Volume 3, Issue 1 pp. 72-80
Original Article
Full Access

Familial multiple sclerosis: Clinical, histocompatibility, and viral serological studies

Roswell Eldridge MD

Corresponding Author

Roswell Eldridge MD

Infectious Disease Branch, the Neuro-Immunology Branch, and the Office of Biometry and Epidemiology, National Institute of Neurological and Communicative Disorders and Stroke, National Institutes of Health, Bethesda, MD

Dr Eldridge, National Institutes of Health, Federal Bldg, Room 6A14, Bethesda, MD 20014Search for more papers by this author
Henry McFarland MD

Henry McFarland MD

Infectious Disease Branch, the Neuro-Immunology Branch, and the Office of Biometry and Epidemiology, National Institute of Neurological and Communicative Disorders and Stroke, National Institutes of Health, Bethesda, MD

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John Sever MD

John Sever MD

Infectious Disease Branch, the Neuro-Immunology Branch, and the Office of Biometry and Epidemiology, National Institute of Neurological and Communicative Disorders and Stroke, National Institutes of Health, Bethesda, MD

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Doris Sadowsky BS

Doris Sadowsky BS

Infectious Disease Branch, the Neuro-Immunology Branch, and the Office of Biometry and Epidemiology, National Institute of Neurological and Communicative Disorders and Stroke, National Institutes of Health, Bethesda, MD

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Helen Krebs RN

Helen Krebs RN

Infectious Disease Branch, the Neuro-Immunology Branch, and the Office of Biometry and Epidemiology, National Institute of Neurological and Communicative Disorders and Stroke, National Institutes of Health, Bethesda, MD

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First published: January 1978
Citations: 43

Abstract

Evaluation of presumed “multiple sclerosis families” and comparison with recently reported families has led us to the following observations: (1) Seven of our original fourteen presumptive multiple sclerosis families had to be eliminated after personal clinical evaluation of family members failed to confirm the diagnosis in a second close relative. (2) No segregation of HLA type was noted between affected and unaffected individuals in our seven bona fide multiple sclerosis families, and no consistent segregation was noted in the twenty-eight families reported elsewhere. This supports other genetic evidence that there is not a single, major gene mapping in the HLA complex which predisposes to multiple sclerosis. (3) The DW 2 antigen was increased in frequency among affected members of our families, and the A3 B7 haplotype was more frequent among affected members of other families reported. But unaffected members also tended to have an increased frequency of these same antigens. (4) No relationship was noted between HLA type and antimeasles antibody titer within our families.

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