Abstract
Introduction
Rheumatoid arthritis (RA) is a chronic systemic autoimmune disease characterized by a symmetrical inflammation of the synovium, resulting in tenderness and destruction of bone and cartilage in various joints, particularly the smaller joints of the hands and feet. Although the cause of RA is unknown, autoimmunity plays a pivotal role in its chronicity and progression. RA affects approximately 1.0% of the general population, women more often than men, and the inflammatory burden of the disease results in functional disability.[1] Several contributors to RA pathogenesis have been identified in recent years: genetic factors (shared epitope on locus HLA-DRB1, but also PTPN22, STAT4, 6q23 and TRAF1/C5), cigarette smoking, auto antibodies (rheumatoid factor (RF), anti-cyclic citrullinated protein antibodies (ACPA)), infectious agents, as well as nutritional and hormonal factors.[2] Ultimately, an interplay between these endoge-nous and exogenous factors has been postulated to break immunological tolerance and trigger the immunological response that manifests itself as RA.[3] The immunological activation of RA leads to infiltration of the synovium by an orchestra of immune cells like T and B cells, macrophages, dendritic cells and fibroblast-like synoviocytes, contributing to the proliferation of cell tissue (i.e. pannus formation) and neovascularization.[4] These immunological processes perpetuate syste-mic inflammatory responses, leading to a chronic, disabling disease which results in the inability to work and an impaired quality of life. [5]
It has been widely observed that disorders with an autoimmune pathogenesis occur with increased frequency in patients with a history of another autoimmune disease (AD). The number of documented cases of a co-occurrence of different autoimmune diseases in a single patient have increased in recent years.
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Corresponding Author
Dr Mir Nadeem
DOI: https://dx.doi.org/10.18535/jmscr/v5i11.208
