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)