MANAGING HYPOPARATHYROIDISM

Guidelines and
strategies for managing hypoparathyroidism

Watch: Clinical Guidelines for the
Management of Hypoparathyroidism
Doctor talking to her patient about hypoparathyroidism.

Therapeutic objectives

International and European guidelines recommend the following therapeutic goals to prevent complications of hypoparathyroidism (HPT)1-3:

Prevent signs and symptoms of hypocalcemia. Maintain serum calcium level slightly below the normal range (no more than 0.5 mg/dL below normal) or in the low normal range.

Potential complications: Tetany, seizures, muscle cramps, paresthesia, other neuromuscular complications, fatigue, poor concentration, memory and cognitive function, impaired quality of life, and congestive heart failure (if severe and chronic).

Maintain calcium phosphate product <55 mg2/dL2.

Potential complications: Ectopic calcifications in the brain, kidney, vascular system, and soft tissues.

Avoid hypercalciuria.

Potential complications: Kidney stones, nephrocalcinosis, renal dysfunction, and end-stage renal disease.

Avoid hypercalcemia.

Potential complications: Symptomatic hypercalcemia (weakness, altered mental status, nausea, and abdominal pain) and increased risk of renal calcification.

Decrease potential for renal and other extraskeletal calcifications.

Potential complications: Renal dysfunction and progression to dialysis or transplantation. Central nervous system calcifications and possible dysfunction (eg, seizures, altered mental activity, and movement disorder), and vision loss.

Key monitoring parameters

Assessing for adequate control of HPT requires monitoring of laboratory values beyond serum calcium and observing their trends over time.

Assess every 3-6 months2,3,*

Assessments3 Target Range3-5
Serum calcium 8.0-9.0 mg/dL
Serum phosphate 2.5-4.5 mg/dL
Calcium phosphate product <55 mg2/dL2
BUN/creatinine or eGFR 90-120 mL/min/1.73 m2
Magnesium1.7-2.6 mg/dL
*Adjust frequency to:
  • Every 1-2 weeks following adjustments in calcium or vitamin D dose
  • At least every 3 weeks during pregnancy

Assess at least once per year3,†

Assessments3 Target Range3
24-hour urine calcium <4 mg/kg body weight daily
Vitamin D >20 ng/mL
Assess more frequently following adjustments in calcium or vitamin D dose

Target-organ evaluations

As clinically indicated1,6:

  • Renal ultrasound or CT scan
  • CNS imaging
  • Electrocardiogram
  • Bone mineral density
  • Ophthalmologic examination

Key management strategies

Calcium1:

  • Calcium requirements can vary, ranging from less than 1 g/d up to 9 g/d.
  • Calcium carbonate is most commonly used, but calcium citrate can be considered in certain clinical situations.

Active vitamin D1:

  • Typical doses of calcitriol (active vitamin D) are between 0.25 μg/d and 2.00 μg/d.
  • Ergo- or cholecalciferol (parent vitamin D) supplementation may be considered.

Thiazide diuretics1:

  • Often used in the presence of hypercalciuria, as they promote calcium retention in the renal tubules.
  • Serum potassium and magnesium should be monitored with diuretic use.

Magnesium6:

  • Used if hypomagnesemia is present, which can be due to diuretic or proton pump inhibitor use.

Phosphate binders1:

  • Only used in situations where serum phosphate levels are markedly elevated (eg, >6.5 mg/dL) and the calcium-phosphate product is of concern.

Dietary changes1:

  • Patients with high serum phosphate levels may need to follow a low-phosphate diet.
  • Patients with high urine calcium levels may need to follow a low-salt diet.

Hormone therapy may be considered for patients who are not adequately controlled.1

Some patients with chronic hypoparathyroidism require large amounts of calcium supplementation.7

BEYOND CALCIUM CONTROL

BUN, blood urea nitrogen; CNS, central nervous system; eGFR, estimated glomerular filtration rate.

REFERENCES:

1. Brandi ML, Bilezikian JP, Shoback D, et al. J Clin Endocrinol Metab. 2016;101(6):2273-2283. 2. Bollerslev J, Rejnmark L, Marcocci C, et al. Eur J Endocrinol. 2015;173(2):G1-G20. 3. Mannstadt M, Bilezikian JP, Thakker RV, et al. Nat Rev Dis Primers. 2017;3:17055. doi:10.1038/nrdp.2017.55. 4. Horwitz MJ, Stewart AF. J Clin Endocrinol Metab. 2008;93(9):3307-3309. 5. Blaine J, Chonchol M, Levi M. Clin J Am Soc Nephrol. 2015;10(7):1257-1272. 6. Shoback DM, Bilezikian JP, Costa AG, et al. J Clin Endocrinol Metab. 2016;101(6):2300-2312. 7. Marcucci G, Cianferotti L, Parri S, et al. Calcif Tissue Int. 2018;103:151-163.