Hepatitis B — Symptoms, Causes & Treatment | MyMedicPlus

Hepatitis B is a liver infection caused by the hepatitis B virus (HBV), a DNA virus transmitted through blood, sexual contact, and mother-to-child (vertical) transmission. Approximately 296 million people have chronic hepatitis B globally, with 1.5 million new infections annually. When acquired in adulthood, HBV becomes chronic in 5–10% of cases; when acquired perinatally (mother-to-child), chronicity occurs in up to 90% of infants. Chronic HBV is a major cause of cirrhosis and hepatocellular carcinoma (liver cancer) globally. A highly effective vaccine has been available since 1982. HBV infection acquired perinatally (mother-to-child) results in chronic infection in up to 90% of exposed infants, compared to only 5–10% of adult-acquired infections — reflecting immature immune response in newborns. Global immunisation programs have substantially reduced HBV prevalence in vaccinated birth cohorts, with WHO targeting global HBV elimination by 2030.

HBV transmission occurs via contact with infected blood (sharing needles, needle-stick injuries, unscreened blood transfusions), sexual intercourse with infected partners, and from an infected mother to her child at birth. The virus is 50–100 times more infectious than HIV through blood contact. High-risk groups include people who inject drugs, sexual partners of infected individuals, healthcare workers, unvaccinated travelers to endemic areas, household contacts of chronically infected individuals, hemodialysis patients, and infants born to HBsAg-positive mothers. Sub-Saharan Africa and East Asia have the highest prevalence (5–10% of the population). Healthcare workers face occupational exposure risk — needle-stick injury with HBV-positive blood carries approximately 6–30% transmission risk without prophylaxis (versus 0.3% for HIV), due to HBV's higher viral titres and environmental stability (HBV survives on dry surfaces for up to 7 days). Tattooing and body piercing with unsterile equipment transmit HBV in settings with inadequate hygiene standards.

Acute HBV infection causes fatigue, nausea, vomiting, abdominal pain, dark urine (cola-colored), clay-colored stools, jaundice (yellowing of skin and eyes), and arthralgias (joint pain). Most adults clear the infection spontaneously within 6 months. Acute liver failure (fulminant hepatitis) occurs in 0.5–1% of acute cases. Chronic HBV is often asymptomatic for years or decades — many patients first present with decompensated cirrhosis or hepatocellular carcinoma. Chronic infection phases range from immune tolerant (high viral load, minimal damage) to immune active (inflammation and fibrosis) to inactive carrier (low replication, minimal risk). Serum sickness-like prodrome — arthralgia, urticaria, and angioedema from immune complex deposition — may precede jaundice by 1–6 weeks in acute HBV. The four chronic HBV infection phases: (1) HBeAg-positive immune tolerant (high viral load, normal ALT, minimal liver damage); (2) HBeAg-positive immune active (elevated ALT, active hepatitis — treatment needed); (3) HBeAg-negative immune control (inactive carrier); (4) HBeAg-negative immune escape (HBeAg-negative chronic hepatitis — HBV core promoter and precore mutations, requires treatment).

Hepatitis B surface antigen (HBsAg) is the primary diagnostic marker — its presence confirms HBV infection (acute or chronic). HBsAg persisting beyond 6 months confirms chronic infection. Hepatitis B e antigen (HBeAg) and hepatitis B virus DNA (HBV DNA) quantify viral replication level. Anti-HBs antibody indicates immunity (either from vaccination or prior resolved infection). Liver function tests (ALT, AST) assess hepatic inflammation. FibroScan (transient elastography) and liver biopsy stage fibrosis. HBV genotype affects treatment duration and natural history. Annual surveillance with liver ultrasound and alpha-fetoprotein (AFP) is recommended for HCC screening in chronic HBV. Hepatitis B core antibody IgM (anti-HBc IgM) is elevated in acute HBV and HBV reactivation, distinguishing it from past infection (anti-HBc IgG total). HBV reactivation — spontaneous or triggered by immunosuppressive therapy — can cause fulminant hepatitis; all patients receiving rituximab, stem cell transplants, or prolonged corticosteroids should be screened for HBsAg and anti-HBc before treatment, with antiviral prophylaxis for HBsAg-positive patients.

