SYSTEMIC LUPUS ERYTHEMATOSUS
Systemic lupus erythematosus (SLE) is a chronic, inflammatory
autoimmune collagen disease resulting from disturbed immune
regulation that causes an exaggerated production of autoanti-
bodies.
Pathophysiology
This disturbance is brought about by some combination of
genetic, hormonal (as evidenced by the usual onset during the
childbearing years), and environmental factors (sunlight
thermal burns). Certain medications, such as hydralazine
(Apresoline), procainamide (Pronesty])isoniazid,chlorpromazine
(Thorazine), and some anticonvulsants, have been implicated in
chemical- or drug-induced SLE. In SLE, the increase in autoanti-
body production is thought to result from abnormal suppressor
I-cell function, leading to immune complex deposition and
tissue damage. Inflammation stimulates antigens, which in turn
stimulate additional antibodies, and the cycle repeats
(remissions and exacerbations).
Clinical Manifestations
Onset is insidious or acute. SLE can go undiagnosed for many
years. The clinical course is one of exacerbations and
remissions.Multisystem features include nephritis,
cardiopulmonary disease, rashes, and more indirect evidence of
systemic inflammation (fever, fatigue, and weight loss).
• Musculoskeletal system: arthralgias and arthritis
(synovitis)are common presenting features. Joint swelling,
Systemic lupus erythematosus (SLE) is a chronic, inflammatory
autoimmune collagen disease resulting from disturbed immune
regulation that causes an exaggerated production of autoanti-
bodies.
Pathophysiology
This disturbance is brought about by some combination of
genetic, hormonal (as evidenced by the usual onset during the
childbearing years), and environmental factors (sunlight
thermal burns). Certain medications, such as hydralazine
(Apresoline), procainamide (Pronesty])isoniazid,chlorpromazine
(Thorazine), and some anticonvulsants, have been implicated in
chemical- or drug-induced SLE. In SLE, the increase in autoanti-
body production is thought to result from abnormal suppressor
I-cell function, leading to immune complex deposition and
tissue damage. Inflammation stimulates antigens, which in turn
stimulate additional antibodies, and the cycle repeats
(remissions and exacerbations).
Clinical Manifestations
Onset is insidious or acute. SLE can go undiagnosed for many
years. The clinical course is one of exacerbations and
remissions.Multisystem features include nephritis,
cardiopulmonary disease, rashes, and more indirect evidence of
systemic inflammation (fever, fatigue, and weight loss).
• Musculoskeletal system: arthralgias and arthritis
(synovitis)are common presenting features. Joint swelling,
