; dose should be adjusted individually to maintain serum calcium levels at low end of the reference range for your laboratory

May decrease effects of tetracyclines, atenolol, salicylates, iron salts, and fluoroquinolones; antagonizes effects of verapamil; large intakes of dietary fiber may decrease calcium absorption and levels

Renal calculi; hypercalcemia; hypophosphatemia; renal or cardiac disease; digitalis toxicity

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

May cause hypercalcemia or hypercalcuria


Calcium carbonate (Tums, Oscal)

An alternative PO form of calcium that can be used to correct mild hypocalcemia and for maintenance therapy (1 g = 400 mg elemental = 20 mEq elemental calcium).

Adult

1-2 g/d elemental calcium PO divided tid/qid

Pediatric

100 mg elemental calcium/kg/d PO initially, then wean as necessary
Infants: 60 mg/kg/d PO elemental calcium
Older children: Require less per kg than infants; dose should be adjusted individually to maintain serum calcium levels at the low end of the reference range for your laboratory

May decrease effects of tetracyclines, atenolol, salicylates, iron salts, and fluoroquinolones; antagonizes effects of verapamil; large intakes of dietary fiber may decrease calcium absorption and levels

Renal calculi; hypercalcemia; hypophosphatemia; renal or cardiac disease; digitalis toxicity

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

May cause hypercalcemia or hypercalcuria

Vitamin D supplements

1,25-Dihyroxyvitamin D, calcitriol, is critical for maintaining serum calcium concentrations. Parathyroid hormone (PTH) deficiency impairs conversion of inactive vitamin D to the active form by renal 1-alpha-hydroxylase. To bypass this PTH-dependent step, the active form of vitamin D is administered and may eliminate the need for PO calcium once the patient has stabilized.


Calcitrol (Rocaltrol)

This drug has a short half-life, and its effects are quickly reversed with withdrawal of the medication in case of hypercalcemia. Calcitriol is available in 0.25- and 0.50-mcg gel cap.

Adult

0.5-2 mcg PO qd

Pediatric

25-50 ng/kg/d PO divided qid; usual dose is 0.25-mcg gel cap qid to treated hypoparathyroidism

Cholestyramine and colestipol decrease absorption of calcitriol; magnesium-containing antacids and thiazide diuretics can increase calcitriol effects

Documented hypersensitivity; hypercalcemia; malabsorption syndrome; vitamin D intoxication

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Adequate response to calcitriol depends on adequate dietary calcium intake; maintain adequate fluid intake

More on Hypoparathyroidism

Overview: Hypoparathyroidism
Differential Diagnoses & Workup: Hypoparathyroidism
Treatment & Medication: Hypoparathyroidism
Follow-up: Hypoparathyroidism
Multimedia: Hypoparathyroidism
References

References

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Further Reading

Keywords

hypoparathyroidism, hypocalcemia, pseudohypoparathyroidism, PHP, pseudopseudohypoparathyroidism, PPHP, polyglandular autoimmune endocrinopathy, DiGeorge syndrome, Barakat syndrome, Kenny-Caffey syndrome, Albright hereditary osteodystrophy, parathyroid insufficiency, familial hypercalciuric hypocalcemia, familial isolated hypoparathyroidism, calcium-sensing receptor hypocalcemia, Kearns-Sayre syndrome, Pearson marrow pancreas, laryngospasm, syncope, seizure, tetany, muscle aches, facial twitching, carpopedal spasm, tetralogy of Fallot, truncus arteriosus, Albright hereditary osteodystrophy, AHO, obesity, treatment, diagnosis

Contributor Information and Disclosures

Author

James CM Chan, MD, Professor of Pediatrics, University of Vermont College of Medicine; Director of Research, The Barbara Bush Children's Hospital, Maine Medical Center
James CM Chan, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Pediatrics, American Association of University Professors, American Chemical Society, American Heart Association, American Medical Association, American Physiological Society, American Society for Bone and Mineral Research, American Society of Nephrology, American Society of Pediatric Nephrology, International Society of Nephrology, New York Academy of Sciences, Society for Experimental Biology and Medicine, and Southern Society for Pediatric Research
Disclosure: Nothing to disclose.

Medical Editor

Thomas A Wilson, MD, Professor of Clinical Pediatrics, Department of Pediatrics; Director of Pediatric Endocrinology, Division of Pediatric Endocrinology, Department of Pediatrics, State University of New York at Stony Brook
Thomas A Wilson, MD is a member of the following medical societies: Endocrine Society, Lawson-Wilkins Pediatric Endocrine Society, and Phi Beta Kappa
Disclosure: Nothing to disclose.

Pharmacy Editor

Mary L Windle, PharmD, Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy, Pharmacy Editor, eMedicine
Disclosure: Pfizer Inc Stock Investment from financial planner; Avanir Pharma Stock Investment from financial planner ; WebMD Salary and stock Employment and investment from financial planner

Managing Editor

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
George P Chrousos, MD, FAAP, MACP, MACE, FRCP(London) is a member of the following medical societies: American Academy of Pediatrics, American College of Endocrinology, American College of Physicians, American Pediatric Society, American Society for Clinical Investigation, Association of American Physicians, Endocrine Society, Lawson-Wilkins Pediatric Endocrine Society, and Society for Pediatric Research
Disclosure: Nothing to disclose.

CME Editor

Merrily P M Poth, MD, Professor, Department of Pediatrics and Neuroscience, Uniformed Services University of the Health Sciences
Merrily P M Poth, MD is a member of the following medical societies: American Academy of Pediatrics, Endocrine Society, and Lawson-Wilkins Pediatric Endocrine Society
Disclosure: Nothing to disclose.

Chief Editor

Stephen Kemp, MD, PhD, Professor, Department of Pediatrics, Section of Pediatric Endocrinology, University of Arkansas and 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, and Southern Society for Pediatric Research
Disclosure: Genentech, Inc. Honoraria Speaking and teaching; Pfizer, Inc. Honoraria Consulting

 
 
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