> Table of Contents > Hypoparathyroidism
Christina Kelly, MD, FAAFP
image BASICS
  • Deficient secretion of parathyroid hormone (PTH)
  • Usually asymptomatic
  • Acute hypoparathyroidism: tetany that is mild (muscle cramps, peri-oral numbness, paresthesias of hands and feet) or severe (carpopedal spasm, laryngospasm, heart failure, seizures, stridor)
  • Chronic: lethargy, anxiety/depression, urolithiasis and renal impairment, dementia, blurry vision from cataracts or keratoconjunctivitis, parkinsonism or other movement disorders, mental retardation, dental abnormalities, and dry, puffy, coarse skin
  • System(s) affected: endocrine/metabolic, musculoskeletal, nervous, opthomalogic, renal
Pediatric Considerations
  • May occur in premature infants
  • Neonates born to hypercalcemic mothers may experience suppression of developing parathyroid glands.
  • Congenital absence of parathyroids
  • May appear later in childhood as autoimmune or APS-1
Geriatric Considerations
Hypocalcemia is fairly common in elderly; however, rarely secondary to hypoparathyroidism
Pregnancy Considerations
  • Use of magnesium as a tocolytic may induce functional hypoparathyroidism.
  • For women with hypoparathyroidism, calcitriol requirements decrease during lactation.
More common in women; affects all ages
Most common after surgical procedure of the anterior neck. Transient hyperparathyroidism is seen after 6.9-46% of thyroidectomies, whereas permanent hypoparathyroidism, 0.9-1.6% at experienced centers.
Wide variation. Autosomal dominant hypocalcemia with hypercalciuria (ADHH): 1/70,000 typically in infancy with hypocalcemic seizures
  • PTH is involved in the control of serum-ionized calcium levels:
    • Mobilizes calcium and phosphorus from bone stores
    • Stimulates formation of 1,25-dihydroxy-vitamin D
    • Stimulates reabsorption of calcium in the distal convoluted tubule and phosphate excretion in proximal tubule
  • Loss of PTH action results in hypocalcemia, hyperphosphatemia, and hypercalciuria.
  • Magnesium is crucial for PTH secretion and activation of the PTH receptor; hypo- or hypermagnesemia may result in functional hypoparathyroidism.
  • Acquired hypoparathyroidism
    • Surgical: removal or damage to parathyroid glands or their blood supply; thyroid, parathyroid, or radical neck surgery for head and neck cancers (1)
    • Autoimmune: isolated or combined with other endocrine deficiencies in polyglandular autoimmune (PGA) syndrome
    • Deposition of heavy metals in gland: copper (Wilson disease) or iron (hemochromatosis, thalassemias), radiation-induced destruction, and metastatic infiltration
    • Functional hypoparathyroidism: associated with hypomagnesemia; hypermagnesemia
    • Congenital
      • Calcium-sensing receptor (CaSR) abnormalities: hypocalcemia with hypercalciuria
      • HDR or Barakat syndrome: deafness, renal dysplasia
      • Familial: mutations of the TBCE gene; abnormal PTH secretions
      • 22q11.2 deletion syndrome
  • Autoimmune: genetic gain-of-function mutation in CaSR
  • Infiltrative: metastatic carcinoma, hemochromatosis, Wilson disease, granulomas
  • Hypo- (alcoholics) or hypermagnesemia: chronic iron overloads
  • Genetic defects may result in X-linked or in autosomal recessive hypoparathyroidism due to abnormal parathyroid gland development; associated with mutations in the transcription factor glial cell missing B (BCMB)
  • Mutations in transcription factors or regulators of parathyroid gland development
    • Component of a larger genetic syndrome (APS-1 or DiGeorge syndrome) or in isolation (X-linked hypoparathyroidism) (2)
    • May be autosomal dominant (DiGeorge), autosomal recessive (APS-1), or X-linked recessive (X-linked hypoparathyroidism) (2)
    • Congenital syndromes
      • 22q11.2 deletion syndrome, familial hypomagnesemia, hypoparathyroidism with lymphedema (2)
      • Hypoparathyroidism with sensorineural deafness
      • ADHH: mutations gain-of-function of the CaSR gene suppressing the parathyroid gland, without elevation of PTH
    • PGA syndrome type I: mucocutaneous candidiasis, hypoparathyroidism, and Addison disease
Neck surgery and neck trauma, neck malignancies, family history of hypocalcemia, PGA syndrome
Intraoperative identification and preservation of parathyroid tissue
  • DiGeorge syndrome
  • PGA syndrome type I
  • Multiple endocrine deficiency autoimmune candidiasis (MEDAC) syndrome
  • Juvenile familial endocrinopathy
  • Addison disease
  • Moniliasis (HAM) syndrome: a polyglandular deficiency syndrome, possibly genetic, characterized by hypoparathyroidism
  • Surgical scar on neck
  • Chvostek sign: ipsilateral twitching of the upper lip on tapping the facial nerve on the cheek. 10% of normal people have positive Chvostek sign.
