This prospective survey suggests that demographics, viral, and host factors in patients with chronic HCV infection are highly variable in India and pose significant challenges for the implementation of broad-scale screening and treatment initiatives.

Background and aimsNon-alcoholic fatty liver disease (NAFLD) is remarkably increasing in developing countries like India, in parallel with the increasing incidence of obesity. Lifestyle modification is a recommended treatment for NAFLD. In most of the previous studies, improvement after lifestyle modification was assessed by liver fibrosis through liver biopsy, but we cannot do a serial liver biopsy in every NAFLD patient. Liver fibrosis can also be assessed by fibroscan non-invasively in NAFLD. This study was designed to evaluate the effect of lifestyle modification on liver enzymes and Fibroscan values in a population with NAFLD.MethodsInitially, 50 NAFLD patients were included in this prospective follow-up study; however, after 6 months of lifestyle modification, only 39 participants were studied. During both the first and second consultations, Fibroscan was carried out. All participants underwent a careful interview, anthropometry measurements and radiological and biochemical tests during every consultation.ResultsAfter 6 months of lifestyle modification, Fibroscan values improved significantly (8.31 ± 0.11kPa vs 7.87 ± 0.12kPa, p=0.009). Alanine aminotransferase (ALT) values also showed improvement during the second consultation (97.25 ± 2.62 U/L vs 66.69 ± 3.95 U/L, p <0.001).ConclusionMeasured by Fibroscan and liver enzymes, it has been found that lifestyle modification is an effective therapy to downgrade hepatic injury in NAFLD patients. Serial Fibroscan can be used to assess the treatment response in NAFLD patients due to its non-invasive nature.

Lifestyle modification improves the hepatic steatosis, and CAP can be used to detect the improvement of hepatic steatosis during follow-up in patients with NAFLD on lifestyle modification. There is no relation between CAP and Fibroscan score in NAFLD patients. Only BMI and weight can predict CAP value independently.

SUMMARYWe investigated an unprecedented outbreak of fulminant hepatitis B virus (HBV) that occurred in Modasa, Gujarat (India) in 2009. Genomic analysis of all fulminant hepatic failure cases confirmed exclusive predominance of subgenotype D1. A1762T, G1764A basal core promoter (BCP) mutations, insertion of isoleucine after nt 1843, stop codon mutation G1896A, G1862T transversion plus seven other mutations in the core gene caused inhibition of HBeAg expression implicating them as circulatingprecore/BCP mutant virus. Two rare mutations at amino acids 89 (Ile→Ala) and 119 (Leu→Ser) in addition to other mutations in thepolymerase (pol)gene may have caused some alteration in either of fourpolgene domains to affect encapsidation of pregenomic RNA to enhance pathogenicity. Sequence similarity among patients' sequences suggested an involvement of a single hepatitis B mutant strain/source to corroborate the finding of gross and continued usage of HBV mutant-contaminated syringes/needles by a physician which resulted in this unprecedented outbreak of fulminant hepatitis B. The fulminant exacerbation of the disease might be attributed to mutations in the BCP/precore/coreandpolgenes that may have occurred due to selection pressure during rapid spread/mutation of the virus.

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