A retired 80-year-old man presented to the emergency department after 10 days of increasing polydipsia, polyuria, dry mouth, confusion, and slurred speech. He also reported that he had gradually and unintentionally lost 20 pounds and had loss of appetite, constipation, and chronic itching. He denied fevers, chills, night sweats, nausea, vomiting, and abdominal pain. Medical history. He had type 2 diabetes mellitus that was well controlled by oral hypoglycemics, hypothyroidism treated with

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... yroxine in stable doses, and chronic hepatitis C complicated by liver cirrhosis without focal hepatic lesions. He also had hypertension, well controlled with hydrochlorothiazide and losartan. For his long-standing pruritus he had tried prescription drugs including gabapentin and pregabalin without improvement. He had also seen a naturopathic practitioner, who had prescribed supplements that relieved the symptoms. Examination. The patient was in no acute distress. He appeared thin, with a weight of 140 lb and a body mass index of 21 kg/m 2 . His temperature was 36.8°C (98.2°F), blood pressure 198/82 mm Hg, heart rate 72 beats per minute, respiratory rate 16 breaths per minute, and oxygen saturation 97%. His skin was without jaundice or rashes. The mucous membranes in the oropharynx were dry. Neurologic examination revealed mild confusion, dysarthria, and ataxic gait. Sensation to light touch, pinprick, and vibration was intact. Generalized weakness was noted. Cranial nerves II through XII were intact. Deep tendon refl exes were symmetrically globally suppressed. Asterixis was absent. The remainder of the physical examination was unremarkable. Laboratory values in the emergency department. We initially suspected he had symptomatic hyperglycemia, but a bedside blood glucose value of 113 mg/dL ruled this out. Other initial laboratory values: • Blood urea nitrogen 31 mg/dL (reference range 9-24) • Serum creatinine 1.7 mg/dL (0.73-1.22; an earlier value had been 1.0 mg/dL) • Total serum calcium 14.4 mg/dL (8.6-10.0) Complete blood cell counts were unremarkable. Computed tomography of the head was negative for acute pathology. In view of the patient's hypercalcemia, he was given aggressive intravenous fl uid resuscitation (2 L of normal saline over 2 hours) and was admitted to the hospital. His laboratory values on admission are shown in Table 1 . Fluid resuscitation was continued while the laboratory results were pending. ■ CAUSES OF HYPERCALCEMIA 1 Based on this information, which is the most likely cause of this patient's hypercalcemia? □ Primary hyperparathyroidism □ Malignancy □ Hyperthyroidism □ Hypervitaminosis D □ Sarcoidosis Traditionally, the workup for hypercalcemia in an outpatient starts with measuring the serum parathyroid hormone (PTH) level. Based on the results, a further evaluation of PTHmediated vs PTH-independent causes of hy-