01993nas a2200253   4500000000100000008004100001260001300042653001500055653001100070653001200081100001100093700001300104700001200117700001400129700001200143700001300155245004800168856004800216300001100264490001600275050001400291520142000305022001401725       2012                            d  c2012 Dec10aBiomarkers10aHumans10aleprosy1 aFava V1 aOrlova M1 aCobat A1 aAlcaïs A1 aMira MT1 aSchurr E00aGenetics of leprosy reactions: an overview.  uhttp://www.scielo.br/pdf/mioc/v107s1/20.pdf  a132-420 v107 Suppl 1  aFAVA 20123 a<p>Type-1 (T1R) and Type-2 (T2R) leprosy reactions (LR), which affect up to 50% of leprosy patients, are aggressive inflammatory episodes of sudden onset and highly variable incidence across populations. LR are often diagnosed concurrently with leprosy, but more frequently occur several months after treatment onset. It is not uncommon for leprosy patients to develop recurring reactional episodes; however, they rarely undergo both types of LR. Today, LR are the main cause of permanent disabilities associated with leprosy and represent a major challenge in the clinical management of leprosy patients. Although progress has been made in understanding the immunopathology of LR, the factors that cause a leprosy patient to suffer from LR are largely unknown. Given the impact that ethnic background has on the risk of developing LR, host genetic factors have long been suspected of contributing to LR. Indeed, polymorphisms in seven genes [Toll-like receptors (TLR)1, TLR2, nucleotide-binding oligomerisation domain containing 2, vitamin D receptor, natural resistance-associated macrophage protein 1, C4B and interleukin-6] have been found to be associated with one or more LR outcomes. The identification of host genetic markers with predictive value for LR would have a major impact on nerve damage control in leprosy. In this review, we present the recent advances achieved through genetic studies of LR.</p>  a1678-8060