Hepatitis — Types, Causes, Symptoms & Treatment Guide — Symptoms, Causes & Treatment | MyMedicPlus

Hepatitis means inflammation of the liver and can be caused by viral infection, alcohol, medications, autoimmune disease, and metabolic conditions. Viral hepatitis — caused by hepatitis viruses A, B, C, D, and E — is the most prevalent form globally. Hepatitis B (HBV) and hepatitis C (HCV) together account for 354 million chronic infections worldwide and are the leading cause of cirrhosis, liver failure, and hepatocellular carcinoma (HCC — liver cancer). Collectively, viral hepatitis causes 1.1 million deaths annually. Hepatitis A and E are acute, self-limiting infections transmitted via contaminated food and water. Hepatitis B is preventable by vaccination; hepatitis C is now curable with direct-acting antivirals (DAAs) achieving over 95% cure rates. Hepatitis — inflammation of the liver from any cause — represents a global public health emergency: viral hepatitis B and C together affect 354 million people worldwide and cause approximately 1.1 million deaths annually through liver cirrhosis and hepatocellular carcinoma, a burden comparable to HIV/AIDS yet dramatically underrecognised and undertreated.

Hepatitis A (HAV): faeco-oral transmission — contaminated water and food, international travel to endemic areas. Hepatitis B (HBV): blood-borne and sexual transmission — vertical (mother to child — most common route globally), unprotected sex, injecting drug use (shared needles), needle-stick injuries, tattoos/piercings with unsterilised equipment. Chronicity risk: 90% of perinatally infected infants develop chronic HBV; only 5% of infected adults become chronic. 296 million people have chronic HBV worldwide. Hepatitis C (HCV): primarily blood-borne — injecting drug use (90% of new infections in high-income countries), pre-1992 blood transfusions, healthcare-related exposure. No vaccine. 58 million have chronic HCV. Hepatitis D (HDV): only infects those with HBV (requires HBsAg); superinfection accelerates liver disease. Hepatitis E (HEV): faeco-oral — contaminated water in developing countries; zoonotic from undercooked pork in developed countries. Other causes: alcohol-related hepatitis (acute alcoholic hepatitis), drug-induced liver injury (DILI — paracetamol, isoniazid, statins, many others), autoimmune hepatitis, non-alcoholic steatohepatitis (NASH).

Acute viral hepatitis (any type): prodrome of fatigue, malaise, anorexia, nausea, right upper quadrant discomfort, low-grade fever, and dark urine and pale stools (preceding jaundice). Clinical jaundice: yellow discolouration of skin and sclera (icterus) due to hyperbilirubinaemia. Hepatomegaly (enlarged, tender liver). Pruritus (itch) from cholestasis. Most acute hepatitis A and E resolve completely within 4-8 weeks. Chronic hepatitis B/C: often entirely asymptomatic for decades — the 'silent epidemic'. Symptoms emerge only with advanced liver disease: fatigue, abdominal distension (ascites), jaundice, oedema, bruising easily (coagulopathy), haematemesis (variceal bleeding), and hepatic encephalopathy (confusion, asterixis — flapping tremor). Physical signs of chronic liver disease: spider naevi, palmar erythema, leuconychia, Dupuytren's, gynaecomastia, splenomegaly, and caput medusae.

Liver function tests (LFTs): ALT and AST elevated (hepatocellular damage); ALP and GGT elevated (cholestasis); bilirubin elevated (jaundice); albumin low and prothrombin time prolonged (reduced synthetic function — indicates severity). Viral serology: Hepatitis A — anti-HAV IgM (acute), anti-HAV IgG (past/vaccinated). Hepatitis B — HBsAg (surface antigen — presence confirms infection); HBeAg (active replication); HBV DNA (viral load — quantitative); anti-HBs (protective immunity from vaccination or resolved infection); anti-HBc IgM (acute HBV). Hepatitis C — anti-HCV antibody (screening); HCV RNA (PCR — confirms active infection); HCV genotype (guides treatment duration). FibroScan (transient elastography) or FIB-4 index for non-invasive liver fibrosis assessment — staging guides treatment urgency and HCC surveillance. Liver biopsy is reserved for diagnostic uncertainty. Ultrasound abdomen: assesses liver size, cirrhotic nodularity, portal hypertension signs (splenomegaly, ascites), and HCC surveillance.

