Biological Therapies and Tuberculosis Infection in Dermatology

Abstract

After contact with a case of transmissible tuberculosis (TB), some of the exposed individuals may be infected and develop an immune reaction against Mycobacterium tuberculosis (Mtb), the causative agent of the disease. The replication of mycobacteria is usually stopped within cellular structures called granulomas, whose integrity relies on a complex interplay between cells and cytokines, the most prominent of them being TNF. In case of deficiency or inhibition of the activity of TNF, the granulomas may disrupt and release the surviving mycobacteria which may multiply, disseminate and lead to active TB disease. Several immune-mediated inflammatory diseases, among which rheumatoid arthritis, Crohn’s disease, ankylosing spondylitis and psoriasis can be treated by biological therapies acting by the inhibition of TNF or cytokines like IL-17 and IL-23. If these therapies, in particular TNF-inhibitors, are administered to people infected by Mtb, there is a risk of decreasing the integrity of granulomas and increasing the probability of mutiplication of mycobacteria and TB reactivation. Therefore, in persons with rheumatological, gastro-enterological and dermatological diseases candidate to biological therapies there is a general recommendation of screening for TB infection (TBI) at baseline. The screening should include also a search for history of prior TB or contact with TB, a test for the presence of TBI, and if scored positive, a chest X-Ray