  • Trousseau sign: painful carpal spasm after 3-minute occlusion of brachial artery with BP cuff. BP cuff inflated to > systolic BP for 3 minutes leads to carpal spasm (flexion of metacarpophalangeal [MCP] joints, extension of interphalangeal [IP] joints, adduction of fingers and thumb).
  • Tetany, laryngo- or bronchospasm, cardiac arrhythmias, refractory heart failure, dyspnea, edema
  • Dry, coarse, puffy hair; brittle nails
  • Loss of deep tendon reflexes
  • Dysrhythmias (secondary hypocalcemia)
  • Cataracts
  • Tooth enamel defects
  • Vitamin D deficiency/resistance
  • Pseudohypoparathyroidism, which presents in childhood, kidney and bone unresponsiveness to PTH; characterized by hypocalcemia, hyperphosphatemia, and, in contrast to hypoparathyroidism, elevated rather than reduced PTH concentrations
  • Hypoalbuminemia, renal failure, malabsorption, familial hypocalcemia, hypomagnesemia
Initial Tests (lab, imaging)
  • Calcium: ionized (low) and total (low) (correct serum calcium level for albumin)
    • Corrected serum calcium = total serum calcium + 0.8 (4 - serum albumin)
  • Phosphorus (high)
  • Intact or “whole” PTH (low or inappropriately normal)
  • Magnesium (low may be cause of hypoparathyroidism; may also be normal)
  • BUN, creatinine, 25-OH vitamin D level (especially in elderly)
  • Urinary calcium (normal or high)
  • Calcium should be monitored after thyroid or parathyroid surgery.
  • Radiographs may show absent tooth roots, calcification of cerebellum, choroid plexus, or cerebral basal ganglia.
Follow-Up Tests & Special Considerations
  • ECG: prolongation of ST and QTc intervals nonspecific repolarization changes, dysrhythmias
  • P.537

  • Urine calcium: Creatinine ratio (normal 0.1 to 0.2) may be low before treatment but should be monitored to prevent stones due to hypercalciuria.
  • Gene sequencing: Evaluation of other hormone levels may be required to diagnose APS-1.
  • Hungry bone syndrome (transient hypoparathyroidism after parathyroid surgery)
    • Hypocalcemia due to hungry bone syndrome may persist despite recovery of PTH secretion from the remaining normal glands. Thus, serum PTH concentrations may be low, normal, or even elevated.
  • Infiltrative: osteoblastic metastasis of prostate, breast, or lung cancer
  • Metabolic/nutritional: renal failure, neonatal hypocalcemia, hypoalbuminemia, malabsorption, calcium (Ca++) chelators, hypomagnesemia
  • Familial hypocalcemia, acute hyperphosphatemia (rare), vitamin D deficiency
  • Autoantibodies against NACHT leucine-rich-repeat protein 5 (NALPS) found in 49% of 73 patients with APS-1 and hypoparathyroidisms
Test Interpretation
Parathyroid gland parenchymal tissue completely or almost completely replaced by fat
  • Monitor ECG during calcium repletion.
  • Maintenance therapy: may require lifelong treatment with calcium and calcitriol
    • Maintain serum calcium in low normal range: 8 to 8.5 mg/dL (2 to 2.12 mmol/L).
  • If hypercalcemia occurs, hold therapy until calcium returns to normal. Treat magnesium deficiency if present.
  • Phosphate binders are required if high calciumphosphate product.
  • Thiazide diuretics combined with a low-salt diet may be used to prevent hypercalciuria, nephrocalcinosis, and nephrolithiasis.
  • Oral calcium administration and vitamin D supplementation after thyroidectomy may reduce the risk for symptomatic hypocalcemia after surgery.
