Systemic lupus erythematosus

Abstract

Guilllermo Ruiz-Irastorza and colleagues1Ruiz-Irastorza G Khamashta MA Castellino G Hughes GRV Systemic lupus erythematosus.Lancet. 2001; 357: 1027-1032Summary Full Text Full Text PDF PubMed Scopus (251) Google Scholar omit an important topic in clinical advances in SLE: the high incidence of drug-related side-effects (other than infection), including diabetes, cataract, bone disease, and neoplasia. Strategies to reduce therapeutic charge over time need to be explored. Steroids and imunosuppressants have greatly changed survival in SLE patients, but, at the present, in long-term survivors with SLE, a crucial issue is to find the best schedules to provide the maximum effect in the induction-remission phase of the disease, with the minimum of side-effects. The decision should eventually be when and how to stop steroids and other major immunodepressant drugs. In 90 patients with SLE nephritis, followed up in our centre since 1968 (mean follow-up 13·7 years [SD 7·9]), the incidence of neoplasia was significantly higher than in the age-matched population living in the same area (nine of 90 at 9·6 years [8·1], odds ratio 3·71 [95% CI 1·7–7·4]). Furthermore, diabetes, cataract and bone disease eventually leading to vertebral fractures arose in eight, ten, and 13 patients, respectively. The figure shows the cumulative doses of cylcophosphamide, prednisone, and azathioprine per year of follow-up. Therefore, we believe that the management long-term therapeutic schedules in SLE patients must be included among the issues to be resolved in the near future. In their section on pregnancy, Ruiz-Irastorza and colleagues deal mainly with antiphospholipid syndrome and not SLE. Management of thrombosis in antiphospholipid syndrome has been validated outside the context of SLE. Therefore, it seems a little confusing to show recommendations for primary antiphospholipid syndrome in a discussion of SLE. However, an important missing point is that, when antiphospholipid antibodies do appear in the context of SLE, attempts to clear these antibodies by conventional immunosuppressive schedules are useless.2Stratta P Canavese C Ferrero S Grill A Schinco PC Montaruli B Failure of the war to the knife against antiphospholipid antibodies by conventional immunosuppressive therapy in systemic lupus erythematosus.Clin Nephrol. 1996; 46: 356PubMed Google Scholar In relation to the role of intravenous immunoglobulin therapies for treatment of SLE or antiphospholipid syndrome complications of pregnancy, Ruiz-Irastorza and colleagues do not mention that intravenous IgG contains detectable amounts of antiphospholipid antibodies, as we have previously shown.3Stratta P Canavese C Ferrero S et al.Catastrophic antiphospholipid syndromes in systemic lupus erythematosus.Ren Fail. 1999; 21: 49-61Crossref PubMed Scopus (13) Google Scholar Lastly, Ruiz-Irastorza and colleagues do not mention that evidence of transient antiphospholipid antibody production in SLE is not related to clinical relevant effects (as are persistent antibodies) has been done by recursive partition analysis.4Stratta P Canavese C Schinco PC et al.Intravenous immunoglobulin contains detectable amounts of antiphospholipid antibodies.Br J Haematol. 1997; 96: 872-873Crossref PubMed Google Scholar Our experience has allowed us to make recommendations to avoid over-treatment of transient antiphospholipid antibodies in SLE patients.5Stratta P Canavese C Segoloni GP Ferrero S Grill A Piccoli G Shaded boundaries between antiphospholipid antibodies syndrome and lupus nephritis: low discriminating power of American Rheumatism Association criteria?.Clin Nephrol. 1997; 47: 138-140PubMed Google Scholar