Antiviral therapy is indicated for patients with active hepatitis (elevated ALT, significant fibrosis, or HBV DNA above threshold). First-line agents are tenofovir disoproxil fumarate (TDF), tenofovir alafenamide (TAF — preferred in renal/bone disease), and entecavir — all highly effective, well-tolerated, and with low resistance rates when taken consistently. Treatment suppresses HBV DNA to undetectable levels but rarely eliminates HBsAg (functional cure) without prolonged therapy. Pegylated interferon alpha (48 weeks) is an alternative offering finite treatment duration with HBsAg seroconversion potential in selected patients. Immediate antiviral therapy is indicated in pregnant HBsAg-positive women with high viral load to prevent mother-to-child transmission. Tenofovir alafenamide (TAF 25 mg daily) — preferred over TDF in patients with osteoporosis, renal impairment (eGFR below 50), or prior pathological fractures due to its lower renal and bone toxicity. Entecavir (0.5 mg daily for treatment-naive; 1 mg for lamivudine-experienced) has a high genetic barrier to resistance (cumulative resistance 1.2% at 5 years). Maternal antiviral treatment (TAF or TDF from week 24–28 of pregnancy) in high-viraemia HBsAg-positive women (HBV DNA above 200,000 IU/mL) significantly reduces mother-to-child transmission risk.

Chronic hepatitis B causes progressive liver fibrosis, with 15–40% of untreated patients developing cirrhosis within 25 years. Decompensated cirrhosis — marked by ascites, variceal bleeding, hepatic encephalopathy, and jaundice — carries a 50% 2-year mortality without liver transplantation. Hepatocellular carcinoma (HCC) develops at an annual rate of 2–5% in patients with HBV-related cirrhosis — HBV is the leading cause of liver cancer globally, responsible for approximately 50% of all HCC cases. HBV can also cause HCC in non-cirrhotic patients (unique among viral hepatitis), particularly with high viral loads or certain HBV genotypes (B and C). Acute liver failure (fulminant hepatitis) occurs in 0.5–1% of acute HBV infection and requires emergency liver transplantation. Extrahepatic manifestations of HBV include polyarteritis nodosa (systemic vasculitis), membranous nephropathy (immune complex deposition in glomeruli), and cryoglobulinemia.

All individuals with confirmed hepatitis B infection (positive HBsAg) should be referred to a hepatologist or gastroenterologist for specialist assessment of disease activity, liver fibrosis staging, and antiviral treatment eligibility — even if the patient feels well. Seek urgent emergency care for: symptoms of acute liver failure in acute hepatitis B (jaundice with encephalopathy — confusion, drowsiness — and coagulopathy — bleeding tendency), or signs of decompensated cirrhosis (massive ascites, haematemesis from oesophageal varices, severe jaundice with encephalopathy). See a GP promptly for: any new jaundice (yellow skin and eyes), dark urine, pale stools, right upper quadrant pain, or marked fatigue in a person at risk of hepatitis B (IVDU, unprotected sex with multiple partners, healthcare worker, travel to endemic area). People who are HBsAg-positive should be vaccinated against hepatitis A (to prevent superinfection) and should inform their sexual partners and close household contacts to enable testing and vaccination.

The hepatitis B vaccine is highly effective — three doses provide long-term protective immunity in over 95% of recipients. It is recommended universally for infants and for unvaccinated adults at risk. Post-exposure prophylaxis with hepatitis B immunoglobulin (HBIG) plus vaccine is given within 24–48 hours of significant exposure. Infants born to HBsAg-positive mothers receive HBIG and vaccine within 12 hours of birth to prevent perinatal transmission. Screen blood and organ donors. Avoid sharing needles, razors, or toothbrushes. Use condoms for sexual protection. All hepatitis B patients should abstain from alcohol to minimize additional liver damage.