1- Definition and Classification
2-Pathophysiology
3-Epidemiology and Risk Factors
4- Cutaneous Manifestations
5– Raynaud’s Phenomenon
6- Lung Involvement
7- Gastrointestinal Manifestations
8- Renal Crisis in Systemic Sclerosis
9- Cardiac Involvement
10- Autoantibodies
11- CREST Syndrome
12- Diagnostic Workup
13- Management Overview
14- Prognosis and Monitoring
15-Differential Diagnosis
Systemic sclerosis (SSc) is a chronic autoimmune connective tissue disease marked by:
Fibrosis of skin and internal organs
Microvascular dysfunction
Immune dysregulation
It is classified into:
Limited cutaneous SSc (lcSSc) – distal skin involvement, slow progression
Diffuse cutaneous SSc (dcSSc) – widespread skin involvement, early visceral disease
Subtypes can be further described by antibody profile and clinical manifestations
Three main pathological features:
Immune activation → autoantibodies (ANA, anti-Scl-70, anticentromere)
Vascular injury → Raynaud’s, digital ulcers
Fibroblast activation → collagen overproduction → fibrosis of skin/organs
Triggers may include silica exposure, viral infections, or environmental toxins.
Female:Male = 4:1
Peak incidence: age 40–60
Risk factors: genetic predisposition (HLA-DR), silica exposure, radiation, certain drugs
Sclerodactyly: tight, shiny, thickened skin on fingers → flexion contractures
Mask-like facies: loss of facial expression, radial furrowing
Telangiectasias, calcinosis
Digital ulcers from vasospasm or infarction
Often begins with puffy fingers before progressing to fibrosis.
Present in >90% of patients (often the first sign)
Triggered by cold or stress → triphasic colour change (white → blue → red)
May progress to digital ulceration or gangrene
-Nailfold capillaroscopy may reveal dilated loops, dropout—used in early diagnosis.
Interstitial Lung Disease (ILD): esp. with anti-Scl-70
Symptoms: dry cough, dyspnoea
PFTs: restrictive pattern, ↓ DLCO
Imaging: HRCT shows fibrosis
Pulmonary Arterial Hypertension (PAH): esp. in lcSSc
Screen with echocardiogram and NT-proBNP
Right heart catheterization is gold standard
-Leading cause of death in systemic sclerosis.
Esophageal dysmotility → reflux, strictures
Delayed gastric emptying
SIBO → bloating, diarrhoea
Watermelon stomach (gastric antral vascular ectasia – GAVE)
Constipation or pseudo-obstruction due to colonic dysmotility
-Barium studies and manometry can aid diagnosis.
Sudden onset malignant hypertension, headache, oliguria
Microangiopathic haemolytic anaemia may occur
Associated with anti-RNA polymerase III antibodies
-Treat immediately with ACE inhibitors (even if creatinine is rising)
Avoid NSAIDs and high-dose steroids—they can precipitate crisis.
Pericarditis
Conduction defects
Myocardial fibrosis → arrhythmias, heart failure
PAH (as above)
-Monitor with ECG, echocardiogram, troponins if symptomatic.
Antibody | Associated Subtype | Clinical Relevance |
---|---|---|
ANA | >90% cases | Screening tool |
Anti-centromere | lcSSc | CREST, PAH, good prognosis |
Anti-Scl-70 (topoisomerase I) | dcSSc | ILD, worse prognosis |
Anti-RNA polymerase III | dcSSc | Renal crisis, skin involvement |
A form of limited SSc with hallmark features:
Calcinosis
Raynaud’s phenomenon
Esophageal dysmotility
Sclerodactyly
Telangiectasia
Associated with anticentromere antibodies and better overall prognosis.
Clinical diagnosis based on skin thickening, Raynaud’s, and serology
Bloods: ANA, Scl-70, centromere, renal profile, CRP
Imaging: HRCT for ILD, echo for PAH
Lung function tests (↓ DLCO = early PAH)
Nailfold capillaroscopy (non-invasive vascular test)
System | Treatment |
---|---|
Raynaud’s | CCBs (nifedipine), sildenafil, iloprost |
Skin | MTX (for early inflammatory skin changes) |
ILD | Mycophenolate, cyclophosphamide, nintedanib |
PAH | Endothelin receptor antagonists (bosentan), sildenafil |
Renal crisis | ACE inhibitors (e.g. captopril) – emergency |
GI | PPIs, prokinetics, rotating antibiotics for SIBO |
Worse prognosis with:
Diffuse skin involvement
Early ILD or PAH
Anti-Scl-70 or anti-RNA pol III positivity
10-year survival ≈ 70–80%
-Mortality mainly from ILD and PAH
MCTD: overlap with lupus, polymyositis, and scleroderma
SLE: ANA+, skin findings, but lacks sclerodactyly
Dermatomyositis: skin changes + muscle weakness
Eosinophilic fasciitis: mimics scleroderma, no Raynaud’s, no autoantibodies