In India, acute hepatitis B with delta-agent without hepatic coma is managed by infectious diseases. Hepatitis B is a viral infection of the liver caused by hepatitis B virus (HBV), a small DNA virus transmitted through blood, sexual contact, and mother-to-child exposure. WHO estimates 296 million people live with chronic hepatitis B and the infection causes around 1.1 million deaths each year from cirrhosis and hepatocellular carcinoma.
Hepatitis B (ICD-10: B16 acute, B18.1 chronic) is an infection of hepatocytes caused by hepatitis B virus (HBV), a partially double-stranded circular DNA virus in the Hepadnaviridae family. The virus has at least eight major genotypes (A-H) and several subgenotypes with regional clustering: genotypes A, D, E predominate in Africa and Europe; B and C in Asia; F and H in the Americas. HBV does not directly kill hepatocytes; liver injury follows the host immune response to infected cells. Infection is divided clinically into acute hepatitis B (lasting up to 6 months from exposure) and chronic hepatitis B (persistent hepatitis B surface antigen positivity for more than 6 months).
The key symptoms of Acute hepatitis B with delta-agent without hepatic coma are: Two-thirds of adult acute hepatitis B infections are asymptomatic; the remaining third experience the prodrome and icteric phases described below., Prodromal flu-like illness with fatigue, low-grade fever, nausea, anorexia, right-upper-quadrant abdominal pain, headache, and joint pains 1-4 weeks before jaundice., Urticaria, polyarthralgia, and serum-sickness-like syndrome in roughly 10% of acute cases, driven by immune complexes., Yellowing of skin and sclera, dark urine, and pale stools developing over 1-2 weeks with peak transaminases at 10-100× upper limit of normal., Right-upper-quadrant tenderness with a slightly enlarged tender liver during the icteric phase., In chronic hepatitis B, most patients are entirely asymptomatic for decades; symptoms (fatigue, mild right-upper-quadrant discomfort) appear when significant fibrosis or active hepatitis is present., Symptoms and signs of cirrhosis in advanced chronic disease: ascites, peripheral oedema, easy bruising, spider naevi, palmar erythema, splenomegaly, encephalopathy..
Diagnosis combines clinical assessment with a defined panel of serological markers, viral nucleic acid testing, and biochemical and imaging staging of liver disease. The initial test is HBsAg: positive HBsAg indicates current HBV infection (acute or chronic). HBsAg present for more than 6 months establishes chronic infection. The complementary panel — anti-HBs (immunity from prior infection or vaccination), anti-HBc total (past or current infection), IgM anti-HBc (acute infection), HBeAg (active replication and high infectivity), anti-HBe (often associated with lower viral replication) — defines the phase of infection. Quantitative HBV DNA by real-time PCR measures viral load and guides treatment decisions and monitoring. Liver function tests (ALT, AST, GGT, alkaline phosphatase, bilirubin, albumin, INR) and platelets define disease activity and synthetic function. Non-invasive markers of fibrosis (FIB-4, APRI), transient elastography (Fibroscan), or shear-wave elastography stage fibrosis without biopsy. Liver biopsy is reserved for ambiguous cases or research. All chronic HBV patients are also tested for HIV, hepatitis C, hepatitis D (HBV/HDV coinfection in 5-10% of chronic HBV), and hepatocellular carcinoma surveillance (abdominal ultrasound and alpha-fetoprotein every 6 months in patients with cirrhosis, family history of HCC, or other high-risk features). Pregnant women are screened universally for HBsAg at first antenatal visit; HBsAg-positive women with HBV DNA above 200,000 IU/mL receive tenofovir disoproxil fumarate from week 28 of pregnancy to reduce mother-to-child transmission. Genotype testing is helpful when interferon therapy is considered (genotype A responds best) but not routine for nucleos(t)ide treatment.
Outcome depends on age at infection, phase of disease, and timely treatment. Adult acute hepatitis B resolves spontaneously in over 95% of immunocompetent adults; chronic infection develops in 90% of perinatally infected infants and 25-50% of children infected aged 1-5. Without treatment, roughly 8-20% of chronic HBV patients develop cirrhosis over 20-30 years; once cirrhosis is established, the annual risk of hepatocellular carcinoma is 2-5%. Effective antiviral therapy with TAF, TDF, or entecavir suppresses HBV DNA in over 95% of patients, normalizes ALT, halts or reverses fibrosis (compensated cirrhosis can regress on long-term therapy), and reduces but does not eliminate HCC risk — surveillance every 6 months continues even on therapy. HBsAg loss (functional cure) is uncommon (under 1% per year on NA therapy, 3-7% with pegIFN) but profoundly reduces HCC and disease-related death. HBV/HDV coinfection progresses faster — 10-20 year cumulative cirrhosis risk approaches 50-70% — and benefits from bulevirtide and pegIFN combinations. Liver transplantation cures end-stage HBV with 5-year post-transplant survival of 75-85% under modern antiviral prophylaxis. The WHO 2030 elimination targets (90% reduction in new infections, 65% reduction in mortality) are achievable with universal birth-dose vaccination, screen-and-treat expansion, and access to affordable generic nucleos(t)ide analogues.
Hepatology referral is recommended for all patients with chronic hepatitis B for staging of liver disease, treatment decision-making, HCC surveillance, and management of comorbidities. Patients with cirrhosis, hepatic decompensation, HCC, HBV/HDV coinfection, complex pregnancy, or pre-immunosuppression need specialist care.
Find specialists →Acute hepatitis B: jaundice and acute symptoms resolve over 2-12 weeks; HBsAg clearance occurs in over 95% of immunocompetent adults within 6 months. Chronic hepatitis B on antiviral therapy: HBV DNA suppression within 6-12 months; ALT normalization within 6-18 months; fibrosis improvement over 1-5 years; HBsAg loss is uncommon and slow (sometimes >10 years on NA). After liver transplant: graft function recovers over weeks; HBV prophylaxis lifelong.
Regular moderate aerobic exercise (150 minutes per week) and resistance training reduce hepatic steatosis, support weight management, and improve quality of life. Vigorous exercise is safe in chronic HBV unless decompensated cirrhosis or active flare is present. Avoid contact sports during severe thrombocytopenia.
Choose a hepatologist or infectious disease specialist familiar with current AASLD, EASL, or APASL guidelines and with access to FibroScan, HBV DNA quantitation, and HCC surveillance imaging. For transplant evaluation, work with a designated transplant centre.
Medically reviewed by AIHealz Medical Editorial Board · May 13, 2026
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