SLE is the most common connective tissue disease involving multiple systems. A wide variety of antibodies are produced against the self antigens.
What happens in Systemic lupus erythematosus (SLE)?
There are round 50 antigen against which autoantibodies are produced and it is likely that this wide spectrum of autoantibody production results from polyclonal B- and T-cell activation. Many auto-antigens in SLE are part of the cell and its nuclear component. Normally these antigens are always hidden from the immune system so they don’t lead to an immune response of productions antibodies. However with the death of the cell some antigens are presented on the cell surface and lead to formation of antibodies against them. The precise mechanism is unknown.
Females of many mammalian species make higher antibody responses than males. Women exposed to estrogen-containing oral contraceptives have an increased risk of developing SLE by 1-2 fold.
Several environmental factors may influence Systemic lupus erythematosus. Exposure to ultraviolet light causes flares of SLE in approximately 70% of patients, possibly by increasing death in skin cells or by altering proteins inside the cells to make them antigenic. Most SLE patients have autoantibodies for 3 years or more before the first symptoms of disease. Children and adults with SLE are more likely to be infected by Epstein Bar Virus (EBV). This virus activates and infects B cells and survives in them for many years.
How is Systemic Lupus Erythematosus is diagnosed?
- Malar rash
- Discoid rash
- Photosensitivity
- Oral ulcers
- Arthritis
- Serositis
- Renal disorder
- Neurologic disorder
- Hematologic disorder
- Immunologic disorder
- Antinuclear antibodies
Treatment of SLE
- Education about the condition. Avoidance of sun and UV light exposure with the use of high-factor sun blocks (SPF 25-50).
- Analgesics
- Disease modifying drugs
- Steroids
- Immunosupressive agents
- Anticoagulants
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