A 55-year-old man comes to the office for follow-up of abnormal serum chemistries found on routine laboratory testing. He has a history of hypertension, for which he is being treated with pharmacologic therapy, weight loss, and dietary salt restriction. Blood pressure is 130/80 mm Hg and pulse is 80/min. BMI is 27 kg/m². Physical examination reveals no abnormalities. Laboratory studies are as follows: Which of the following is most likely responsible for these findings?

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11ec160b_38d1_12eb_9249_314d195efaa3_MD0001_00 Thiazide diuretics (eg, chlorthalidone, hydrochlorothiazide) are some of the most widely used agents for treatment of hypertension. However, thiazides, especially in higher doses, can cause a variety of metabolic complications, including hypercalcemia, hyperglycemia, hyperlipidemia, hyponatremia, and hypokalemia. The incidence of the individual side effects is relatively low, and, patients rarely experience all of the potential adverse effects. Thiazides increase renal Ca²⁺ reabsorption, leading to hypercalcemia and hypocalciuria. This occurs through 2 major mechanisms: The increase in circulating calcium suppresses parathyroid hormone (PTH) release, leading to a new steady state with a mildly elevated serum calcium concentration and low serum PTH. (Choice A) Familial hypocalciuric hypercalcemia is a benign disorder caused by mutations in the calcium-sensing receptor in the parathyroid gland and kidneys. Higher calcium levels are required to suppress secretion of PTH, leading to mild hypercalcemia and hypocalciuria. However, unlike in patients taking thiazide diuretics, PTH is high-normal or mildly elevated. (Choice B) Hyperthyroidism can cause hypercalcemia due to increased osteoclastic bone resorption, but serum calcium in hypothyroidism is usually normal. (Choices D and E) Primary hyperparathyroidism is caused by parathyroid hyperplasia or adenoma; it is characterized by hypercalcemia with elevated or inappropriately normal PTH levels. Secondary hyperparathyroidism is usually seen in patients with chronic kidney disease and is due to phosphate retention and decreased production of 1,25-dihydroxyvitamin D; these disturbances lead to decreased intestinal calcium absorption, hypocalcemia, hyperphosphatemia, and a compensatory increase in PTH secretion. This patient has a decreased PTH level. Educational objective: Thiazide diuretics cause hypercalcemia by increasing the distal tubular reabsorption of Ca²⁺. The increased circulating calcium levels result in suppression of parathyroid hormone, which distinguishes this effect from hyperparathyroidism.

A 55-Year-Old Man Comes to the Office for Follow-Up of Abnormal