This file owns three connective tissue diseases unified by autoantibody-driven subtyping: Sjögren's syndrome (sicca + anti-Ro/La + lymphocytic sialadenitis), systemic sclerosis (scleroderma) with its diffuse vs limited/CREST split driven by anti-Scl-70 vs anti-centromere autoantibodies, and inflammatory myopathies (polymyositis, dermatomyositis, inclusion body myositis, anti-synthetase syndrome). The unifying clinical reasoning is autoantibody → predicted organ pattern: each specific autoantibody points to a specific clinical phenotype with predictable extra-cutaneous and extra-glandular manifestations.
Prerequisites
Systemic Lupus Erythematosus & Mixed Connective Tissue Disease (the ANA-pattern → specific-autoantibody algorithm; anti-Ro/La as the link between Sjögren's, SLE, and neonatal lupus / congenital heart block; secondary Sjögren's recognition in established autoimmune disease)Approach to Inflammatory Arthritis & Rheumatoid Arthritis (the four-pillar inflammatory arthritis framework, particularly the third pillar — extra-articular features locating the systemic disease — and the principle that complement consumption distinguishes SLE from RA, with normal complement in scleroderma/Sjögren's/myopathies)Cytokine biology, particularly Type I interferon signature in DM and IFN-γ in PMType II antibody-mediated mechanisms relevant to DM perimysial complement deposition; Type IV CD8+ T cell-mediated mechanism in PM endomysial patternBasic histology (skeletal muscle organization — perimysium vs endomysium; salivary and lacrimal gland exocrine architecture)