Hypoparathyroidism is an endocrinological disorder characterized by parathyroid hormone (PTH) deficiency. The most common cause of hypoparathyroidism is damage or injury to the parathyroid glands during anterior neck surgery, which leads to impaired PTH synthesis and/or secretion. Other causes include genetic conditions and autoimmune or infiltrative parathyroid gland destruction. Congenital disorders affecting parathyroid gland development typically manifest in childhood. Pseudohypoparathyroidism manifests similarly to hypoparathyroidism but is caused by resistance to PTH rather than insufficient hormone levels. Hypocalcemia is the primary manifestation of both hypoparathyroidism and pseudohypoparathyroidism, and can cause symptoms ranging from muscle cramps to seizures or heart failure. Chronic hypoparathyroidism can cause basal ganglia calcifications (resulting in ), cataracts, and skeletal and dental abnormalities. The presence of hypocalcemia and concurrent low (or inappropriately normal) PTH levels on two separate occasions ≥ 2 weeks apart confirms the diagnosis. Management typically includes correcting hypocalcemia through calcium and vitamin D supplementation and monitoring for complications. PTH replacement therapy may be indicated in selected patients.
- Postoperative: most commonly occurs as the result of accidental injury to parathyroids (or their blood supply) during thyroidectomy, parathyroidectomy, or radical neck dissection
- Autoimmune: : second most common cause
- Nonautoimmune destruction
- Functional hypoparathyroidism: caused by hypermagnesemia or hypomagnesemia (reversible) 
Acute manifestations 
- Extrapyramidal disorders
- Ocular disease
- Skeletal manifestations
- Dental abnormalities
- Cutaneous manifestations: dry, puffy, coarse skin
Both results must be present on two separate occasions, ≥ 2 weeks apart. 
medical emergency. Do not wait for confirmation of the underlying etiology to initiate . is a
Additional studies 
The following findings help support the diagnosis, monitor for complications, and guide management.
- Blood tests
- Urine : typically elevated
Genetic testing: Obtain for patients with nonsurgical hypoparathyroidism and any of the following
- Age < 40 years
- Family history of nonsurgical hypoparathyroidism
- Syndromic pattern (e.g., features of )
Renal imaging 
- Assess for nephrocalcinosis and nephrolithiasis at the time of diagnosis.
- Options include CT abdomen or renal ultrasound.
Postthyroidectomy assessment 
Pseudohypoparathyroidism type 1A (PHP1A)
- Definition: end-organ (i.e., bones and kidneys) resistance to parathyroid hormone (PTH) despite sufficient PTH synthesis due to a defective Gs protein α subunit
- Pathophysiology: mutations in GNAS1 → impaired encoding of α subunit → missing activation of adenylate cyclase when PTH binds to Gs → resistance to PTH in kidney and bone tissue
- Clinical features
- Definition: extremely rare condition that mimics PHP1A but without end-organ resistance to PTH
- Clinical features:
- Diagnostics: normal calcium, PTH, and phosphate
The differential diagnoses listed here are not exhaustive.
Indications for urgent include:
- Disposition: hospital admission for cardiac monitoring if IV is indicated
Therapeutic regimens are adjusted and dosages titrated to achieve target serum levels.
Vitamin and mineral supplementation: indicated for all patients
- Calcium (e.g., calcium carbonate or calcium citrate): target serum calcium at or slightly below the LLN
- Vitamin D (e.g., cholecalciferol, ergocalciferol, or calcitriol): to maintain serum 25[OH]D level above 20–30 ng/dL 
- Magnesium (e.g., magnesium oxide): to maintain normal serum magnesium levels
- PTH replacement therapy (subcutaneous recombinant human PTH 1–84)
- Thiazide diuretics
Regular follow-up studies facilitate early identification of complications.