INFECTION IN SYSTEMIC LUPUS ERYTHEMATOSUS

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The improved survival of systemic lupus erythematosus (SLE) patients since the 1950s is the result of not only better treatment of SLE, but also supportive treatment of renal failure (transplant and dialysis) and the wealth of antibiotics now available. Ironically, the wider use of immunosuppressives, especially the alkylating drugs, and the longer survival of patients with renal insufficiency and renal failure have made the identification and appropriate treatment of infection in SLE an on-going challenge.

It has always seemed extremely ironic that SLE patients have an increased risk for infection, given that they exhibit so many signs of B-cell hyperactivity. SLE patients, after all, are characterized by having hypergammaglobulinemia and elevated antibody titers to multiple viruses and other pathogens. It is this paradox—that SLE patients, whose immune systems attack themselves, are often unable to mount an effective attack against outside agents—that is explored in this article.

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Address reprint requests to Michelle Petri, MD, MPH, Division of Rheumatology, Johns Hopkins School of Medicine, 1830 East Monument Street, Suite 7500, Baltimore, MD 21205

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From the Department of Medicine, Johns Hopkins University School of Medicine, and Hopkins Lupus Cohort, Baltimore, Maryland