CASE 1 HYPERCALCEMIA

A 44-year-old woman was hospitalized with hypercalcemic crisis.

Six years before she had total abdominal hysterectomy and oophorectomy.

Four years before she was told of a total calcium of 11.5 mg/dl (8.5-10.3). Subsequently, it varied between 10.7 and 11.5 mg/dl. C-terminal parathyroid hormone was 640 ng/ml (<340) with simultaneous calcium of 11.0 mg/dl. The patient was started on conjugated equine estrogen 0.625 mg. daily. It caused the calcium to decline 0.8 mg/dl.

Three weeks ago she developed anorexia, nausea and began a total seven pound weight loss. She was hospitalized elsewhere with low grade fever and orthostatic hypotension which responded to fluid administration. Laboratory studies at that time included the following results: calcium 17.2 mg/dl; phosphate 2.3 mg/dl (2.5-4.5); chloride 111 meq/l (100-106); glucose 100 mg/dl (70-110); creatinine 1.0 mg/dl (<1.2); free thyroxine 1.2 ng/dl (0.9-1.9), alkaline phosphatase 255 U/l (50-110) and 24 hour urinary calcium excretion 8.5 mg/kg (1.5 to 4.5). Radiographs of the chest and breasts, a protein electrophoresis and renal ultrasound were negative. A dual energy bone mineral density of the lumbar spine had a T score of minus 3.4 (values below 2.5 are considered to be major demineralization).

She was hydrated with 0.9% NaCl solution, ranging from 4.0 to 1.5 liters daily. Pamidronate, 60 mg given intravenously over four hours, caused the calcium to decline to normal over four days. She was dismissed and asked to drink two quarts of Gatorade each day.

Six days later she was admitted to our hospital after a motor vehicle accident caused compound fractures of both tibiae. During the next three days she developed symptoms of severe gastritis, polyuria and lapsed into coma. There was no history of peptic ulcer disease, constipation, fractures, urolithiasis, hypertension or familial endocrinopathy.

Her temperature was 37 degrees C. She was 56 inches tall, weighed 122 pounds, had a blood pressure of 135/90 mm Hg and a pulse of 100 per minute. She was comatose, appeared cachectic and had dry skin. No lymphadenopathy was found. There was a 2.5 cm mass just lateral to the lower pole of the right thyroid lobe. The remaining examination was normal.

Her laboratory studies were as in Table 1. Ultrasonographic exam of the neck showed a well-circumscribed, rounded, homogeneous, hypoechoic mass measuring 2.0 x 4.0 cm inferior and lateral to the inferior aspect of the right lobe of the thyroid gland. Treatment was as outlined in Table 1. An operation was performed.

1. What is the diagnosis?

2. What things exclude benign familial hypercalcemia? 

3. What would you anticipate as possibilities at cervical exploration? 

4. What do you think caused the initial excessive urinary output? 

5. What were helpful and harmful occurrences associated with the patient’s hypomagnesemia?

6. Outline the principles involved in the treatment of the patient’s hypercalcemia with each of the following:

7. Assuming the patient became hypocalcemic shortly postoperatively, to what would you attribute the hypocalcemia? What clues would you have about the cause?