Master Systemic Lupus Erythematosus (SLE) Mechanism, Treatment and Complications with Picmonic for Medicine

The etiology is not completely understood. The presence of many different autoantibodies demonstrates a lack of self-tolerance. This combined with external triggers such as UV radiation may play a part in the pathophysiology.

As with other autoimmune diseases females are affected to a higher degree than males. It is more common in African-American patients than Caucasians.

Local or systemic glucocorticoids are used for acute exacerbations and systemic glucocorticoids are used for severe manifestations.

Used for symptoms of minimal severity.

This is the best longterm therapy for constitutional, cutaneous and articular manifestations.

Used for patients with active glomerulonephritis.

Occurs in up to 50% of SLE patients and is due to immune complex deposition in the glomeruli, tubular or peritubular capillary basement membranes or larger blood vessels. The most common type is diffuse proliferative glomerulonephritis.

These noninfectious vegetations are smaller, 1-3 mm, than vegetations in infective endocarditis and rheumatic heart disease. They are also present on both sides of the heart valve unlike infective endocarditis and rheumatic heart disease.

This is no longer known as lupus anticoagulant syndrome because it is in fact a procoagulant state. Antiphospholipid antibodies cause a hypercoagulable state due to endothelial injury. It is characterized by elevated antiphospholipid antibodies in conjunction with 1 or more of the following: 1) venous thromboembolism, 2) arterial thrombosis, 3) fetal loss.

This disease is similar to SLE; however, it is due to certain drugs such as sulfonamides, hydralazine, INH, procainamide and phenytoin (SHIPP) among others. Anti-dsDNA and anti-Smith antibodies are typically absent while anti-histone antibodies are classically present. Treatment involves discontinuing the offending drug and starting the patient on prednisone if needed.