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October 1969

Pathology and Ultrastructure of the Human Parathyroid Glands in Chronic Renal Failure

Author Affiliations

Boston; Galveston, Tex

From the Department of Pathology, Harvard Medical School, and the Edwin S. Webster Laboratory of the James Homer Wright Pathology Laboratories, Massachusetts General Hospital, Boston (Dr. Roth); and the Department of Surgical Pathology, University of Texas Medical Branch, Galveston (Dr. Mar-; shall). Dr. Roth is a faculty research associate (PRA-44) of the American Cancer Society.

Arch Intern Med. 1969;124(4):397-407. doi:10.1001/archinte.1969.00300200009002

Since the classical studies of Castleman and Mallory,1 it has been universally recognized that severe renal disease results in hyperplasia of the parathyroid glands. This study and subsequent ones have confirmed the impression that the hyperplasia of the parathyroid glands resulted in clinical hyperparathyroidism, and to distinguish this process from that in which the defect lay initially in the parathyroid gland, the former has been termed "secondary hyperparathyroidism." Though the mechanisms are not clear, experimental studies have demonstrated that parathyroid hormone secretion and synthesis 2,3 and cellular proliferation of the parathyroid gland are controlled by the level of the ionized serum calcium.

This communication will describe the anatomical structure of the parathyroids in 200 patients with secondary hyperparathyroidism. This structure will be correlated with clinical symptoms and chemical values. An electron microscopic study of the parathyroids of a patient with severe secondary hyperparathyroidism resulting in osteitis fibrosis cystica will

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