Liver cirrhosis
End-stage scarring of the liver from any chronic insult. Once compensated cirrhosis becomes decompensated (ascites, varices, encephalopathy, jaundice) the prognosis worsens sharply — but lifestyle change + treatment can stop or reverse early disease.
What it is
Cirrhosis is the final common pathway of chronic liver injury: normal hepatocytes are progressively replaced by fibrous scar tissue and regenerative nodules. The architecture of the liver is permanently disturbed, leading to portal hypertension, impaired synthetic function (clotting factors, albumin), impaired detoxification (ammonia → encephalopathy) and increased risk of hepatocellular carcinoma. Globally the leading causes are chronic hepatitis B and C, alcohol-related liver disease, and non-alcoholic steatohepatitis (NASH). The disease moves through a 'compensated' phase — usually silent, picked up on lab work or imaging — to 'decompensated' — ascites, variceal bleeding, hepatic encephalopathy, jaundice. Compensated cirrhosis can be stable for years; decompensated cirrhosis has a 5-year mortality around 50–80% without transplant.
Key lab markers
- ALT, AST — often normal or only mildly elevated in established cirrhosis (the burned-out liver has fewer hepatocytes to release enzymes). AST > ALT ratio >1 hints at alcohol or advanced fibrosis.
- GGT, alkaline phosphatase — rise in cholestatic patterns and alcohol-related disease.
- Bilirubin — rises late as synthetic and excretory function fail.
- Albumin — falls when the liver can no longer make enough protein.
- INR / prothrombin time — prolongs because clotting factors aren't made.
- Platelets — fall (portal hypertension → splenic sequestration); a platelet count <150 in someone with chronic liver disease is a classic clue.
- AFP — useful for hepatocellular carcinoma screening every 6 months.
- MELD score — combines bilirubin + INR + creatinine + sodium for prognosis and liver-transplant prioritisation.
Symptoms
Compensated cirrhosis is usually silent. Decompensation brings:
- Jaundice
- Abdominal swelling from ascites
- Leg oedema
- Easy bruising and bleeding (gum bleeds, nosebleeds)
- Spider angiomas, palmar erythema
- Vomiting blood or black stools (variceal bleeding)
- Confusion, sleep-wake inversion, tremor (hepatic encephalopathy)
- Fatigue and weight loss
- Itching
When to discuss with a doctor
Any abnormality in the liver-panel profile of a patient with risk factors (chronic hepatitis, heavy alcohol use, NAFLD) warrants a hepatology referral. Low platelets + low albumin + slightly elevated bilirubin in someone with chronic liver disease is the classic compensated-cirrhosis pattern and merits ultrasound elastography (Fibroscan) for staging. Any decompensation event (variceal bleed, ascites, encephalopathy) is an emergency. Hepatocellular-carcinoma screening every 6 months is recommended once cirrhosis is established. Mediora.AI flags the synthetic-function pattern; full evaluation and transplant assessment belong with hepatology.