General Medicine

SLE (Systemic Lupus Erythematosus) = multisystem autoimmune disease; F:M = 9:1 ; African-American > Caucasian; peak 15–40 years; characterised by loss of tolerance to nuclear antigens + immune complex deposition.

• SLICC 2012 Criteria (replace old ACR; ≥ 4 criteria OR biopsy-proven lupus nephritis + ANA or anti-dsDNA):

• Treatment: Hydroxychloroquine (all SLE — reduces flares + renal disease + mortality ); Steroids (flares); Azathioprine (maintenance); Cyclophosphamide or Mycophenolate (Class III/IV lupus nephritis ); Belimumab (anti-BLyS); Voclosporin (CNI — lupus nephritis)
• Cutaneous manifestations in detail: acute - malar (butterfly) rash sparing nasolabial folds, photosensitive; subacute - annular/papulosquamous lesions; chronic - discoid lupus (scarring, follicular plugging, dyspigmentation; discoid alone does not equal SLE); bullous lupus; livedo reticularis.
• Systemic features: musculoskeletal (arthralgia/non-erosive arthritis - Jaccoud arthropathy); renal (lupus nephritis - most serious; urinalysis shows protein, RBC casts; classification I-VI on biopsy); haematological (lymphopenia, haemolytic anaemia, thrombocytopenia); CNS (psychosis, seizures, cerebrovascular disease); serositis (pleuritis, pericarditis).
• Investigations: ANA (screening; 99% sensitive), anti-dsDNA (disease-specific, correlates with activity/nephritis), anti-Sm (highly specific), low complement C3/C4 (active disease), urinalysis and eGFR (nephritis surveillance), FBC (cytopenias), direct Coombs test.
• Monitoring & prognosis: SLEDAI disease activity index guides treatment; hydroxychloroquine reduces flares and mortality in all patients; avoid triggers (sunlight, OCP, sulfonamides); mortality from nephritis, infections and cardiovascular disease.

Anaphylaxis = severe, life-threatening, generalised hypersensitivity reaction. Mechanism: Type I hypersensitivity (IgE-mediated; sensitised mast cells + basophils → cross-linked by antigen → massive histamine + tryptase + leukotrienes release → vasodilation + ↑ permeability + bronchospasm).

• Common triggers: Drugs (penicillin #1 drug; aspirin, NSAIDs; cephalosporins; IV contrast; anaesthetic agents); Foods (peanuts, tree nuts, shellfish); Insect stings (bee/wasp venom); Latex; Blood products; Exercise-induced
• Clinical: Urticaria + angioedema + flushing; bronchospasm (wheeze; stridor); hypotension + tachycardia (distributive shock); laryngeal oedema (stridor + hoarseness); nausea/vomiting; abdominal pain

• Pathogenesis: Type I (IgE-mediated) - prior sensitisation produces IgE bound to mast cells; re-exposure causes cross-linking and massive mast cell/basophil degranulation releasing histamine, tryptase, leukotrienes and prostaglandins; non-IgE (anaphylactoid) reactions (contrast, opioids) produce the same mediators directly.
• Investigations: serum mast cell tryptase at 1-3 h after reaction (confirms anaphylaxis; useful even retrospectively); skin prick/intradermal testing and specific IgE serology 4-6 weeks later to confirm the trigger; exclude hereditary angioedema (normal tryptase, low C4).
• Biphasic reaction & discharge: a second reaction can occur 8-72 h later without re-exposure in 5-20% of cases; patients should be observed for at least 6 h after full recovery; prescribe two adrenaline auto-injectors (EpiPen) and refer to allergy.
• Prevention: avoid the trigger, wear a medical alert bracelet, carry adrenaline auto-injectors, and have a written anaphylaxis action plan.

ARF = acute inflammatory condition following Group A Streptococcal (GAS) pharyngitis (not skin infection); mediated by molecular mimicry (streptococcal M protein antigens → antibodies cross-react with cardiac tissue ). Incubation: 2–4 weeks after throat infection.