Hepatitis A and E: supportive care — rest, adequate hydration, and nutrition. Avoid alcohol and hepatotoxic medications. Most recover fully. Rare fulminant hepatic failure from HAV or HEV may require liver transplantation. Hepatitis B treatment (chronic): tenofovir alafenamide (TAF) or entecavir — first-line oral antivirals; suppress HBV DNA replication to undetectable levels; take indefinitely as they do not eradicate infection (HBsAg rarely clears). Pegylated interferon alpha-2a (48-week course): 10-20% achieve functional cure (HBsAg clearance) — suitable for young patients with high ALT and low HBV DNA. Treat all patients with active viral replication and liver damage. Hepatitis C treatment: sofosbuvir/velpatasvir (Epclusa) 12 weeks or glecaprevir/pibrentasvir (Mavyret) 8 weeks — pangenotypic oral DAA regimens achieving over 95% cure (SVR). All chronic HCV patients should receive treatment. HIV coinfection requires careful drug interaction assessment. Alcoholic hepatitis: abstinence is essential; prednisolone improves short-term survival in severe cases (Maddrey Discriminant Function over 32); pentoxifylline no longer recommended. Autoimmune hepatitis: prednisolone + azathioprine.

Acute hepatitis can progress to acute liver failure (ALF) — particularly with hepatitis B (HBV) and hepatitis E in pregnancy — with coagulopathy (INR greater than 1.5), hepatic encephalopathy, and mortality of 50-80% without liver transplantation. Chronic hepatitis B and C are the leading causes of liver cirrhosis and hepatocellular carcinoma (HCC) globally. Cirrhosis from chronic viral hepatitis leads to progressive portal hypertension with variceal haemorrhage (15-20% mortality per episode), ascites (50% 2-year mortality once established), spontaneous bacterial peritonitis (30% per-episode mortality), hepatic encephalopathy, and hepatorenal syndrome. HCC develops in 2-4% of HCV-cirrhotic patients and 2-5% of HBV-cirrhotic patients annually — global estimates attribute 810,000 deaths per year to viral hepatitis-related HCC. HBV reactivation in immunosuppressed patients (chemotherapy, biologic therapy) causes acute severe hepatitis and liver failure — prophylactic antiviral therapy (tenofovir or entecavir) is mandatory in HBsAg-positive patients receiving immunosuppression. Autoimmune hepatitis progressing to cirrhosis causes liver failure requiring transplantation in 13-20% of patients. Extrahepatic manifestations of HCV include cryoglobulinaemic vasculitis, membranoproliferative glomerulonephritis, non-Hodgkin lymphoma, and type 2 diabetes. HBV is associated with polyarteritis nodosa and membranous nephropathy.

Hepatitis A and B vaccination: Hepatitis A vaccine (2 doses) is recommended for travellers to endemic regions, food handlers, MSM, and close contacts of cases. Hepatitis B vaccine (3-dose schedule) is universal infant vaccination in most countries; catch-up vaccination for all unvaccinated adults. HBV vaccination provides over 95% protection. No vaccine for HCV or HEV. HBV and HCV harm reduction: sterile needles and syringes for people who inject drugs; safe sex with correct condom use; safe medical procedures with sterile equipment. Post-exposure prophylaxis (PEP): HBV immunoglobulin (HBIG) + vaccination for needle-stick from HBsAg-positive source if unvaccinated. All HBsAg-positive pregnant women should have viral load measured — if HBV DNA above 200,000 IU/mL, maternal tenofovir from 28 weeks prevents vertical transmission. HCC surveillance: liver ultrasound every 6 months in all patients with cirrhosis (any cause) and in non-cirrhotic HBV patients with specific risk factors.

Seek emergency care for acute hepatic failure symptoms: progressive jaundice with confusion or altered consciousness (encephalopathy), coagulopathy (unusual bruising or bleeding), severe abdominal distension (ascites), haematemesis (vomiting blood from varices), or collapse — these indicate decompensated liver disease requiring urgent specialist care. See your doctor promptly for unexplained jaundice, dark urine and pale stools lasting over a few days, right upper quadrant pain, or significant fatigue with known risk factors for hepatitis (travel to endemic areas, injection drug use, blood transfusion history). Get tested for hepatitis B and C if you have ever shared needles, had a blood transfusion before 1992, or have a parent with hepatitis B — both conditions are curable or controllable when found early.