Molecular signatures in systemic lupus erythematosus: distinction between disease flare and infection

The clinical scenario of a febrile, acutely ill, immunocompromised patient with immunocompromised lupus remains challenging despite advances in technology and improved understanding of pathogenic mechanisms. Infection is a major contributor to morbidity and mortality in systemic lupus erythematosus (SLE); infection-related hospitalisation rates range from 10% to 35%1–4 and mortality rates range from 29% to 53%.5 ,6 The disease itself and most treatment strategies are immunosuppressive, rendering patients with SLE more susceptible to severe infection with common organisms and opportunistic pathogens. Both infection and lupus flare can incite clinically indistinguishable inflammatory responses. Consequently, appropriate therapy may be delayed or patients are treated for both conditions while awaiting results of time-consuming investigations for bacterial and viral infections. The potential consequences of treating infection with immunosuppression are obvious and may contribute to the high mortality rates. Antibiotics given unnecessarily also have potential toxicities. A biomarker that would accurately and rapidly differentiate between flare and infection would provide an extremely valuable guide to more directed, precise therapy, likely leading to significantly decreased morbidity and mortality. Microarray technology offers an unbiased, systems biology approach to study the expression level of thousands of genes simultaneously and genome-wide transcriptional studies have emerged as a powerful investigational tool to study complex diseases as well as infection.7 The objective of this exploratory study was to use whole blood gene expression profiling to identify specific RNA expression profiles that would differentiate systemic inflammation related to SLE disease flare from infection in acutely ill patients with lupus. We hypothesised that the molecular signature associated with active disease and no infection in patients with SLE will differ from the molecular signature in patients with SLE with infection. Comparison groups consisted of SLE subjects with inactive disease and healthy controls. ### Study design Blood samples for microarray analysis were obtained from two …

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