• JONES CRITERIA 2015 (Revised) — 2 major OR 1 major + 2 minor + evidence of preceding GAS infection:

• Evidence of GAS infection: Raised ASOT (anti-streptolysin O titre) > 200 IU/mL in adults; anti-DNase B titre; throat culture; recent positive rapid antigen test

▶ TREATMENT: Benzylpenicillin 1.2 MIU IM single dose (eradicate GAS) THEN Benzathine penicillin for prophylaxis;
Carditis: Bed rest + Prednisolone 2 mg/kg/day × 4–6 weeks;
Arthritis: Aspirin 100 mg/kg/day (4–6 wks) — dramatic relief within 24h;
Chorea: Haloperidol ± Carbamazepine

• Secondary prophylaxis: Benzathine penicillin 1.2 MIU IM every 3–4 weeks for years (duration based on carditis severity: no carditis = 5 years or to 21 yrs; mild carditis = 10 yrs or to 25 yrs; severe residual carditis = lifelong )

Gout = clinical syndrome from hyperuricaemia (> 6.8 mg/dL ) → monosodium urate (MSU) crystal deposition in joints, periarticular soft tissues (tophi ), and kidneys. M > F; peak 4th–5th decade; HLA-B association.

• Acute gout: Sudden onset monoarthritis (especially 1st MTP joint = podagra — 75%; also ankle, knee, wrist); exquisitely painful; red, hot, swollen; fever; peak within 24 hrs; resolves spontaneously in 1–2 weeks; triggers: purine-rich foods (red meat, organ meat, shellfish ), alcohol (beer ), dehydration, diuretics, trauma
• Chronic tophaceous gout: Tophi (deposits of MSU crystals) — ear pinnae, tendons, joints, periarticular; urate nephropathy; renal stones
• Diagnosis: Synovial fluid aspirate — GOLD STANDARD: negatively birefringent, needle-shaped MSU crystals under polarised light (appear yellow when parallel, blue when perpendicular to compensator axis ); serum uric acid (may be normal during acute attack ); X-ray: punched-out erosions with overhanging edges (Martel's sign ) in chronic; DECT (dual-energy CT) identifies urate deposits

▶ Acute attack: NSAIDs (indomethacin 50 mg TDS ) — first-line (avoid if PU/renal disease); OR Colchicine 0.5 mg 2–4×/day (blocks tubulin → inhibits neutrophil migration; SE: diarrhoea ); OR Prednisolone 30–40 mg OD (if NSAIDs/colchicine contraindicated); DO NOT start urate-lowering during acute attack

▶ Urate-lowering therapy (chronic prevention; start ≥ 2 weeks after acute attack resolves ):
Allopurinol 100 mg OD → titrate to 300–900 mg OD; xanthine oxidase inhibitor; first-line; target uric acid < 6 mg/dL (< 5 mg/dL with tophi); SIDE EFFECTS: Allopurinol hypersensitivity syndrome (HLA-B*5801 association especially in Asian/CKD patients — SJS/TEN — screen before starting in Han Chinese/Thai/Korean patients )
Febuxostat 80–120 mg OD — non-purine xanthine oxidase inhibitor; effective in CKD
Cover with colchicine 0.5 mg OD × 6 months during initiation (prophylactic ) to prevent flares

APLA syndrome = acquired thrombophilia due to antiphospholipid antibodies (aPL) [Lupus anticoagulant (LA), anticardiolipin (aCL), anti-β2-glycoprotein I (anti-β2GPI)] → arterial AND venous thrombosis + pregnancy morbidity (recurrent miscarriage ).

• Primary APLA: No underlying disease; Secondary: SLE (most common underlying disease — 30–40% of SLE have aPL )
• Clinical features: DVT; PE; arterial thrombosis (stroke, MI); recurrent pregnancy loss (≥ 3 miscarriages < 10 weeks OR ≥ 1 fetal death > 10 weeks) ; thrombocytopenia; Libman-Sacks endocarditis (non-bacterial; mitral valve ); livedo reticularis (mottled violaceous skin pattern); Sneddon's syndrome (livedo + stroke)
• Diagnosis: Sapporo criteria — clinical (thrombosis/pregnancy morbidity) + lab: LA (by DRVVT; APTT paradoxically prolonged in vivo but thrombotic ) + aCL IgG/IgM + anti-β2GPI IgG/IgM; must be positive on 2 occasions ≥ 12 weeks apart
• Catastrophic APLA (CAPS) — rare; multi-organ thrombosis < 1 week; mortality 50%; treat with anticoagulation + steroids + plasmapheresis/IVIg + eculizumab
• Pathogenesis: antiphospholipid antibodies (lupus anticoagulant, anticardiolipin IgG/IgM, anti-beta2-glycoprotein-I) activate endothelium and platelets, impair fibrinolysis and inhibit anticoagulant pathways, producing a prothrombotic state.
• Investigations: LA by dilute Russell viper venom time (dRVVT) or APTT; anticardiolipin and anti-B2GPI by ELISA; must be positive on two occasions at least 12 weeks apart to avoid false positives (infection-related transient antibodies).
• Treatment nuances: indefinite anticoagulation for thrombotic APLA; target INR 2-3 (or 3-4 for arterial events or recurrence on adequate anticoagulation); DOACs are less effective than warfarin in triple-positive APLA (LA + anticardiolipin + anti-B2GPI); LMWH throughout pregnancy with low-dose aspirin.

