Steatorrhea, Functional Hypoparathyroidism, and Metabolic Bone Defect

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Abstract
A common cause of osteomalacia is the fecal loss of calcium and vitamin D during steatorrhea of diverse etiology.1 Chemical alterations in the blood most frequently accompanying this osseous disorder are (1) slight-to-moderate reduction of serum calcium, (2) moderate-to-severe reduction of serum phosphorus, and (3) elevated alkaline phosphatase activity. The skeletal and biochemical abnormalities have been attributed in part to secondary hyperplasia of the parathyroid glands.1-4 The latter could enhance the rate of demineralization of the skeleton, maintain the serum calcium despite the calcium and vitamin D deficiency, and lower the serum phosphorus by increasing its renal clearance. If, during the steatorrheic syndrome, this hyperplasia of the parathyroid glands led to their functional failure, the chemical effects of hypoparathyroidism would be added to those of vitamin D and calcium deficiency. Marked hypocalcemia would develop, normal or elevated serum phosphorus would replace the hypophosphatemia, and the degree of skeletal

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