Annals of the rheumatic diseases · 2003
Antiphospholipid antibody in localised scleroderma.
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Sato S, Fujimoto M, Hasegawa M, Takehara K
Аннотация
OBJECTIVE: To investigate the prevalence and clinical correlation of antiphospholipid antibodies in localised scleroderma.
METHODS: Antibodies against cardiolipin (aCL) or beta(2)-glycoprotein I were examined by enzyme linked immunosorbent assay (ELISA) in 48 patients with localised scleroderma (18 patients with generalised morphoea, 20 with linear scleroderma, and 10 with morphoea). Twenty one of these patients were investigated for lupus anticoagulant (LAC) by screening and confirmatory coagulation tests.
RESULTS: Patients with generalised morphoea, the severest form of localised scleroderma, had significantly raised levels of IgM or IgG aCL relative to normal controls (n=21) and patients with systemic sclerosis (n=20). The IgM isotype was predominant, with the frequency of IgM aCL (61%) higher than that of IgG aCL (28%). Levels of aCL were similar for patients with linear scleroderma or morphoea and normal controls. IgM aCL were associated with a greater number of lesions, especially plaque lesions, wider distribution of lesions, and the presence of immunological abnormalities including antinuclear antibodies, rheumatoid factor, IgM antihistone antibodies, IgG anti-single stranded DNA antibodies, and raised serum interleukin 6 levels in patients with localised scleroderma. LAC was detected in 5/7 (71%) patients with generalised morphoea. However, pulmonary embolism was seen in only one patient with generalised morphoea. None of patients with localised scleroderma exhibited anti-beta(2)-glycoprotein I antibodies.
CONCLUSIONS: These results suggest that aCL and LAC are the major autoantibodies in patients with generalised morphoea.
METHODS: Antibodies against cardiolipin (aCL) or beta(2)-glycoprotein I were examined by enzyme linked immunosorbent assay (ELISA) in 48 patients with localised scleroderma (18 patients with generalised morphoea, 20 with linear scleroderma, and 10 with morphoea). Twenty one of these patients were investigated for lupus anticoagulant (LAC) by screening and confirmatory coagulation tests.
RESULTS: Patients with generalised morphoea, the severest form of localised scleroderma, had significantly raised levels of IgM or IgG aCL relative to normal controls (n=21) and patients with systemic sclerosis (n=20). The IgM isotype was predominant, with the frequency of IgM aCL (61%) higher than that of IgG aCL (28%). Levels of aCL were similar for patients with linear scleroderma or morphoea and normal controls. IgM aCL were associated with a greater number of lesions, especially plaque lesions, wider distribution of lesions, and the presence of immunological abnormalities including antinuclear antibodies, rheumatoid factor, IgM antihistone antibodies, IgG anti-single stranded DNA antibodies, and raised serum interleukin 6 levels in patients with localised scleroderma. LAC was detected in 5/7 (71%) patients with generalised morphoea. However, pulmonary embolism was seen in only one patient with generalised morphoea. None of patients with localised scleroderma exhibited anti-beta(2)-glycoprotein I antibodies.
CONCLUSIONS: These results suggest that aCL and LAC are the major autoantibodies in patients with generalised morphoea.