Overview
This lecture explains systemic lupus erythematosus (SLE), a systemic autoimmune disease affecting multiple organs, its causes, diagnostic criteria, and management.
Definition and Pathogenesis
- Systemic lupus erythematosus (SLE) is a systemic autoimmune disease causing inflammation in various organs.
- "Systemic" means affecting multiple organs; "erythematosus" refers to skin redness; "lupus" refers to wolf, due to skin lesion appearance.
- SLE occurs when immune cells attack the body's own tissues (autoimmunity).
- Both genetic susceptibility and environmental triggers (e.g., UV light) contribute to SLE development.
- UV radiation can cause cell damage and apoptosis, exposing nuclear antigens to the immune system.
- People with certain genes have poor clearance of apoptotic bodies and produce antinuclear antibodies (ANA).
- Antinuclear antibodies bind nuclear antigens, forming complexes that deposit in tissues and cause inflammation (type III hypersensitivity).
- Other triggers include smoking, infections, certain drugs, and hormones like estrogen.
- SLE is much more common in women, especially during reproductive years.
Symptoms and Diagnostic Criteria
- Classic symptoms: fever, joint pain, and rash, especially in women of childbearing age.
- Diagnosis requires at least 4 of 11 criteria:
- Malar (butterfly) rash over cheeks.
- Discoid rash—chronic, patchy redness, may scar.
- Photosensitivity—rashes on sun-exposed skin.
- Oral or nasal mucosal ulcers.
- Serositis—inflammation around lungs (pleuritis) or heart (pericarditis).
- Arthritis—pain in two or more joints.
- Renal disorders, e.g., proteinuria or glomerulonephritis.
- Neurologic disorders—seizures or psychosis.
- Hematologic disorders—anemia, leukopenia, or thrombocytopenia.
- Presence of antinuclear antibodies (ANA).
- Other specific autoantibodies (anti-Smith, anti-dsDNA, antiphospholipid).
Antibodies and Complications
- Anti-Smith and anti-dsDNA antibodies are more specific for SLE.
- Antiphospholipid antibodies (anticardiolipin, lupus anticoagulant, anti-beta2 glycoprotein I) can cause antiphospholipid syndrome, increasing clot risk.
- SLE features both type III (immune complex mediated) and type II (antibody mediated) hypersensitivity reactions.
Treatment and Management
- SLE has periods of flare-ups and remission.
- Management aims to prevent flares (sun protection) and reduce inflammation (corticosteroids/immunosuppressants).
- Severe cases may require long-term anticoagulation for clot prevention.
Key Terms & Definitions
- Systemic lupus erythematosus (SLE) — An autoimmune disease affecting multiple organs.
- Autoimmune disease — The immune system attacks the body’s own tissues.
- Antinuclear antibody (ANA) — Antibody attacking nuclear components; present in SLE.
- Type III hypersensitivity — Tissue damage from immune complex deposition.
- Type II hypersensitivity — Tissue damage from antibodies targeting specific cells.
- Antiphospholipid syndrome — Clotting disorder caused by antiphospholipid antibodies.
- Photosensitivity — Skin reaction following sun exposure.
Action Items / Next Steps
- Review the 11 diagnostic criteria for SLE.
- Study the differences between type II and type III hypersensitivity reactions.
- Read about common SLE treatments and their mechanisms.