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Article [Cutaneous lupus induced by etanercept in rheumatoid arthritis] 2008
Abourazzak FE, Guggenbuhl P, Perdriger A, Meadeb J, Gando-Cocley N, Chevrant-Breton J, Hajjaj-Hassouni N, Chalès G. · Service de rhumatologie, hôpital El-Ayachi, CHU de Rabat-Salé, 10000 Rabat-Salé, Maroc. · Rev Med Interne. · Pubmed #18676065 No free full text.
Abstract: Therapy with anti-TNFalpha in rheumatoid arthritis may induce autoimmune disorders. Induction of autoantibodies is frequently observed, but lupus-like syndrome is rare and few cases only have been reported. We report a 41-year-old female, treated with etanercept for a rheumatoid arthritis, who developed a cutaneous lupus induced without any other organ involvement, associated with high ANA and DNA antibody titres. The skin biopsy and the histological analysis with immunofluorescence confirmed the diagnosis. The anti-TNFalpha treatment was stopped. Corticosteroids were increased and hydroxychloroquine administered because skin lesions persist after three months.
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Article Analysis of TNFalpha microsatellites in 35 patients with primary Sjögren's syndrome. 2000
Guggenbuhl P, Veillard E, Quelvenec E, Jego P, Semana G, Jean S, Meadeb J, Chalès G, Perdriger A. · Rheumatology Department, Rennes Teaching Hospital, France. · Joint Bone Spine. · Pubmed #10963076 No free full text.
Abstract: OBJECTIVES: Although the cause of Sjögren's syndrome remains unknown, many arguments suggest a role for both environmental and genetic factors. An association with HLA molecules has been established. Other genes on the short arm of chromosome 6 may be involved, most notably the TNF gene, which may be pivotal in the development of the epithelial lesions. METHODS: We investigated TNFalpha microsatellites in 35 patients with primary Sjogren's syndrome and in 146 healthy controls. RESULTS: The frequency of the TNFalpha10 allele showed a non-significant increase in the Sjögren's disease group (28.6% vs 15.8%; P = NS). We found significant increases when we considered only those Sjögren's disease patients with joint manifestations (N = 24; 37.5% vs 15.7%; P < 0.05) or only those with anti-Ro(SSA) antibodies (N = 10; 50% vs 15.7%; P < 0.05). CONCLUSION: Our data support a role for the TNFalpha10 allele in primary Sjögren's syndrome, particularly those forms with joint symptoms and anti-Ro(SS-A) antibodies.
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