▶ Treatment: Anticoagulation — Warfarin (target INR 2–3; INR 3–4 for arterial thrombosis); LMW heparin in pregnancy (warfarin teratogenic) + low-dose aspirin 75 mg OD; DOACs INFERIOR to warfarin in aPL (especially high-risk triple-positive patients)

Ankylosing spondylitis (AS) = chronic inflammatory arthropathy of axial skeleton (sacroiliac joints + spine) with characteristic bamboo spine in late disease. HLA-B27 association (90% ). M:F = 3:1; onset 15–40 years.

• Clinical features: Insidious onset low back pain + morning stiffness > 1 hour (inflammatory — improves with exercise, not rest — opposite of mechanical back pain); pain at night/rest (characteristic ); sacroiliac joint tenderness (FABER test = hip Flexion + ABduction + External Rotation); progressive spinal stiffness
• Tests of spinal mobility:

• Schober's test — marks 5 cm below + 10 cm above posterior superior iliac spine; on maximal forward flexion, normal = increased distance ≥ 5 cm; AS = < 5 cm (restricted flexion)
• Occiput-to-wall distance (cervical involvement) — patient stands against wall; inability to touch occiput to wall = cervical fusion

• Extra-articular: Acute anterior uveitis (most common EAM — painful red eye; photophobia; affects HLA-B27+ patients); Aortic regurgitation; pulmonary fibrosis (upper lobe ); cardiovascular (AV block); psoriasis; IBD (Crohn's/UC )
• Radiological: Sacroiliitis (earliest X-ray finding — bilateral, symmetrical ); bamboo spine (syndesmophytes + fusion of vertebrae); square vertebrae (Romanus lesion — early sign); MRI (inflammatory changes before X-ray evidence )
• Lab: ESR ↑; CRP ↑; HLA-B27 positive (90%) ; RF negative (seronegative spondyloarthritis )

▶ NSAIDs (first-line; continuous — also suppress disease activity); physiotherapy (essential); anti-TNF biologic (adalimumab/etanercept/infliximab — for NSAID-refractory active AS; dramatically improve mobility + reduce pain); IL-17A inhibitors (Secukinumab/Ixekizumab) — second-line biologic; effective for both axial and peripheral disease + psoriasis

REACTIVE ARTHRITIS (ReA)

Reactive arthritis (previously Reiter's syndrome) = aseptic inflammatory arthritis occurring 1–4 weeks after infection at a distant site (NOT direct infection of joint). Organisms: GU tract — *Chlamydia trachomatis* (#1 STI-triggered); GI tract — *Campylobacter, Salmonella, Shigella, Yersinia *.

• Classic triad (Reiter's triad): Arthritis + Urethritis/Cervicitis + Conjunctivitis; also: circinate balanitis (painless erosive penile lesion); keratoderma blennorrhagicum (palmo-plantar pustular lesions resembling psoriasis )
• Lab: HLA-B27 positive (70–80%); RF negative; urine/urethral PCR for Chlamydia

▶ Management: Treat infection (Chlamydia: doxycycline 100 mg BD × 7 days or azithromycin 1g single dose); NSAIDs (arthritis); Sulfasalazine/methotrexate (chronic); anti-TNF if refractory

• Investigations: ESR/CRP raised; RF negative; HLA-B27 positive in 70-80%; urethral/cervical/stool PCR for the triggering organism; X-ray in chronic disease shows periostitis and enthesitis.
• Complications: chronic arthritis in 15-20%, eye involvement (uveitis - anterior, can impair vision), cardiac conduction defects with axial disease, and potentially disabling enthesitis.
• Ankylosing spondylitis key points: sacroiliitis (bilateral, grade II bilateral or III/IV unilateral on X-ray) is the hallmark; symptoms improve with exercise; treat with NSAIDs first-line, then anti-TNF biologics if refractory; assess with BASDAI activity score.

