Systemic Lupus Erythematosus and Virus C Infection - Diagnosis, Evolution and Treatment Particularities

Abstract

Abstract Lupus erythematosus (SLE) is an autoimmune disease with a broad spectrum of clinical and immunologic manifestations. Hepatitis C virus (HCV) has been postulated as a potential etiologic or triggering agent among other viruses and it appears to be associated with the presence of autoimmune disorders, even mimicking SLE clinically and serologically. Data on the association between HCV infection and SLE are scarce, but an interaction between these two conditions seems possible. As for treatment options, it is well known that the classic antiviral therapy with interferon may aggravate preexisting autoimmunity, unmask previously silent autoimmune processes, or even cause the emergence of de novo autoimmune disease, including SLE. Interferon-free treatment seems to be more efficacious, safer and more tolerable. However, it is important that clinicians be aware that DAAs (direct acting antivirals) can also trigger lupus-like immune complex-mediated glomerulonephritis. There is scant data on the use of immunosuppressive drug therapy in HCV patients. It seems that enhanced HCV replication due to immunosuppression does not lead to clinically significant sequelae and growing evidence has been reported that supports its efficacy and safety. Patients with SLE and virus C infection are a special category, a fact that the clinician needs to take in consideration in order to a better approach, all the more as these patients are at increased risk for developing end-stage renal disease and have a lower survival rate than general population.