Hepatitis — Symptoms, Causes & Treatment | MyMedicPlus

Hepatitis is inflammation of the liver from any cause, resulting in hepatocyte damage and impaired liver function. It encompasses a spectrum from acute self-limiting illness to chronic progressive disease leading to cirrhosis and liver failure. The most common causes are viral hepatitis (A, B, C, D, E), alcoholic hepatitis, non-alcoholic steatohepatitis (NASH), autoimmune hepatitis, and drug-induced liver injury. Viral hepatitis B and C together affect approximately 354 million people globally and are the leading preventable causes of liver cancer worldwide. Hepatitis collectively causes an estimated 1.1 million deaths annually — a burden comparable to HIV/AIDS and tuberculosis — yet remains significantly underdiagnosed and undertreated. Non-alcoholic fatty liver disease (NAFLD), now reclassified as metabolic dysfunction-associated steatotic liver disease (MASLD), is the fastest-growing cause of chronic hepatitis globally, driven by the rising prevalence of obesity, type 2 diabetes, and metabolic syndrome.

Viral hepatitis types: Hepatitis A and E are transmitted fecally-orally (contaminated food and water) and cause acute, self-limiting illness. Hepatitis B is transmitted via blood, sexual contact, and perinatally. Hepatitis C is predominantly blood-borne. Hepatitis D (delta) only co-infects with HBV. Non-viral causes include excessive alcohol consumption (alcoholic hepatitis), obesity and metabolic syndrome (NASH), autoimmune attack on liver cells (autoimmune hepatitis), medications (paracetamol overdose, anti-TB drugs, statins, herbal supplements), and rare metabolic conditions (Wilson's disease, alpha-1 antitrypsin deficiency). Risk factors for accelerated liver disease progression include coinfection with multiple hepatitis viruses or HIV, concurrent heavy alcohol consumption, pre-existing metabolic liver disease, and immunosuppression — each substantially increasing the rate of progression from chronic hepatitis to cirrhosis and hepatocellular carcinoma.

Acute hepatitis from any cause presents with fatigue, nausea, vomiting, right upper abdominal pain, loss of appetite, fever (especially in HAV and HEV), dark urine, pale stools, and jaundice (yellowing of skin and whites of the eyes). Chronic hepatitis is often asymptomatic for years. Signs of advanced chronic liver disease (cirrhosis) include spider angiomata, palmar erythema, splenomegaly, ascites, variceal bleeding, and encephalopathy. Autoimmune hepatitis more commonly presents in young women with concurrent autoimmune conditions (thyroid disease, ulcerative colitis) and may present with acute liver failure. In acute hepatitis A and E, a prodrome of fever and right upper quadrant pain classically precedes jaundice by several days. Pruritus (generalized skin itch) from bile salt accumulation may accompany deep jaundice in cholestatic presentations and can be severe and distressing.

Liver function tests (LFTs) assess hepatic inflammation (ALT, AST) and function (bilirubin, albumin, prothrombin time). Viral hepatitis serology and molecular testing (HBsAg, anti-HCV antibody, HCV RNA, HAV IgM, HEV IgM) identify the causative virus. Autoimmune hepatitis screen includes ANA, anti-smooth muscle antibody (ASMA), anti-liver kidney microsomal antibody (anti-LKM1), and IgG levels. Abdominal ultrasound assesses liver size, echogenicity, biliary system, and portal hypertension signs. FibroScan measures liver stiffness indicating fibrosis stage. Liver biopsy is the gold standard for staging chronic hepatitis and confirming autoimmune hepatitis diagnosis. Liver elastography (FibroScan) provides non-invasive assessment of hepatic stiffness correlating with fibrosis stage, reducing the need for liver biopsy in most patients. FIB-4 score (derived from age, ALT, AST, and platelet count) and APRI score are validated non-invasive fibrosis markers widely used in clinical practice to guide hepatitis management decisions.

Viral hepatitis A and E are self-limiting — supportive care with hydration and rest is sufficient; alcohol must be avoided during recovery. Hepatitis B: antiviral therapy (tenofovir, entecavir) for active chronic disease; vaccination for prevention. Hepatitis C: 8–12 weeks of direct-acting antivirals (sofosbuvir/velpatasvir or glecaprevir/pibrentasvir) cure 95%+ of patients. Autoimmune hepatitis: oral corticosteroids (prednisolone) with azathioprine achieve remission in 65–80% of patients — lifelong maintenance therapy is typically required. Alcoholic hepatitis: alcohol abstinence is essential; severe cases (Maddrey Discriminant Function above 32) benefit from corticosteroids. Drug-induced hepatitis resolves after stopping the causative agent. For MASLD/NASH, weight loss of 7–10% body weight significantly reduces hepatic inflammation and fibrosis; semaglutide (GLP-1 receptor agonist) and resmetirom (thyroid hormone receptor-β agonist) have demonstrated significant histological benefit in clinical trials. Liver transplantation remains the definitive treatment for end-stage liver failure from any hepatitis cause.

Acute liver failure — rapid severe loss of hepatic function — can complicate severe acute hepatitis A, B, E, drug-induced injury, or autoimmune hepatitis and requires emergency liver transplant assessment. Chronic hepatitis from any cause can progress to cirrhosis (irreversible fibrosis causing portal hypertension) and hepatocellular carcinoma (HCC). Cirrhotic complications include ascites, spontaneous bacterial peritonitis, variceal hemorrhage (life-threatening gastrointestinal bleeding), hepatorenal syndrome, and hepatic encephalopathy. HBV and HCV together account for approximately 75% of worldwide HCC. Viral hepatitis reactivation can occur with immunosuppressive therapy and cancer chemotherapy in chronically infected patients.

Vaccinate against hepatitis A (2 doses) and hepatitis B (3 doses) — both are highly effective. Hepatitis B vaccine also prevents hepatitis D (delta). No vaccine exists for hepatitis C. Practice safe sex, avoid sharing needles or personal hygiene items, and ensure blood products are screened. Abstain from or limit alcohol to prevent alcoholic and toxic hepatitis. Avoid unnecessary over-the-counter medications and herbal supplements in the presence of any liver disease. Review all medications with your hepatologist — many common drugs can cause drug-induced liver injury. Annual liver ultrasound and AFP testing for HCC surveillance in all patients with cirrhosis from any cause.

Seek emergency care immediately (999/911) for: jaundice with fever and right upper quadrant pain (Charcot's triad — possible ascending cholangitis or fulminant hepatitis); jaundice with confusion, altered consciousness, or drowsiness (possible acute liver failure with hepatic encephalopathy — a life-threatening emergency); or vomiting blood or black tarry stools (variceal haemorrhage from portal hypertension). See a GP urgently for: new onset jaundice at any age; unexplained fatigue, right upper quadrant pain, and loss of appetite persisting more than 2 weeks; known exposure to viral hepatitis (needle sharing, sexual exposure, contaminated blood product); abnormal liver function tests found on routine blood tests; or positive viral hepatitis serology on screening. High-risk individuals should be proactively tested for hepatitis B and C: people who inject drugs (past or present), men who have sex with men, people born in high-prevalence countries (sub-Saharan Africa, East/South-East Asia, Eastern Europe), and anyone who received a blood transfusion before 1992 (pre-screening era). Chronic hepatitis B and C are now highly treatable — testing and early treatment prevents cirrhosis and liver cancer.