IgA Vasculitis: Etiology, Treatment, Biomarkers and Epigenetic Changes

IgA, previously called Henoch-Schonlein vasculitis, is an essential immune component that drives the host immune response to the external environment. As IgA has the unique characteristic of a flexible response to broad types of microorganisms, it sometimes causes an autoreactive response in the host human body. IgA vasculitis and related organ dysfunction are representative IgA-mediated autoimmune diseases; bacterial and viral infections often trigger IgA vasculitis. Recent drug developments and the presence of COVID-19 have revealed that these agents can also trigger IgA vasculitis. These findings provide a novel understanding of the pathogenesis of IgA vasculitis. In this review, we focus on the characteristics of IgA and symptoms of IgA vasculitis and other organ dysfunction. We also mention the therapeutic approach, biomarkers, novel triggers for IgA vasculitis, and epigenetic modifications in patients with IgA vasculitis.

Automated summary

IgA, previously known as Henoch-Schonlein vasculitis, is an important immune component that can respond flexibly to various microorganisms, but may also cause autoreactive responses in the host human body, leading to IgA vasculitis and other autoimmune diseases. Bacterial and viral infections are often triggers of IgA vasculitis, while recent research has found that drugs and COVID-19 can also trigger this disease.