Abstract
Systemic lupus erythematosus is a chronic, autoimmune disorder which may have even fatal consequences, particularly if it affects vital organs of the human body. It is typically manifested by inflammation of various organ systems. The course of the disease includes sporadic flare-ups, or relapses, which may lead to irreversible damage of the organs. The focus is on the suppression of clinical symptoms, inhibition of the formation of autoantibodies induce remission, preventing relapse and irreversible organ damage while maintaining the best possible quality of life for the patient. The traditional treatment of SLE include corticosteroids, cyclophosphamide and cyclosporine A, in severe forms are widely used in addition to azathioprine and high doses of immunoglobulins. In recent years, intensive research into the pathogenesis of SLE appeared other potential targets for therapeutic intervention.
Highlights
As in other autoimmune diseases, etiology of SLE is still a subject of various hypotheses
They include mainly antibodies to double-stranded DNA and anti-nucleosome antibodies [2,3,4,5]
These complexes are produced by activated neutrophils which, as in case of sepsis, form neutrophil extracellular traps (NETs) and trigger activation of immature plasmacytoid dendritic cells in a Toll-like receptor 9 (TLR9) manner
Summary
As in other autoimmune diseases, etiology of SLE is still a subject of various hypotheses. After administration of hydroxychloroquine’s, skin lesions may improve as early as within several days, but joint-related symptoms get better as late as after 6-10 weeks These medications are not effective in case of increased temperature, hematopoiesis disorders and involvement of vital organs of the body [9]. Intravenous methylprednisolone pulse therapy is used in SLE in life-threatening conditions, such as rapidly progressive renal failure, acute manifestations of CNS involvement and severe thrombocytopenia. Immunosuppressive preparations are used mainly in patients with involvement of visceral organs, who do not respond to glucocorticoid therapy, do not tolerate it, and require high maintenance doses of glucocorticoids or when the disease repeatedly reactivates during this therapy. The azathioprine dosage is reduced by 6075% if azathioprine is administered simultaneously with allopurinol which blocks its metabolic degradation
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