| dc.description.abstract | Autoimmune diseases (ADs) are chronic and heterogeneous conditions that affect specific target organs or multiple organ systems. They are caused by the interactions over time between hereditary and environmental factors leading to a breakdown in immune tolerance and the ensuing tissue damage. The fact that these disorders share several clinical signs and symptoms (i.e., subphenotypes such as arthritis, alopecia, fatigue, photosensitivity, Raynaud's phenomenon as well as non-specific autoantibodies, e.g., antinuclear antibodies, rheumatoid factor, anti-Ro antibodies), physiopathological mechanisms (e.g., type I interferon activation, reduced B and T cell regulatory function), and genetic factors at both the MHC and non-MHC loci, has been called the autoimmune tautology and indicates that they have several common mechanisms [1]. One of the strongest arguments supporting the autoimmune tautology is polyautoimmunity, defined as the presence of more than one AD in a single patient [2,3]. When three or more ADs coexist, this extreme phenotype is called multiple autoimmune syndrome (MAS) [4]. Polyautoimmunity has been described in most of the ADs including systemic lupus erythematosus (41%), type 1 diabetes mellitus (35%), Sjögren's syndrome (33%), primary biliary cirrhosis (32%), antiphospholipid syndrome (28%), vitiligo (27%), systemic sclerosis (26%), autoimmune thyroid diseases (15%), multiple sclerosis (15%), rheumatoid arthritis (15%), myasthenia gravis (13%), and alopecia areata (10%). The main factors associated with polyautoimmunity are familial autoimmunity (i.e., the presence of diverse ADs in a nuclear family) and Amerindian ancestry. Based on polyautoimmunity and depending on severity, ADs may be categorized as major and minor diseases. In this sense, how polyautoimmunity affects major ADs has not fully evaluated. | |
