Clinical Features of Systemic Lupus Erythematosus <br /> Systemic lupus erythematosus (SLE) is a chronic systemic autoimmune disease with variable clinical presentation. SLE can affect all organs and the involvement of major organs can be life threatening. The exact pathological mechanisms of SLE remain elusive, and the etiology of SLE is known to be multifactorial <br />There is no single clinical laboratory test currently useful as an indicator of clinical disease activity. Attempts to establish markers have led to studies exploring titers of antibodies to double-stranded DNA (antidsDNA), levels of complement, erythrocyte sedimentation rate, and complement deposition on red blood cells. One approach to identify markers of disease activity is to investigate expression levels of genes thought to be involved in the pathogenesis or maintenance of SLE. The variable expression of cytokines determined by these genes is thought to contribute to SLE itself, as well as to the heterogeneity of SLE <br />The difficulty with cytokines is both their pleiotropic effects as well as the complex interactions among cytokines in some cases leading to both pro-inflammatory and anti-inflammatory effects. Further, cytokines thought to be involved in the pathogenesis of SLE, such as interferon alpha, may not vary in states of high or low disease activity <br /> The disease is much more prevalent in women than men, especially in the fertile age. The risk of flares after use of sex hormones as contraceptives or hormone-replacement therapy, as well as in physiological conditions such as pregnancy and puerperium is increased. Hypoandrogenism has been described in men with SLE, and androgen therapy is sometimes recommended for the treatment of some SLE manifestationsCortisol hormone, a glucocorticoid produced by the adrenal glands and one of the main stress hormones, might play a particularly important role here, because circulating levels of this hormone increase in situations of novelty, uncertainty, and uncontrollability <br />Systemic Lupus Erythematosus is considered to be complex multi-genetic autoimmune disease. Genetic factors confer a predisposition to the development of SLE. Genes that contribute to the pathogenesis of systemic lupus are classified as follows: 1. Genes that cause a break in tolerance for the self-antigens. 2. Genes that lead to immune dysregulation. It is also suggested that multiple mutations (inherited or somatic) may be needed before a selfreactive clone B and T lymphocytes bypasses sequential tolerance check points resulting in the emergence of autoimmune disease <br />