Hypoparathyroidism

Hypoparathyroidism is deficient secretion of parathyroid hormone (PTH), the hormone that maintains blood calcium. PTH normally raises serum calcium by stimulating bone resorption, increasing renal calcium reabsorption, promoting phosphate excretion, and activating vitamin D. When PTH is deficient, the result is the defining laboratory pattern: hypocalcemia with hyperphosphatemia.

The most common cause is iatrogenic — accidental removal of or damage to the parathyroid glands during thyroidectomy or other neck surgery, since the four small parathyroids sit on the posterior surface of the thyroid. Other causes include autoimmune destruction of the glands and congenital absence of the parathyroids, as in DiGeorge syndrome, where failure of the third and fourth pharyngeal pouches to develop leaves the patient without parathyroids and thymus.

The symptoms are those of hypocalcemia, driven by increased neuromuscular excitability: perioral numbness, tingling of the fingers, muscle cramps, and in severe cases tetany, laryngospasm, and seizures. Two classic bedside findings are Chvostek sign (facial muscle twitching when the facial nerve is tapped) and Trousseau sign (carpal spasm when a blood pressure cuff is inflated on the arm). A prolonged QT interval may appear on ECG.

Hypoparathyroidism is a high-yield endocrine topic on the USMLE Step 1 exam, which tests the lab pattern of low calcium with high phosphate, the post-surgical and congenital causes, and recognition of Chvostek and Trousseau signs.