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Article
January 1962

Steatorrhea, Functional Hypoparathyroidism, and Metabolic Bone Defect

Author Affiliations

LOS ANGELES

From Wadsworth Hospital, Veterans Administration Center, and the Departments of Medicine, University of California Medical Center, and Mount Sinai Hospital, Los Angeles.; Senior Resident in Medicine and Fellow in Metabolic Diseases, Veterans Administration Center, and Clinical Assistant in Medicine, U.C.L.A. Medical Center, Los Angeles (Dr. Bernstein); Chief, Metabolic Section, Veterans Administration Center, and Associate Professor of Medicine, U.C.L.A. Medical Center, Los Angeles (present address: Department of Medicine, Mount Sinai Hospital, 8720 Beverly Blvd., Los Angeles 48 (Dr. Kleeman); Associate Chief, Metabolic Service, Veterans Administration Center, and Assistant Clinical Professor of Medicine, U.C.L.A. Medical Center, Los Angeles (present title: Chief, Metabolic Section, Veterans Administration Center, Los Angeles) (Dr. Dowling); Attending Specialist in Medicine, Veterans Administration Center, and Associate Clinical Professor of Medicine, U.C.L.A. Medical Center, Los Angeles (Dr. Maxwell).

Arch Intern Med. 1962;109(1):43-49. doi:10.1001/archinte.1962.03620130045007
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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