Systemic Lupus Erythematosus (SLE)

• Constitutional: Fatigue, fever, weight loss.
• Mucocutaneous: Malar rash (butterfly rash), discoid lesions, photosensitivity. Oral/nasal ulcers, alopecia.
• Musculoskeletal: Arthralgia/arthritis (non-erosive), myositis. Renal: Lupus nephritis (proteinuria, hematuria, casts). Hematologic: Cytopenias (anemia, leukopenia, thrombocytopenia). Neuropsychiatric: Headaches, seizures, psychosis, cognitive dysfunction. Serositis: Pleuritis, pericarditis.
• Red flags: Rapidly progressive glomerulonephritis, CNS lupus, thrombotic events (associated with antiphospholipid antibodies).

• Etiology: Genetic predisposition (e.g., HLA-DR2/DR3, IRF5, STAT4).
  Environmental triggers (e.g., UV light, infections, drugs, hormones). Epigenetic factors and immune dysregulation.
• Pathophysiology:
  • Autoantibodies (e.g., anti-dsDNA, anti-Smith) form immune complexes deposited in tissues, activating complement and causing inflammation.
  • Type I interferon pathway activation, B-cell hyperactivity, and defective clearance of apoptotic debris.

• Prevention: Avoid triggers (e.g., UV exposure, sulfa drugs).
  Regular monitoring and early treatment to prevent flares.
• Follow-up: Frequent assessment of disease activity (e.g., SLEDAI score).
  Monitoring for organ involvement (e.g., renal function, urinalysis). Screening for comorbidities (e.g., osteoporosis, cardiovascular risk). Vaccinations (avoid live vaccines on immunosuppressants).

Note: SLE requires lifelong, multidisciplinary management (rheumatology, nephrology, dermatology). Treatment is tailored to disease severity and organ involvement. Patient education on medication adherence, lifestyle modifications, and pregnancy planning (if applicable) is crucial. Prognosis has improved with earlier diagnosis and advanced therapies, but organ damage remains a major cause of morbidity and mortality.