Systemic lupus erythematosus (SLE) is a multisystem disease that preferentially affects women of childbearing age. This disorder is both more common and more severe in individuals of African and Asian ancestry. The etiology of SLE is not well understood, although genetics and environmental stimuli clearly are involved. Whether this disease is caused by a T-cell, B-cell, or other immunologic malfunction is debated, but all would agree that clearly autoantibodies such as antinuclear antibodies and anti–double-stranded DNA contribute to the pathophysiology of this disorder. This multisystem disease can affect the skin, joints, lungs, heart, kidneys, and central nervous system. Most of the morbidity and mortality is from renal and central nervous system (CNS) involvement, although accelerated atherosclerosis has recently been appreciated as a major contributor to disease burden. The treatment of SLE has improved over the past decade with less reliance on high-dose corticosteroids and more emphasis on immunosuppressive agents. It is our hope that future research into the pathophysiology of this disorder and the development of more specific therapy, such as biologics, will improve the outcome of this disease.
Central Nervous System Melioidosis in Systemic Lupus Erythematosus: A Clinical Vignette
