CA 8.6 - 10.3 HIGH

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HYPERCALCEMIA, a serum calcium level greater than 10. 3 mg/dL. Symptoms include anorexia, nausea, vomiting, constipation, weakness, fatigue, confusion, stupor, polyuria, nephrolithiasis, and coma. Symptoms usually manifest only at serum levels greater than 12 mg/dL, and their severity is usually increased in rapidly evolving cases of hypercalcemia. The majority of cases are associated with either primary hyperparathyroidism or cancer (humoral hypercalcemia of malignancy or secondary to metastatic bone involvement) even though the list of possible causes is extensive. The serum chloride may be helpful in attempting to make this distinction in patients with normal renal function. Parathyroid hormone causes bicarbonate wasting; thus, patients with primary hyperparathyroidism manifest a mild hyperchloremic acidosis. Patients with humoral hypercalcemia of malignancy (HHM) often have serum chloride levels lower than 100 mEq/L and the diagnosis may be confirmed by the finding of an elevated parathyroid hormone related peptide (PTHrP) level although testing is often unnecessary (there is usually a history of a cancer diagnosis or symptoms of an advanced malignancy). Familial hypocalciuric hypercalcemia (FHH) is an autosomal dominantly inherited disorder that is usually benign with the only known complication in adults being pancreatitis. FHH is characterized by normal PTH levels (although PTH levels may be mildly elevated) and a low 24-hour urine calcium level (less than 100 mg/day). Granulomatous diseases (sarcoidosis, tuberculosis, histoplasmosis, disseminated candidiasis, leprosy, coccidioidomycosis, berylliosis, and eosinophilic granuloma) cause hypercalcemia through the overproduction of 1,25 dihydroxyvitamin D. Hypercalcemia secondary to granulomatous disease is characterized by elevated levels of serum 1,25 dihydroxyvitamin D, normal levels of serum 25 hydroxyvitamin D, depressed levels of serum PTH, and slightly increased levels of serum phosphate. When associated with renal insufficiency, anemia, and bone pain in patients over 50 years of age, multiple myeloma should be ruled out as the cause.

Electrocardiographic manifestations of hypercalcemia include a shortened QT interval. Hypercalcemia increases susceptibility to digitalis toxicity. Abnormal calcium values should be corrected in the presence of abnormal albumin values; however, the calculated correction factor (subtracting 0. 8 mg/dL calcium for every 1 gram/dL albumin is above normal or adding 0. 8 mg/dL calcium for every 1 gram/dL albumin is below normal) may be inaccurate, and an ionized calcium level (normal 4.6-5.1 mg/dL) should be obtained in critical cases.

Therapy for mild asymptomatic hypercalcemia entails intravenous normal saline with or without lasix (10-40 mg intravenously every 6 hours as needed). Lasix therapy should not be initiated until the patient is well hydrated. The above measures may reduce the serum calcium by 1. 6-2. 4 mg/dL. Severe symptomatic hypercalcemia should be treated with pamidronate disodium administered in a single 24-hour infusion of 60-90 mg or zoledronic acid (4 mg IV over 15 minutes). Because pamidronate has a slow onset, it should be given along with a rapid-acting agent in severe cases. Calcitonin is an effective rapid-acting medication that can be given along with pamidronate. Calcitonin is administered subcutaneously every 12 hours at a dosage of 4 IU/kg. Once hypercalcemia is corrected, prophylactic measures against recurrence include a low phosphorous diet, discontinuation of calcium and vitamin D supplements, adequate hydration, and determination and correction of the cause.