SPONDYLOARTHRITIS (SpA) OVERVIEW

• Seronegative spondyloarthropathies (RF negative; HLA-B27 associated; axial + peripheral joint disease):

OA = most common joint disease; non-inflammatory (morning stiffness < 30 min ); cartilage degradation + subchondral bone changes + osteophyte formation; no systemic inflammation (CRP/ESR normal ); joints: DIP (Heberden's nodes ) + PIP (Bouchard's nodes ) + 1st CMCJ (carpometacarpal ); weight-bearing joints (knees, hips ); spine (cervical + lumbar spondylosis); NOT MCP/wrist (unlike RA ).

• Radiology: LOSS of joint space + osteophytes (bony spurs) + subchondral sclerosis + subchondral cysts (the 4 OA X-ray signs — mnemonic: LOSS)
• Synovial fluid: Non-inflammatory (< 2000 WBC/μL; clear/yellow; viscous)

▶ Non-pharmacological (cornerstone): Weight loss (for knee/hip OA — each kg weight loss = 4 kg force reduction on knee ); physiotherapy; walking aids; heat/cold therapy; patient education

▶ Pharmacological: Paracetamol (1st line; mild); Topical NSAIDs (diclofenac gel — effective + less GI risk for small joints); Oral NSAIDs (moderate pain; with PPI ); Intra-articular corticosteroid injections (for inflammatory flares; max 3–4/year ); Duloxetine (central sensitisation); Intra-articular hyaluronic acid (viscosupplementation — for knee OA)

• Joint replacement surgery (TKR/THR) — for severe/refractory OA; dramatically improves pain and function; gold standard for advanced knee/hip OA
• Joints affected and features: knees (commonest), hips, distal interphalangeal (Heberden nodes) and proximal interphalangeal (Bouchard nodes) joints of the hands, thumb base (first carpometacarpal), and cervical/lumbar spine; spares MCP and wrist (unlike RA).
• Pathology: cartilage breakdown driven by mechanical stress and inflammatory mediators; subchondral bone remodelling produces sclerosis and cysts; marginal osteophytes form; synovial fluid is non-inflammatory.
• Investigations: largely clinical; X-ray shows joint space narrowing, osteophytes, subchondral sclerosis and cysts; synovial fluid is non-inflammatory (WBC < 2000); blood tests are normal (no raised inflammatory markers in primary OA).

Inflammatory Myopathies = idiopathic inflammatory disorders of skeletal muscle. Main types: Polymyositis (PM) (pure muscle inflammation); Dermatomyositis (DM) (muscle + characteristic skin rash); Inclusion Body Myositis (IBM) (elderly; resistant to treatment).

• Clinical features: Proximal muscle weakness (symmetrical; difficulty climbing stairs, rising from chair, lifting arms overhead; NOT from myalgia); dysphagia (pharyngeal muscle); myalgia (variable); NO sensory loss; NO fasciculations (unlike LMN)
• DM-specific skin features:

• Heliotrope rash — violaceous periorbital rash (especially upper eyelids); pathognomonic
• Gottron's papules — violaceous papules over MCP/PIP extensor surfaces; pathognomonic
• V-sign (anterior chest); Shawl sign (posterior neck/shoulders); Mechanic's hands (hyperkeratotic palms)

• Investigations: ↑↑ CK (markedly elevated — hallmark; serial monitoring ); ↑ LDH; ↑ aldolase; EMG (myopathic pattern — small-amplitude, brief, polyphasic MUPs); MRI muscle (shows oedema/inflammation ); muscle biopsy (gold standard — PM: CD8 T-cell infiltrate; DM: perifascicular atrophy + perivascular B-cell/CD4 infiltrate ); myositis-specific antibodies (anti-Jo-1 — anti-synthetase syndrome: ILD + myositis + arthritis + fever + Mechanic's hands )
• Malignancy association — DM especially; screen for malignancy in all DM at diagnosis (CT chest/abdomen/pelvis ± PET)

▶ Prednisolone 1 mg/kg/day × 4–6 weeks then taper; Methotrexate or Azathioprine as steroid-sparing agents; IVIg 2 g/kg (for refractory or acute severe with dysphagia/ILD); Rituximab (anti-Jo-1+ or DM)

