Approaching the Extrinsic Etiopathogenesis of Behcet’s Disease: Can Microbes Prompt This Ailment?

Behçet’s disease (BD) is a multisystem idiopathic vasculitis that demonstrates multi-systematic manifestations of which mucosal, ocular, gastrointestinal and vascular manifestations come atop. Since autoimmunity cannot fully explain BD, it is recently considered midway between auto inflammation and autoimmunity. Ironically, the serological test of anti-nuclear antibody (ANA) is usually negative. Autoantibodies, furthermore, do not play a significant role in aggravating the condition, nor do B cells [1].

To date, intrinsic etiology of BD are mostly leveled at a defective HLA-B51 allele with or without tumor necrosis factor and MHC class I chain related alleles [2] whereas extrinsic factors include local geographical influence [3], pertaining to the Silk Road: an ancient trading route between the Mediterranean and East Asia, and contagious microbial involvement. Again, all these controversial allegations are rebuttable by the unquestionable hitting of BD in genetically-free cases, outside the geoepidemiological territory. Recently, open-label clinical trials in Japan and Turkey have shown infliximab to be effective in ocular Behçet’s disease [4]. Other treatment modalities combine steroids with colchicine, interferon (IFN)-α, cyclosporine, or azathioprine [5] or recruit Dapsone [6,7]. Azathioprine [8], interferon (IFN)-α [9] and three anti-TNF-α compounds, infliximab, adalimumab, and etanercept, have shown favorable results on preliminary tests [10,11]. Recently, Davatchi., et al. [12] concluded that rituximab is efficient in severe ocular manifestations of BD. Scanning theses therapeutic agents, there appears no mainstay treatment line. This reflects the inconclusive understanding of BD etiopathogenesis.ecbvr-img1

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