Introduction
Systemic lupus erythematosus (SLE) is a multisystem inflammatory disease of unknown etiology. Clinical signs and manifestations, laboratory signs, course and prognosis in patients vary and vary from patient to patient. Almost all organs of the human body are affected by the disease. In this disease, autoantibodies are produced against cell components and as a result, immunological reactions and inflammation caused by them cause cell and tissue damage in various systems. (1) These autoantibodies are not only diagnostically related. They may also relate to specific clinical subtypes (2) the American College of Rheumatology (ACR) revised criteria for SLE (3), as well as the latest classification of International Systemic Lupus Clinic Clinics (SLICC) in the diagnosis of SLE. Is used (4). The prevalence and incidence of SLE varies according to the population and the method used for diagnosis, but studies have shown that the incidence is 1 to 25 per 100,000 worldwide. Also, the reported prevalence of SLE in the United States is 20 to 150 cases per 100,000 people (5). In Iran, according to the latest studies, the prevalence of lupus is 40 per 100,000 people in urban society (6, 7). SLE can affect any organ and varies dramatically from patient to patient. Clinical manifestations are mainly a mixture of major skin, musculoskeletal, blood, serological, renal, or CNS complaints. The cause of SLE is still unknown but is likely to be multifactorial (8). Many studies have shown the role of genetic (9), hormonal (10), immunological (11) and environmental factors (12) in the pathogenesis of the disease. Due to the role of immune complexes in the pathogenesis of the disease, some of these antibodies are considered laboratory findings to meet the clinical criteria of SLE. Clinical manifestations and mortality in this disease or due to tissue damage caused by the disease itself and Or due to the side effects of various drugs used to treat lupus (13)