• Subtypes: polymyositis (PM) - pure muscle, adults; dermatomyositis (DM) - muscle plus skin, also occurs in children; inclusion body myositis (IBM) - distal and finger flexor weakness, dysphagia, elderly, steroid-resistant; antisynthetase syndrome (anti-Jo-1 antibody, ILD, mechanic hands, Raynaud).
• Investigations in full: creatine kinase (can be > 10,000 IU/L in acute PM/DM), aldolase, LDH; EMG (myopathic - short, small, polyphasic motor unit potentials); MRI (guides biopsy site - shows muscle oedema); muscle biopsy (perimysial inflammation in DM, endomysial in PM, rimmed vacuoles in IBM); myositis-specific antibodies (anti-Jo-1, anti-Mi-2, anti-MDA5).
• Complications: ILD (especially anti-Jo-1 positive), aspiration pneumonia (pharyngeal weakness), cardiac disease, and malignancy association (screen DM patients with CT chest/abdomen/pelvis, consider PET-CT).

• Classification: large vessel - GCA (temporal arteritis, age > 50, ESR > 50, jaw claudication, treat with prednisolone 1 mg/kg/day to prevent blindness) and Takayasu (young women, aorta and branches); medium vessel - PAN (hepatitis B, aneurysms, mononeuritis multiplex), Kawasaki; small vessel - GPA, MPA, EGPA (all ANCA-associated), IgA vasculitis (Henoch-Schonlein), cryoglobulinaemia.
• GPA clinical features in detail: upper airways (sinusitis, nasal crusting/epistaxis, saddle-nose deformity, subglottic stenosis), lower airways (nodules, cavitating lesions, haemoptysis), and kidneys (rapidly progressive glomerulonephritis - cellular crescents on biopsy); cANCA/anti-PR3 is the specific marker.
• Treatment: induction - rituximab or cyclophosphamide plus high-dose steroids; maintenance - azathioprine or rituximab; monitor disease activity with ANCA titres, CRP, and renal function.

Systemic sclerosis (SSc) = multisystem autoimmune disease characterised by vasculopathy + fibrosis (collagen deposition) affecting skin, lungs, heart, kidneys, GI tract. F:M = 4:1.

• Raynaud's phenomenon = episodic vasospasm of digits → colour change: WHITE (ischaemia — pallor) → BLUE (deoxygenation — cyanosis) → RED (reperfusion — rubor) on exposure to cold/stress
• Sclerodactyly: Thickening + tightening of skin of fingers; cannot make a fist; loss of finger creases; 'rat-bite' ulcers at fingertips (ischaemia); telangiectasia; beaking of nose ; microstomia (small mouth )
• GI: Oesophageal dysmotility (GERD; waterbrash; dysphagia); GAVE (gastric antral vascular ectasia — 'watermelon stomach' ); malabsorption (SIBO )

▶ Raynaud's: Nifedipine (CCB) first-line; Sildenafil; Iloprost (severe); sympathectomy

▶ ILD: Mycophenolate (MRC Scleroderma trial) or Cyclophosphamide; Nintedanib (anti-fibrotic — ILD-SSc )

▶ Scleroderma renal crisis: ACE inhibitors (captopril/enalapril) — even if Cr ↑; dramatically improve survival; do NOT use steroids (↑ SRC risk )

• Investigations: ANA (>95%); anti-centromere antibody (lcSSc specific); anti-Scl-70/topoisomerase I (dcSSc specific, predicts ILD); HRCT chest (ILD - ground glass, then honeycombing); echo and right heart catheter (PAH); OGD/manometry (GI involvement); hand X-ray (calcinosis, acroosteolysis).
• Complications: interstitial lung disease and pulmonary arterial hypertension are the leading causes of death; scleroderma renal crisis (acute HTN + AKI - treat urgently with ACE inhibitor); malabsorption from bacterial overgrowth; digital ulcers and gangrene.
• CREST syndrome: Calcinosis, Raynaud, oEsophageal dysmotility, Sclerodactyly, Telangiectasia - a limited variant with better prognosis but still at risk of PAH.

