Hepatitis B

Also known as: Hep B

Infection caused by hepatitis B virus (HBV, hepadnavirus, partially double-stranded DNA), transmitted via percutaneous/mucosal exposure to infected blood/body fluids; perinatal (major route in endemic regions), sexual contact, needle-sharing, occupational exposure.

Risk of chronicity is inversely related to age at infection: ~90% of perinatally infected infants become chronic carriers vs. ~5% of immunocompetent adults.

Classified by phase/course:

Acute hepatitis B: self-limiting in most immunocompetent adults, resolves within 6 months
Chronic hepatitis B: HBsAg persists >6 months; further subdivided by phase — immune-tolerant, immune-active (HBeAg-positive or -negative chronic hepatitis), inactive carrier state, resolved
Fulminant hepatitis: rare, acute liver failure

Acute infection: often asymptomatic/subclinical (especially in young children); when symptomatic: prodrome of malaise, anorexia, nausea, low-grade fever, followed by jaundice, dark urine, pale stools, right upper quadrant discomfort, hepatomegaly
Extrahepatic manifestations (immune complex-mediated): polyarteritis nodosa, membranous glomerulonephritis, serum sickness-like syndrome (rash, arthralgia ; can precede jaundice)
Fulminant hepatic failure (rare, <1%): coagulopathy, encephalopathy, jaundice : high mortality without transplant
Chronic infection: often asymptomatic for years/decades; may present with fatigue, or with complications of cirrhosis/hepatocellular carcinoma at advanced stage
Extrahepatic in chronic infection: cryoglobulinemia, vasculitis

Serological markers; interpretation is key:

HBsAg: surface antigen, marker of current infection (acute or chronic) ; positive >6 months defines chronic infection
Anti-HBs: surface antibody, indicates immunity (from resolved infection or vaccination)
HBeAg: marker of active viral replication/high infectivity
Anti-HBe: seroconversion marker, generally indicates lower replication (though precore/core promoter mutant strains can have high viral load despite anti-HBe positivity)
Anti-HBc IgM: acute/recent infection marker
Anti-HBc IgG: past or chronic infection marker (persists lifelong)
HBV DNA (viral load): quantifies replication, guides treatment decisions and monitors response

Interpretation patterns:

Acute infection: HBsAg+, IgM anti-HBc+, HBeAg often +
Chronic infection: HBsAg+ (>6 months), IgG anti-HBc+, IgM anti-HBc-
Resolved infection: HBsAg-, anti-HBs+, anti-HBc+ (IgG)
Vaccinated (immune): anti-HBs+ only, anti-HBc negative
"Window period": HBsAg negative, anti-HBs not yet positive, IgM anti-HBc positive (only marker detectable)

Additional workup for chronic infection: LFTs, HBV DNA level, HBeAg/anti-HBe status, HDV co-infection screening (anti-HDV, especially in endemic areas/high-risk groups), HIV/HCV co-infection screening, liver fibrosis assessment (transient elastography or biopsy), HCC surveillance (AFP + ultrasound 6-monthly if cirrhotic or high-risk per guidelines; e.g., Asian males >40, African >20, family history of HCC).

Differentials for acute presentation: hepatitis A/C/E, drug-induced liver injury, autoimmune hepatitis, alcohol-related hepatitis, EBV/CMV hepatitis.

Acute hepatitis B: supportive care in most cases (rest, hydration, avoid hepatotoxic substances/alcohol); antivirals generally not required unless severe/fulminant (coagulopathy, encephalopathy); then entecavir/tenofovir and urgent liver transplant unit referral.

Chronic hepatitis B ; treatment indicated based on HBV DNA level, ALT, fibrosis stage, and HBeAg status (per AASLD/EASL/WHO criteria):

Generally treat if: HBV DNA >2000 IU/mL with elevated ALT and/or significant fibrosis/cirrhosis on biopsy or non-invasive assessment; all patients with cirrhosis (compensated or decompensated) regardless of viral load/ALT; HBeAg-positive with high viral load and elevated ALT persisting
First-line antivirals (high barrier to resistance, preferred):
Tenofovir disoproxil fumarate 300mg od, or tenofovir alafenamide 25mg od (better renal/bone safety profile)
Entecavir 0.5mg od (1mg od if lamivudine-experienced/resistant)
Pegylated interferon-alfa-2a: alternative for selected patients (younger, HBeAg-positive, low viral load, wanting finite treatment duration) ; subcutaneous weekly injection for 48 weeks, more side effects (flu-like symptoms, cytopenias, mood disturbance) but potential for HBsAg loss/functional cure in a subset
Treatment typically long-term/indefinite with nucleos(t)ide analogs (especially in cirrhosis) ; stopping criteria complex, specialist-guided, risk of flare/decompensation on discontinuation

Monitoring: HBV DNA, LFTs every 3–6 months on treatment; HCC surveillance (ultrasound ± AFP) 6-monthly in cirrhotic patients or high-risk groups regardless of treatment status; renal function monitoring on tenofovir.