Acute Hypoparathyroidism
  • Hypoparathyroid with severe symptoms (tetany, seizures, cardiac failure, laryngospasm, bronchospasm)
    • IV calcium gluconate: 1 or 2 g, each infused over a period of 10 minutes. Central venous catheter is preferred because calcium-containing solutions can irritate surrounding tissues. Follow with infusion of 10 g calcium gluconate in 1 L 5% dextrose water at a rate of 1 to 3 mg calcium gluconate/kg body weight/hr (1)[B].
  • Hypomagnesemia: acutely: 1 to 2 g IV q6h. Longterm magnesium oxide tablets (600 mg) once or twice per day
  • Maintenance: See “First Line” treatment for chronic hypoparathyroidism.
Chronic Hypoparathyroidism
First Line
  • Adults
    • Oral calcium: calcium salts: 1 to 3 g/day PO. For geriatric patients, consider using calcium citrate instead of calcium carbonate.
    • Calcitriol: (vitamin D 1, 25-dihydroxycholecalciferol): 0.25 &mgr;g/day. Doses 0.5 to 2.0 &mgr;g/day are usually required (2)[A].
  • Children
    • Oral elemental calcium: 25 to 50 mg/kg daily
    • Calcitriol: 0.25 &mgr;g daily for age >1 year
Second Line
Cholecalciferol 10,000 to 50,000 U duration of action 4 to 8 weeks
Endocrinologist, nephrologist, ophthalmologist
Parathyroid hormone 1 to 34 and 1 to 84 SC
  • Improved well-being and increased bone mineral density have been shown with PTH therapy, but other long-term benefits have not (3).
Autotransplantation of cryopreserved parathyroid tissue: restores normocalcemia in 23% of cases
Admission Criteria/Initial Stabilization
Laryngospasm, seizures, tetany, QT prolongation
Discharge Criteria
Resolution of hypocalcemic symptoms, patient educated on hypoparathyroidism and treatment
Patient Monitoring
  • Goal is a total corrected serum calcium level in low normal range (8 to 8.5 mg/dL or 2 to 2.12 mmol/L), 24-hour urine calcium <300 mg, and calciumphosphate product <55.
  • Outpatient measurement of serum calcium, phosphate, magnesium, and creatinine weekly to monthly during initial management; for changes in medication, check weekly or every other week; when stable, measure every 3 to 6 months (3)[A].
  • Measure 24-hour urinary calcium secretion yearly.
  • If symptoms of renal stone disease or increasing Cr, get renal imaging (3)[A].
  • Annual slit-lamp and ophthalmologic evaluations are recommended.
  • DEXA scan (2)[A]
Low-phosphate diet in patients with hyperphosphatemia
Hypoparathyroidism following neck surgery is often transient. Length of required treatment may vary depending on origin.
1. Al-Azem, Khan A. Hypoparathyroidism. Best Pract Res Clin Endocrinol Metab. 2012;26(4):517-522.
2. Bilezikian JP, Khan A, Potts JT Jr, et al. Hypoparathyroidism in the adult: epidemiology, diagnosis, pathophysiology, target-organ involvement, treatment, and challenges for future research. J Bone Miner Res. 2011;26(10):2317-2337.
3. Bollerslev J, Rejnmark L, Marcocci C, et al. European Society of Endocrinology Clinical Guideline: treatment of chronic hypoparathyroidism in adults. Eur J Endocrinol. 2015;173(2):G1-G20.
Additional Reading
  • Michels TC, Kelly KM. Parathyroid disorders. Am Fam Physician. 2013;88(4):249-257.
  • National Institute of Child Health and Human Development. Hypoparathyroidism: For researchers and health care practictioners. https://www.nichd.nih.gov/health/topics/hypopara/resources/pages/providers.aspx
  • E20.9 Hypoparathyroidism, unspecified
  • P71.4 Transitory neonatal hypoparathyroidism
  • E89.2 Postprocedural hypoparathyroidism
Clinical Pearls
Often asymptomatic; consider if hypocalcemic with fatigue and circumoral or distal extremity paresthesias.
  • Correct the serum calcium level for albumin level.
  • Monitor calcium after thyroid or parathyroid surgery.
  • Serum levels of magnesium and 25-OH should be measured to rule out deficiency that could contribute to reduced serum calcium levels.