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Fredda Ginsberg-Fellner, MD; Mary E. Witt, MD; Bonita H. Franklin, MD; Soroku Yagihashi, MD; Yayoi Toguchi, MD; Michael J. Dobersen, PhD; Pablo Rubinstein, MD; Abner Louis Notkins, MD

JAMA. 1985;254(11):1469-1472.

Abstract
A longitudinal investigation was conducted from 1977 to 1984 on 178 families in which one or more of the children had insulin-dependent diabetes mellitus. Of 351 nondiabetic sibs followed up for an average of 54 months, ten have, thus far, become diabetic. Eight sibs were HLA identical to their diabetic proband and nine had HLA-DR3 and/or HLA-DR4. Islet cell surface antibody and islet cell cytoplasmic antibody were found from two to 74 months before the onset of clinical diabetes in 100% and 90%, respectively, of the children. A decrease in insulin secretion was observed in all of these children on entry into the study and was detected in the absence of elevated plasma glucose concentrations. The data suggest that the triad of HLA identity, pancreatic islet cell antibodies, and depressed insulin secretion identifies those sibs who are at high risk of developing insulin-dependent diabetes mellitus.

(JAMA 1985;254:1469-1472)

Author Affiliations
From the Division of Pediatric Endocrinology and Metabolism, Department of Pediatrics, Mount Sinai School of Medicine, New York (Drs Ginsberg-Fellner, Witt, Franklin, and Toguchi); the Laboratory of Oral Medicine, National Institutes of Health, Bethesda, Md (Drs Yagihashi, Dobersen, and Notkins); and the Laboratory of Immunogenetics, Lindsley F. Kimball Research Institute, New York Blood Center, New York (Drs Toguchi and Rubinstein).

Footnotes
Reprint requests to Division of Pediatric Endocrinology and Metabolism, Department of Pediatrics, Mount Sinai School of Medicine, 1 Gustave L. Levy Place, New York, NY 10029 (Dr Ginsberg-Fellner).

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