Hypoparathyroidism
Hypoparathyroidism is characterized by insufficient PTH production, leading to hypocalcemia and hyperphosphatemia. The most common cause is inadvertent removal or damage to the parathyroid glands during thyroid or neck surgery. Chronic hypocalcemia causes neuromuscular irritability, cognitive effects, and long-term complications including cataracts and basal ganglia calcification.
Symptoms
Perioral numbness and tingling, hand and foot cramps, muscle spasms, carpopedal spasm, Chvostek's sign (facial muscle twitch with cheek tap), Trousseau's sign (carpal spasm with blood pressure cuff), and -- in severe hypocalcemia -- seizures, laryngospasm, or cardiac arrhythmia.
Causes and risk
Surgical hypoparathyroidism after thyroidectomy or parathyroidectomy is the most common cause. Autoimmune destruction (isolated or part of autoimmune polyendocrine syndrome), hypomagnesemia, infiltrative diseases (hemochromatosis, Wilson's), and genetic causes (DiGeorge syndrome) are less common.
How it is evaluated
Low serum calcium with low or inappropriately normal PTH confirms the diagnosis. Phosphorus is elevated. We check 25-OH-D, magnesium, creatinine, and 24-hour urine calcium. ECG (QTc prolongation). Regular surveillance includes kidney ultrasound to monitor for nephrocalcinosis from treatment.
Treatment
Active vitamin D (calcitriol) and calcium supplements are the mainstay. Magnesium repletion is essential when deficiency contributes. Thiazide diuretics reduce urine calcium excretion. PTH replacement (recombinant PTH 1 -- 84, Natpara) is approved for patients not controlled on conventional therapy. The goal is to maintain calcium in the low-normal range to prevent both symptoms and hypercalciuria.