Hepatitis B & C

Our hepatitis management programme at Shree Hospitals is structured around five steps that move from accurate virological characterisation through liver disease staging, treatment indication assessment, antiviral therapy initiation and monitoring, and long-term surveillance for complications.

 

The majority of patients referred with "hepatitis B positive" or "hepatitis C positive" results have not had their viral phase characterised, their liver fibrosis staged, or their treatment eligibility assessed - a critical gap that our approach closes systematically.

 

Step 1 - Complete Virological Characterisation

 

For hepatitis B, complete serological profiling establishes the patient's phase of chronic infection and guides treatment decisions. HBsAg (hepatitis B surface antigen) confirms chronic infection.

 

HBeAg (hepatitis B e antigen) and anti-HBe distinguish HBeAg-positive (immune-active or immune-tolerant) from HBeAg-negative chronic hepatitis B. HBV DNA quantification by PCR measures viral replication level - the primary determinant of treatment eligibility (treatment threshold: ALT elevated AND HBV DNA above 2,000 IU/mL; or DNA above 20,000 IU/mL regardless of ALT; or advanced fibrosis regardless of viral level).

 

Anti-HBc (IgG) confirms past exposure; anti-HBs confirms immunity. HDV co-infection is tested by anti-delta antibody in all HBsAg-positive patients from endemic regions. For hepatitis C, the diagnostic pathway begins with anti-HCV antibody (positive in chronic infection and past resolved infection); HCV RNA by PCR confirms active viraemia; HCV genotyping (Genotypes 1–6, with GT3 predominating in India at approximately 50%) was historically critical for treatment selection but is now less essential with pan-genotypic regimens.

 

Step 2 - Liver Fibrosis Staging

 

Treatment urgency for both HBV and HCV is informed by liver fibrosis stage. All hepatitis B and C patients undergo non-invasive fibrosis assessment: Fibroscan (transient elastography) and FIB-4 index calculation.

 

F3–F4 fibrosis (Fibroscan above 9–10 kPa) changes management significantly - it mandates immediate treatment regardless of HBV DNA level, triggers HCC surveillance, initiates variceal screening endoscopy, and in HCV mandates immediate treatment without waiting for any further workup.

 

NAFLD co-existing with hepatitis B or C - increasingly common in Indian urban patients - accelerates fibrosis progression and is identified by Fibroscan CAP score.

 

Step 3 - Hepatitis B Antiviral Therapy

 

First-line hepatitis B antiviral therapy at Shree Hospitals uses either entecavir (0.5mg daily for treatment-naive patients; 1mg daily in lamivudine-experienced) or tenofovir disoproxil fumarate (TDF 300mg daily) or tenofovir alafenamide (TAF 25mg daily - preferred in patients with renal impairment or osteoporosis risk).

 

All three achieve HBV DNA suppression to undetectable levels in over 95% of patients by 48 weeks and maintain suppression indefinitely with continued therapy.

 

Treatment does not eradicate hepatitis B - cccDNA (covalently closed circular DNA) persists in hepatocyte nuclei as a viral reservoir that cannot be eliminated with current agents. HBsAg loss - "functional cure" -occurs in less than 10% of patients even after many years of therapy but is the endpoint that allows eventual treatment cessation.

 

Step 4 - Hepatitis C Direct-Acting Antiviral (DAA) Cure

 

Hepatitis C treatment in 2024 is transformatively simple compared with the interferon-based era: 8–12 weeks of once-daily oral direct-acting antiviral tablets cure over 95% of all patients across all HCV genotypes.

 

First-line pan-genotypic regimens at Shree Hospitals: sofosbuvir/velpatasvir (SOF/VEL, Epclusa) 400/100mg once daily for 12 weeks in all genotypes including GT3 - the predominant Indian genotype - with or without ribavirin in decompensated cirrhosis; or glecaprevir/pibrentasvir (GLE/PIB, Maviret) 300/120mg once daily for 8 weeks in non-cirrhotic treatment-naive patients of all genotypes, or 12 weeks in compensated cirrhosis.

 

SVR12 - sustained virological response 12 weeks after completing treatment, confirmed by undetectable HCV RNA - is the definition of cure. SVR12 dramatically reduces liver-related mortality, decompensation risk, and HCC risk, though existing cirrhosis does not regress completely and HCC surveillance continues even after cure in cirrhotic patients.

 

Step 5 - Long-Term Monitoring and HCC Surveillance

 

Hepatitis B patients on antiviral therapy require 3-monthly monitoring during the first year (HBV DNA, ALT, eGFR and phosphate for patients on TDF given its renal tubular effects), then 6-monthly monitoring in stable suppression.

 

HBeAg seroconversion (loss of HBeAg and development of anti-HBe) is a treatment milestone associated with lower long-term HCC risk, though not treatment cessation in most patients.

 

HCC surveillance - 6-monthly ultrasound with AFP - is mandatory for all HBV cirrhotics and for HBV patients with significant fibrosis (F3–F4) or those with HBsAg positivity combined with HCC family history or age above 40 in males/50 in females even without cirrhosis.

 

Post-SVR12 hepatitis C patients with cirrhosis continue 6-monthly HCC surveillance indefinitely - cure reduces but does not eliminate the elevated cirrhotic HCC risk.