Abstract
Vasculitis is pathologically identified as specific cellular inflammation, vessel destruction, and tissue necrosis. Current classifications of vasculitis such as the Chapel Hill Classification (CHCC) and American College of Rheumatology (ACR) guidelines are not sufficiently adequate for clinicians to diagnose vasculitis. The biomarkers that are currently in clinical use such as PR3-ANCA and MPO-ANCA, only help in diagnosing small vessel vasculitis and their sensitivity and specificity are not sufficient. However, recent developments related to the pathogenesis and etiopathogenesis of vasculitis have the potential to contribute to new and improved biomarkers. The determination of diverse roles of ANCA and synergistic effects of infection, genetic, environmental factors and drugs on pathogenesis is quite important. The demonstration of a new autoantibody directed to hLAMP-2 and the resemblance to some microbial structures, in addition to the determination of the possible roles of hepatitis B and C on vasculitis are important findings. These hints may lead to new biomarker developments, providing a better method to diagnose vasculitis. The evidence on T cell immunity as circulatory and lesional will likely contribute to the development of new drugs for vasculitis.
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