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Related Subjects: |Chronic liver disease |Cirrhosis |Alkaline phosphatase (ALP) |Liver Function Tests |Ascites Assessment and Management |Budd-Chiari syndrome |Autoimmune Hepatitis |Primary Biliary Cirrhosis |Primary Sclerosing Cholangitis |Wilson disease |Hereditary Haemochromatosis |Alpha-1 Antitrypsin (AAT) deficiency |Non alcoholic steatohepatitis (NASH) |Spontaneous Bacterial Peritonitis |Alcoholism and Alcoholic Liver Disease |Hepatitis C
Chronic Liver Disease (CLD) refers to progressive liver injury lasting >6 months, often asymptomatic until advanced. It encompasses fibrosis, cirrhosis, portal hypertension, and hepatocellular carcinoma (HCC) risk. Early detection, identification of cause, and risk stratification are essential to prevent complications and guide referral, consistent with NICE guidance (NG50, NG145, NG196, CKS).
Chronic liver disease results from sustained injury to hepatocytes and/or biliary epithelium, triggering inflammation and activation of hepatic stellate cells, which drive extracellular matrix deposition and fibrosis. Progression from fibrosis to cirrhosis alters hepatic architecture, leading to portal hypertension, synthetic dysfunction (coagulopathy, hypoalbuminaemia), and impaired metabolism. Ongoing cholestasis in biliary diseases further promotes bile acid toxicity and fat‑soluble vitamin deficiency. Immune dysregulation and genetic predisposition modulate susceptibility to injury and fibrosis.
| Cause / Aetiology | Key Features / Diagnosis | Initial Management (UK, NICE-aligned) |
|---|---|---|
| 🍺 Alcohol-related liver disease (ARLD) | AST:ALT >2; macrocytosis, thrombocytopenia; history of high alcohol intake; imaging: steatosis/cirrhosis | Brief intervention, alcohol abstinence support, nutrition & thiamine, refer to hepatology if advanced |
| 🥩 Non-alcoholic fatty liver disease (NAFLD / MASLD) | Obesity, T2DM, dyslipidaemia; ALT>AST or mild elevation; ultrasound: steatosis; Fib-4/APRI for fibrosis | Weight loss, exercise, control diabetes/lipids, statins if indicated; refer if high fibrosis risk |
| 🦠 Viral hepatitis (HBV, HCV) | HBsAg/HBcAb, HCV Ab + PCR; raised ALT/AST; risk factors: travel, transfusion, tattoos, IV drugs | HCV: DAAs (curative), HBV: antiviral therapy per viral load & fibrosis; vaccination if indicated; refer hepatology |
| 🩷 Autoimmune hepatitis (AIH) | Raised ALT/AST, ↑ IgG; ANA/SMA/anti-LKM1; biopsy: interface hepatitis with plasma cells | Prednisolone taper + azathioprine (or MMF if intolerant); monitor ALT/AST & IgG; hepatology follow-up |
| 💚 Primary biliary cholangitis (PBC) | Cholestatic pattern (ALP ≫ ALT), ↑ IgM; AMA-M2 positive; pruritus, fatigue, xanthelasma | UDCA 13–15 mg/kg/day; manage pruritus; monitor LFTs 3–6 monthly; hepatology follow-up; consider OCA/bezafibrate if non-responder |
| 🌀 Primary sclerosing cholangitis (PSC) | Cholestatic LFTs; men 30–40 yrs; MRCP: multifocal strictures “beading”; strong UC association | No disease-modifying drug; manage complications; ERCP for dominant strictures; transplant if advanced; colonoscopy 1–2 yearly if IBD |
| 🧬 Genetic / Metabolic | Haemochromatosis: high ferritin/iron saturation; Wilson’s: low ceruloplasmin, Kayser-Fleischer rings; A1AT deficiency: low alpha-1 antitrypsin | Phlebotomy (haemochromatosis), chelation (Wilson), lifestyle & surveillance; specialist referral |
| 💊 Drug-induced / toxic | History of hepatotoxic drugs (methotrexate, amiodarone, herbal supplements); LFT pattern variable; exclude other causes | Stop offending agent, monitor LFTs, manage complications, refer if persistent or advanced |
| ☢️ Cholestatic / vascular / other | Budd–Chiari: abdominal pain, ascites, US doppler: hepatic vein obstruction; biliary obstruction: cholestatic LFTs, imaging | Anticoagulation or interventional radiology (Budd–Chiari), ERCP/surgery for obstruction; specialist referral |
💡 Tip: Always assess for **fibrosis severity** (FIB-4/APRI, elastography) to guide referral; manage reversible causes early to prevent progression to cirrhosis.
Refer to autoimmune table above (AIH, PBC, PSC, overlap syndromes) for disease‑specific therapy and monitoring.
💡 Chronic liver disease often develops silently — a high index of suspicion, careful history (especially alcohol, metabolic risk factors, viral exposure), and early fibrosis assessment improve outcomes. Referral to hepatology is indicated for moderate or advanced disease, decompensation, or if aetiology is unclear.