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Monoclonal IgG Gammopathy and Hyperparathyroidism

RICHARD N. DEXTER, M.D., F.A.C.P.; FRANKLIN MULLINAX, M.D.; HERSCHEL L. ESTEP, M.D.; and RALPH C. WILLIAMS JR., M.D., F.A.C.P.
[+] Article and Author Information

Supported in part by USPHS grants AM 07126, AM 1369 IMB, AM 13824 IMB, and CA 07350, National Institutes of Health, Bethesda, Md.; Garland P. Smithie Memorial Grant for Cancer Research T-467, American Cancer Society, New York, N.Y.; and the Charles W. Thomas Arthritis Fund (Publication No. 48), Medical College of Virginia, Richmond, Va.

▸Requests for reprints should be addressed to Richard N. Dexter, M.D., Indiana University Medical Center, 1100 W. Michigan St., Indianapolis, Ind. 46202.


Indianapolis, Indiana, Richmond, Virginia, and Albuquerque, New Mexico


Ann Intern Med. 1972;77(5):759-764. doi:10.7326/0003-4819-77-5-759
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Three patients with hypercalcemia had serum IgG monoclonal gammopathies. In none of the cases could a diagnosis of multiple myeloma be established, and other clinical findings were most compatible with primary hyperparathyroidism. Parathyroid exploration showed a parathyroid adenoma in two patients and parathyroid hyperplasia in the third. The hypercalcemia but not the gammopathy disappeared after removal of abnormal parathyroid tissue in all three patients. One of the monoclonal IgG proteins was of the kappa type, and two were of the lambda type; no shared idiotypic specificities could be shown. No definite evidence for a specific parathyroid-directed antibody was found by immunofluorescence studies. Clinically, the finding of a monoclonal immunoglobulin pattern in a patient with hypercalcemia does not necessarily indicate multiple myeloma, nor does it exclude primary hyperparathyroidism.

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