Low Viral Load Does Not Exclude Significant Liver Damage in Patients with Chronic HBV Infection in Bangladesh

Background: In general, it is assumed that patients with chronic hepatitis B virus (HBV) infection with high viral load exhibit increased liver damages. Accordingly, the treatment guidelines emphasize on reducing viral load in chronic HBV carriers. The ethical and scientific basis of these observations was mainly accumulated from investigations from developed countries of the world. More than 80% chronic HBV carriers live in the developing nations of the world, but little is known about relationship between HBV viral load and extent of liver damages in these countries. In this study, we addressed this issue to provide insights about this. Methods: In this retrospective study we reviewed the records of 210 chronic hepatitis B (CHB) patients from our pool of 561 Bangladeshi CHB patients. All of these 210 patients had low HBV DNA (<105 copies/ml by PCR). Of them 16 were HBeAg +ve and rest 194 HBeAg -ve. They have also been tested for other serologic markers of HBV (i.e. HBsAg, anti-HBe), HCV (i.e. anti-HCV) and serum alaninetransaminase (ALT) level. All patients also underwent per-cutaneous liver biopsy. Results: 37.5% (6/16) HBeAg +ve patients with low HBV DNA had significant hepatic necro-inflammation (HAI-NI ≥7), whereas this figure was 31.44% (61/194) in case of HBeAg -ve patients. On the other hand significant hepatic fibrosis (HAI-F ≥3) was observed in 31.25% (5/16) and 14.4% (28/194) in HBeAg +ve and -ve patients respectively. Conclusion: This study shows that a correlation could not be established between viral load and liver damage in patients with CHB in Bangladesh. A significant percentage of patients with low HBV DNA may have marked hepatic necro-inflammation and fibrosis, more so in case of HBeAg +ve CHB. Further study may be needed to find out the influence of other factors on liver damages in CHB patients in developing nations like Bangladesh, where about 8 million chronic HBV carriers are living. Most of these patients have not been characterized and treatment modalities have not been defined for them. Our study may suggest the research direction for management of these cases. Key Words: Low HBV DNA; Chronic hepatitis B; Hepatic necro-inflammation; Hepatic fibrosis.DOI: 10.3329/bsmmuj.v1i1.3693 BSMMU J 2008; 1(1): 19-2

25 Low Viral Load Does Not Exclude Significant Liver Damage in Patients with Chronic HBV Infection in Bangladesh

Background: In general, it is assumed that patients with chronic hepatitis B virus (HBV) infection with high viral load exhibit increased liver damages. Accordingly, the treatment guidelines emphasize on reducing viral load in chronic HBV carriers. The ethical and scientific basis of these observations was mainly accumulated from investigations from developed countries of the world. More than 80 % chronic HBV carriers live in the developing nations of the world, but little is known about relationship between HBV viral load and extent of liver damages in these countries. In this study, we addressed this issue to provide insights about this. Methods: In this retrospective study we reviewed the records of 210 chronic hepatitis B (CHB) patients from our pool of 561 Bangladeshi CHB patients. All of these 210 patients had low HBV DNA (<105 copies/ml by PCR). Of them 16 were HBeAg +ve and rest 194 HBeAg-ve. They have also been tested for other serologic markers of HBV (i.e. HBsAg, anti-HBe), HCV (i.e. anti-HCV) and serum alaninetransaminase (ALT) level. All patients also underwent per-cutaneous liver biopsy. Results: 37.5 % (6/16) HBeAg +ve patients with low HBV DNA had significant hepatic necro-inflammation (HAI-NI>7), whereas this figure was 31.44 % (61/194) in case of HBeAg-ve patients. On the other hand significant hepatic fibrosis (HAI-F>3) was observed in 31.25 % (5/16) and 14.4 % (28/194) in HBeAg +ve and-ve patients respectively. Conclusion: This study shows that a correlation coul

Antimicrobial Susceptibility of Helicobacter pylori Strains Isolated in Bangladesh

Antimicrobial susceptibility of 120 Helicobacter pylori isolates to metronidazole, tetracycline, clarithromycin, and amoxicillin was determined, and 77.5, 15, 10, and 6.6% of the isolates, respectively, were resistant. Only rdxA inactivation and both rdxA and frxA inactivation were responsible for metronidazole resistance in 66% (8 of 12) and 33% (4 of 12) of the isolates, respectively