The aim of this study was to determine whether the different autoantibodies predict early damage in patients with systemic lupus erythematosus (SLE). The patients comprised a prospective inception cohort of 205 patients with SLE, 154 on follow-up for at least five years after diagnosis. Eight patients who died before the fifth year of disease course were included in analyses comprising survival. Organ damage was measured using the Systemic Lupus International Collaborating Clinics--American College of Rheumatology damage index (SDI). Endpoints were the development of some (SDI > or = 1) or severe (SDI > 2) damage at five years after diagnosis or the combined outcome 'SDI > or = 1 or death at five years'. Autoantibodies [anti-DNA, anti-Ro, anti-La, anti-Sm, anti-U1RNP, any anti-ENA and antiphospholipid (aPL)] were included in univariate and multivariate analysis. 'Age at diagnosis' was also included as an independent variable in multivariant analyses. Sapporo criteria were used to define aPL positivity. Eighty-four patients (54.5%) had accrued damage at five years, 17 patients (11.0%) having severe damage. Patients with aPL had damage in a higher proportion (63.2% any damage, 17.6% severe damage). Only aPL were related to damage in univariate analysis (P = 0.03). In logistic regression models, aPL were the only independent predictors of damage at five years (OR 1.94, 95% CI 1.01-3.73), severe damage at five years (OR 3.34, 95% CI 1.11-10.03) and increasing damage since diagnosis (OR 2.46, 95% CI 1.24-4.87). No autoantibody was a predictor of the outcome 'SDI > or = 1 or death at five years'. The conclusion was that aPL predict early damage in patients with SLE.

Cardiovascular disease is a major cause of morbidity and mortality in patients with systemic lupus erythematosus (SLE). Antiphospholipid syndrome (APS) is one of the most important causes of thrombosis in SLE. In addition, an association between hyperhomocysteinemia and increased cardiovascular risk has also been reported. Our aim is to analyse the association of thrombosis with plasma total homocysteine (ptHcy), antiphospholipid antibodies (aPL) and other vascular risk factors in SLE patients. Fasting plasma levels of ptHcy, vitamin B12, folate, total cholesterol and creatinine were measured in 117 SLE patients. Clinical and immunological data were obtained from our prospective computerized database. aPL-positivity was defined according to Sapporo criteria. There was no association between aPL and ptHcy. ptHcy was higher in patients with arterial (median 13.02 versus 10.16 micromol/L, P = 0.010) but not venous thrombosis. In the subgroup analysis, this association was only seen in aPL-negative patients. In logistic regression, aPL (OR 6.60, 95% CI 1.86-23.34) and ptHcy (OR 1.10, 95% CI 1.01-1.19) were independently associated with arterial thrombosis. However, when hypertension, smoking and plasma total cholesterol were added to the model, only aPL (OR 7.38, 95% CI 2.02-26.91) and hypertension (OR 7.70, 95% CI 2.33-25.39), but not ptHcy, remained independently related to arterial events. aPL was the only variable independently related to venous thrombosis (OR 7.68, 95% CI 1.60-36.86). ptHcy concentrations are higher in SLE patients with arterial thrombosis. No interaction between homocysteine and aPL was found. Raised ptHcy may be a marker of increased vascular risk in aPL-negative SLE patients. The role of homocysteine as a marker of vascular risk may depend on the presence of traditional risk factors, although a modest intrinsic effect cannot be entirely excluded.