ABSTRACT
Helicobacter pylori [H. pylori] is recognized as the causative agent of peptic and duodenal ulcers, gastric adenocarcinoma, and low-grade mucosa-associated lymphoid tissue [MALT] lymphoma. In the present study, we investigate the genotoxic damage of lysates of H, pylori in human B lymphocytes. Human B lymphocytes were treated with 0, 10, 20, and 30 microg/mL of total protein concentration of lysates obtained from H. pylori isolates from dyspeptic patients. Direct H. pylori-induced DNA damage was investigated by the in vitro cytokinesis-block micronucleus assay which detects chromosomal fragments and maldistributed whole chromosomes. The total mean micronuclei number [tMMN] observed per 1000 binucleus B cells significantly correlated with increasing protein concentration of H pylori lysates [r[2]=0.994, p=0.006]. The highest tMMN [3.81-fold] was observed in cells treated with 30 microg/mL of H, pylori lysate [12.43 +/- 1.91] when compared with the control [3.26 +/- 0.48]. This study provides evidence of the direct effect of H, pylori in chromosomal breakage of human B lymphocytes, which might lead to the development of abnormal B cells. Long-term infection by H. pylori has been implicated in epithelial cell damage as a result of continuous induction of the immune system by bacterial antigens. However, the results of this study propose that persistent H. pylori infection could also directly damage B lymphocyte DNA from which gastric MALT lymphoma arises
ABSTRACT
The level of HBsAg in some chronic hepatitis B virus [HBV]-infected individuals may decline over time so that it is not detectable in serum. To assess the efficacy of HBV vaccine in those who lost their HBsAg without seroconverssion to anti-HBs antibody. From April 1993 to December 2008, of 1603 chronic HBV-infected individuals, 34 [22 men and 12 women] became HBsAg-negative in follow-up visits, with no detectable anti-HBs antibody and HBV DNA in their sera. They received HBV vaccination at 0, 1 and 6 months [case group]. Fifty-two subjects [30 men and 22 women] who were negative for HBsAg, anti-HBs and anti-HBc antibody, received HBV vaccination according to the said schedule [control group]. Anti-HBs antibody was assessed one month after the last dose of vaccination in the both groups. The mean +/- SD age of the case and control groups was 38 +/- 12.7 and 33.4 +/- 8.6 years, respectively [p=0.07]. The sex distribution between these two groups were similar [p=0.652]. The mean +/- SD years of follow-up for the case group was 7.6 +/- 4.5 years. Anti-HBs antibody level >/= 10 IU/L was found in 8 [24%] subjects in the case group and in 45 [87%] in the control group [p<0.001]. The mean +/- SD anti-HBs antibody level in the case group was 68 +/- 32.66 and in the control group 344.6 +/- 38.9 IU/L [p<0.001]. We found that nearly 24% of chronic HBsAg-positive subjects who lost their HBsAg responded to HBV and the remaining cases need to be followed for occult HBV infection