A 56-year-old woman comes to the emergency department due to acute dyspnea and cough. She has a history of chronic obstructive pulmonary disease (COPD) treated with inhaled albuterol, tiotropium, and fluticasone. The patient's other medical problems include hypertension and hypothyroidism, for which she takes lisinopril, hydrochlorothiazide, and levothyroxine. She also takes a daily over-the-counter supplement containing vitamin D and calcium carbonate. The patient has a 25-pack-year smoking history but quit after the diagnosis of COPD was made 4 years ago. She experienced menopause at age 49 and has no history of low trauma fracture or loss of height. Blood pressure is 140/80 mm Hg, pulse is 108/min, and respirations are 24/min. Oxygen saturation is 94% on 2 L of oxygen via nasal cannula. BMI is 29 kg/m². Chest examination reveals coarse rhonchi bilaterally, and the remainder of the physical examination is unremarkable. Laboratory results are as follows: The patient is admitted to the hospital and treated with systemic glucocorticoids, antibiotics, and inhaled bronchodilators. On the third day of hospitalization, repeat serum calcium is 11.2 mg/dL and parathyroid hormone is 60 pg/mL (normal: 10-65). Which of the following is the most likely cause of this patient's hypercalcemia?

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11ec193a_97a0_380d_853d_c157fe92a60d_MD0002_00 This patient has mild, asymptomatic hypercalcemia associated with a nonsuppressed parathyroid hormone (PTH) level. This is most consistent with primary hyperparathyroidism (PHPT). Although PTH is elevated in a majority of patients with PHPT, approximately 10%-20% of these patients have PTH levels that are only borderline elevated or in the upper half of the normal range (as in this patient). Normally, even mild hypercalcemia suppresses PTH to very low levels (usually <20 pg/mL); therefore, hypercalcemia associated with a nonsuppressed PTH level suggests inappropriate PTH secretion due to PHPT. Familial hypocalciuric hypercalcemia can also cause PTH-dependent hypercalcemia, but this is much less common. (Choice A) Up to 50% of total circulating calcium is protein-bound. Dehydration can increase the serum albumin concentration, with a corresponding increase in the bound calcium fraction, although, the ionized calcium concentration (and albumin-corrected serum calcium concentration) is normal. However, this patient's serum albumin is normal and her calcium level does not need to be corrected. (Choice B) Thiazide diuretics increase urinary reabsorption of calcium and can occasionally cause mild hypercalcemia, but PTH in such patients is suppressed. More frequently, thiazide diuretics worsen or unmask hypercalcemia in patients with an underlying bone and calcium disorder (eg, PHPT). (Choice C) Malignancy is the most common cause of PTH-independent hypercalcemia and is usually due to secretion of PTH-related protein by cancer cells. Hypercalcemia due to malignancy is typically more severe than in PHPT, and serum PTH is very low. (Choice E) Excess intake of vitamin D (iatrogenic or accidental) can lead to vitamin D toxicity with resulting hypercalcemia. Excess intake of calcium carbonate for treatment of acid reflux or prevention of osteoporosis can cause milk-alkali syndrome and also lead to severe hypercalcemia. However, PTH in these disorders is suppressed. Educational objective: Hypercalcemia normally suppresses parathyroid hormone (PTH) secretion to very low levels. In the setting of hypercalcemia, a high-normal PTH level suggests primary hyperparathyroidism. Although PTH is elevated in most patients with primary hyperparathyroidism, it is only borderline or high-normal in 10%-20% of these patients. __________ References: Primary hyperparathyroidism: skeletal and non-skeletal effects, diagnosis and management. (http://www.ncbi.nlm.nih.gov/pubmed/21943558)

A 56-Year-Old Woman Comes to the Emergency Department Due to Acute