Definition of SLE?
Chronic autoimmune disease causing immune complex–mediated inflammation in multiple organs (skin, joints, kidneys, CNS, blood).
Epidemiology of SLE?
Female predominance (9:1), peak 20–40 yrs.
Pathogenesis of SLE?
Loss of self-tolerance → autoantibody formation (ANA, dsDNA, Sm) → immune complexes → complement activation → tissue injury.
Main genetic risk?
HLA-DR2, HLA-DR3.
Environmental triggers?
UV light, EBV, drugs, smoking.
Type of hypersensitivity in SLE?
Type III (immune complex–mediated).
Typical skin features?
Malar rash sparing nasolabial folds, discoid lesions, photosensitivity, oral ulcers, alopecia.
Typical joint pattern?
Symmetric, non-erosive polyarthritis (hands, wrists).
Major renal manifestation?
Proteinuria, haematuria, hypertension → lupus nephritis.
Serositis features?
Pleuritis, pericarditis causing pleuritic chest pain.
Neuro features?
Seizures, psychosis, myelitis, stroke-like episodes.
Haematologic findings?
Anaemia, leucopenia, lymphopenia, thrombocytopenia.
Screening antibody for SLE?
ANA (sensitive, not specific).
Most specific antibodies for SLE?
Anti-dsDNA, Anti-Sm.
Antibody predicting renal disease?
Anti-dsDNA ↑ correlates with lupus nephritis.
Complement pattern in active SLE?
Low C3/C4 due to immune complex consumption.
Antibodies linked with neonatal lupus?
Anti-Ro (SSA), Anti-La (SSB).
Antibody associated with overlap/MCTD?
Anti-RNP.
Antiphospholipid antibodies in SLE?
Anticardiolipin, lupus anticoagulant, β2-glycoprotein → thrombosis risk.
2019 EULAR/ACR entry criterion for SLE?
Positive ANA ≥1:80.
Treatment goal in SLE?
Remission or low activity with minimal steroid exposure.
Universal baseline drug in SLE?
Hydroxychloroquine (HCQ).
HCQ safe dose?
≤ 5 mg/kg/day actual body weight.
HCQ eye monitoring?
Baseline exam + annual after 5 years (earlier if high risk).