Prevention:

Vaccination: universal infant vaccination (birth dose within 24 hours critical for perinatal transmission prevention), catch-up vaccination for unimmunized, at-risk adults
Hepatitis B immunoglobulin (HBIG): for neonates born to HBsAg-positive mothers (combined with vaccine, within 12 hours of birth), post-exposure prophylaxis (needlestick, sexual exposure) in non-immune individuals
Pregnancy: maternal HBV DNA >200,000 IU/mL : offer tenofovir in 3rd trimester to reduce perinatal transmission risk (in addition to infant HBIG + vaccine)
Screen and vaccinate household/sexual contacts of chronic carriers
Standard precautions for healthcare workers, needle-exchange programs, blood product screening

Referral: hepatology/gastroenterology for all chronic HBV requiring treatment decision, cirrhosis, HCC surveillance, or coinfection (HIV/HCV/HDV).

References

AASLD / EASL / WHO hepatitis B guidelines

Clinical toolsCalculators

BMI GCS EDD Parkland Formula

Corrected Sodium Corrected Calcium Anion Gap Creatinine Clearance Insulin Calculations qSOFA Wells PE Wells DVT CHA₂DS₂-VASc HAS-BLED CURB-65 Centor/McIsaac

Alcoholic Hepatitis

Alcohol-associated (alcoholic) hepatitis is an acute inflammatory liver injury resulting from heavy alcohol consumption, typically in the context of a recent significant increase in intake superimposed on a background of chronic alcohol use, representing a distinct acute clinical syndrome from the broader spectrum of alcohol-related liver disease that also includes steatosis and cirrhosis (see that entry).

Severity ranges from mild, self-limiting disease to severe disease with high short-term mortality.

LFTs show a characteristic pattern: AST typically elevated but rarely above 300 to 400 IU/L, with an AST:ALT ratio greater than 2 (reflecting relative ALT deficiency from alcohol-related pyridoxal-5-phosphate depletion), alongside elevated bilirubin and, in more severe disease, prolonged INR
FBC often shows a neutrophilic leukocytosis (can mimic sepsis and should prompt active screening for concurrent infection, which is common and important not to miss) and macrocytic anemia
Severity is stratified using the Maddrey discriminant function: DF = 4.6 × (patient's PT − control PT in seconds) + serum bilirubin (mg/dL); a DF of 32 or above indicates severe disease with significant short-term mortality risk and is the threshold used to consider corticosteroid therapy
The Glasgow Alcoholic Hepatitis Score and MELD score are alternative/complementary severity and prognostic tools used in some centers
Liver biopsy (transjugular, given the frequent coagulopathy) is reserved for diagnostic uncertainty rather than routine use
Active screening for infection (given the elevated risk and the fact that untreated infection is a contraindication to corticosteroid therapy) and for other alcohol-related complications (Wernicke's encephalopathy risk, pancreatitis)

Alcohol abstinence is the single most important intervention, with addiction support and management of alcohol withdrawal (see general alcohol withdrawal principles) initiated concurrently
Nutritional support is essential given near-universal malnutrition in this population, with adequate protein intake (1.2 to 1.5 g/kg/day, not restricted despite hepatic impairment, given evidence that protein restriction worsens outcomes) and thiamine supplementation (given before or with any glucose administration, to prevent precipitating Wernicke's encephalopathy)
Corticosteroids: prednisolone 40 mg PO od for 28 days, then tapered, is considered for severe disease (DF ≥32) in the absence of active infection, GI bleeding, or renal failure, following screening and treatment of any infection first; benefit is modest and short-term (improved 28-day but not clearly improved 90-day or long-term survival in more recent trial evidence), and response is reassessed at day 7 using the Lille score, with corticosteroids stopped if the Lille score indicates non-response, since continued treatment offers no benefit and adds infection risk in non-responders
Pentoxifylline was historically used as an alternative or adjunct but current evidence does not support a clear survival benefit, and it has been largely superseded by the corticosteroid-with-Lille-score-reassessment approach above
Screen for and treat infection aggressively given the significantly elevated risk and its major impact on mortality
Liver transplantation is increasingly considered for select patients with severe, corticosteroid-non-responsive alcoholic hepatitis at specialist centers with structured sobriety and psychosocial assessment protocols, a significant shift from historical rigid sobriety-duration requirements
Manage complications of decompensation (ascites, encephalopathy, coagulopathy) per the principles in the Cirrhosis entry

Referral: hepatology for all cases, urgently for severe disease (DF ≥32) given the corticosteroid decision window and mortality risk; addiction services for alcohol use disorder management.

Hepatitis B

Overview

Clinical Features

Diagnosis

Management

Overview

Clinical Features

Diagnosis

Management