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© 1994 British Society for Rheumatology

research-article

FAMILIAL SCLERODERMA—EVIDENCE FOR ENVIRONMENTAL VERSUS GENETIC TRIGGER

C. O. STEPHENS*,, D. C. BRIGGS{dagger}, J. WHYTE{ddagger}, C. M. ARTLETT§, A. B. SCHERBAKOV||, N. OLSEN, N. G. GUSSEVA||, N. J. MCHUGH{ddagger}, P. J. MADDISON{ddagger}, K. I. WELSH§ and C. M. BLACK*

*Royal Free Hospital London
{dagger}Tissue Typing, Middlesex Hospital London
{ddagger}RNHRD Bath
§Churchill Hospital Oxford, UK
||Institute of Rheumatology Moscow, Russia
Vanderbilt Hospital Nashville, TN, USA

Correspondence to: Correspondence to: C. O. Stephens, Bloomsbury Rheumatology Unit, Arthur Stanley House, 40–50 Tottenham St, London W1P 9PG, UK.

Families with more than one case of scleroderma are unusual. Four families each with two members (in one case monozygotic twins) with scleroderma (systemic sclerosis, SSc) were identified. Clinical, immunogenetic and autoantibody studies were carried out. Multicase SSc families cited in the literature were reviewed.

Each family pair shared cutaneous subset of disease severity, and SSc-associated autoantibody. HLA typing showed two pairs shared an HLA-DR allele associated with scleroderma (DR3 or DR5), while one also had alleles reported in association with their SSc-specific autoantibody. Review of dates and ages of onset suggested that the timing of onset of scleroderma is more likely to have an environmental trigger than to be encoded genetically.

KEY WORDS: Scleroderma, Systemic sclerosis, Immunogenetics, Environment


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