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Clinical Course and Necropsy

J. EARLE WHITE, M.D.; CHARLES CHAPMAN BINFORD, M.D.; ROSCOE R. ROBINSON, M.D.; WILLIAM G. BLACKARD, M.D.

Arch Intern Med. 1963;111(4):460-464.

	Since this article does not have an abstract, we have provided the first 150 words of the full text PDF and any section headings.

The etiology of rachitic bone disease associated with hypophosphatemia, which requires large doses of vitamin D for treatment, has been a subject of dispute. Albright, Butler, and Bloomberg¹ have attributed the syndrome to parathyroid hyperplasia secondary to calcium malabsorption, whereas Fanconi and Girardet² have proposed an intrinsic and primary renal tubular defect in phosphate reabsorption. Evidence bearing on each of these mechanisms has been presented by Blackard, Robinson, and White³ in a study of a kindred and the propositus who necropsy is described here. Secondary hype parathyroidism appeared clinically to fit the data obtained better than did a renal tubular defect. The present report describes the patient's course during subsequent follow-up for one year and includes the only necropsy findings in proved familial hypophosphatemia known to us.

Summary of the Initial Case Report³

A 44-year-old electrician entered the Veterans Administration Hospital because of arthralgias and paresthesias. . . . [Full Text PDF of this Article]

Author Affiliations
DURHAM, N.C.

Clinical Investigator, Veterans Administration Hospital (Dr. White); Assistant Resident in Pathology, Duke University Medical Center and Veterans Administration Hospital (Dr. Binford); Clinical Investigator, Veterans Administration Hospital (Dr. Robinson); formerly, Assistant Resident, Duke University Medical Center (Dr. Blackard).; From the Departments of Medicine and Pathology, Duke University Medical Center Division of Endocrinology and Veterans Administration Hospital.

Footnotes
Received for publication Oct. 9, 1962; accepted Nov. 6.

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