- Clinical science
Hypoparathyroidism may be due to a variety of mechanisms, including destruction of parathyroid glands (autoimmune or surgical), abnormal parathyroid gland development, altered regulation of parathyroid hormone (PTH), or impaired PTH action on end organs. The resulting hypocalcemia can trigger a variety of symptoms, ranging from muscle cramps to seizures or heart failure. Manifestations of chronic hypoparathyroidism, however, are quite specific, and include basal ganglia calcifications (resulting in movement disorders), cataracts, and skeletal and dental abnormalities. Laboratory findings in hypoparathyroidism include hypocalcemia with low or inappropriately normal PTH, hyperphosphatemia, and normal renal function. Treatment usually includes correcting the hypocalcemia through calcium and vitamin D supplementation and treatment of the underlying cause.
- Postoperative: (most common cause of hypoparathyroidism in adults): secondary to thyroidectomy, parathyroidectomy, or radical neck dissection
- Autoimmune: second most common cause
- Nonautoimmune destruction:
Pseudohypoparathyroidism (type 1A):
- Etiology: defective Gs protein alpha subunit
- Pathophysiology: end-organ resistance to parathyroid hormone (PTH) despite sufficient PTH synthesis.
- Clinical features: persistent hypocalcemia dispite increased levels of PTH, developmental delay, short stature, obesity, shortened 4th and 5th finger (Albright hereditary osteodystrophy)
- Acute manifestations: symptoms of hypocalcemia (see )
- Extrapyramidal disorders : symptoms include parkinsonism, dystonia, hemiballismus, choreoathetosis, oculogyric crises, or dementia
- Ocular disease: cataracts, keratoconjunctivitis
- Skeletal: increased bone mineral density, osteosclerosis
- Dental abnormalities: dental hypoplasia, failure of tooth eruption, defective root formation
- Cutaneous manifestations: dry, puffy, coarse skin
The differential diagnoses listed here are not exhaustive.