• SLICC 2012: ≥ 4 criteria (at least 1 clinical + 1 immunological) OR biopsy-proven lupus nephritis + ANA or anti-dsDNA
• EULAR/ACR 2019: Entry criterion = ANA ≥ 1:80; then additive scoring system; score ≥ 10 = SLE; more sensitive and specific than SLICC
• Key antibodies: ANA (99% sensitive; screening ); anti-dsDNA (60% sensitivity; 99% specific for SLE; correlates with disease activity + renal disease ); anti-Smith (most specific; 25–30% sensitive); anti-histone (drug-induced lupus ); anti-Ro/SSA (neonatal lupus + subacute cutaneous lupus ); anti-La/SSB; antiphospholipid Abs
• Complement: Low C3 + C4 = active lupus (especially nephritis)
• Clinical criteria (SLICC 2012): acute/chronic cutaneous lupus; oral ulcers; non-scarring alopecia; synovitis; serositis (pleuritis/pericarditis); renal (proteinuria > 500 mg/day or RBC casts); neurological (seizure, psychosis, mononeuritis); haemolytic anaemia; leucopenia/lymphopenia; thrombocytopenia.
• Immunological criteria (SLICC): ANA; anti-dsDNA; anti-Sm; antiphospholipid antibodies; low complement (C3, C4, CH50); direct Coombs positive without haemolytic anaemia.
• Differential diagnosis: RA (erosive, RF/CCP positive), drug-induced lupus (anti-histone antibodies, resolves on stopping drug), mixed connective tissue disease (anti-U1RNP), undifferentiated connective tissue disease.
• 2019 EULAR/ACR criteria in detail: entry criterion is ANA >= 1:80; then additive scoring across 7 domains (constitutional, haematological, neuropsychiatric, mucocutaneous, serosal, musculoskeletal, renal); immunological criteria include anti-dsDNA, anti-Sm, antiphospholipid antibodies, low complement, and direct Coombs; total score >= 10 = SLE.
• Monitoring disease activity: SLEDAI-2K score; check anti-dsDNA and complement C3/C4 every 3-6 months (rise in dsDNA + fall in C3/C4 predicts flare); monitor urine ACR for nephritis; regular blood pressure and lipid assessment (cardiovascular risk is markedly increased).

• Approach to monoarthritis: septic arthritis must always be excluded first - joint aspiration is mandatory if an acutely swollen hot joint is present; send aspirate for Gram stain, culture, cell count and crystals; start antibiotics immediately if septic arthritis is clinically likely.
• Approach to polyarthritis: determine the pattern - additive versus migratory; symmetrical (RA) versus asymmetrical (SpA, reactive, psoriatic); small joint (RA) versus large joint (OA, reactive, gout); inflammatory (morning stiffness, systemic features, elevated CRP) versus non-inflammatory (OA).
• Investigations: FBC, ESR, CRP, uric acid, RF, anti-CCP, ANA, HLA-B27; X-ray of affected joints; joint aspiration (crystals - gout: negative birefringent monosodium urate; pseudogout: positive birefringent calcium pyrophosphate).
• Septic arthritis management: joint aspiration for diagnosis and drainage; empirical antibiotics (flucloxacillin IV for Staphylococcus coverage; ceftriaxone for gonococcal in young adults; add anti-MRSA cover if risk factors); daily aspiration or surgical washout if not improving; duration 4-6 weeks IV then oral.
• Crystal arthropathy: gout - hyperuricaemia (urate deposition in joints, tophi, renal stones); acute attack treated with NSAIDs, colchicine, or prednisolone; prophylaxis with allopurinol or febuxostat; pseudogout (CPPD) - calcium pyrophosphate crystals, affects elderly, wrists and knees, associated with hyperparathyroidism, haemochromatosis and hypomagnesaemia.

• Pattern of ANA: reported on immunofluorescence as homogeneous (anti-dsDNA/histone), speckled (anti-Sm, anti-Ro, anti-La, anti-RNP), nucleolar (Scl-70, RNA polymerase III), centromere (lcSSc); the pattern helps guide further specific antibody testing.
• Key disease-specific antibodies: anti-dsDNA (SLE, especially nephritis); anti-Sm (SLE specific); anti-Ro/SSA (Sjogrens, neonatal lupus, subacute cutaneous SLE); anti-La/SSB (Sjogrens); anti-Jo-1 (antisynthetase myositis + ILD); anti-centromere (lcSSc/CREST); anti-Scl-70 (dcSSc with ILD); anti-U1RNP (MCTD).
• Interpretation: a positive ANA alone does not diagnose disease - it is positive in 5% of the healthy population and also in infections, malignancy, and other autoimmune diseases; always correlate with the clinical picture and specific antibody profile.