AIM: Hepatitis B virus (HBV) e antigen (HBeAg)-negative variants are reported to harbor 1896 precore mutants, and predict a worse clinical outcome. The aim of this study was to estimate the incidence of a precore mutation (1896) in both patients with chronic hepatitis B (CH-B) infection and blood donors in a tertiary care hospital in south India. METHODS: One hundred and twenty-two consecutive HBV DNA-positive CH-B patients (group I) and 102 HBsAg-positive 'healthy' blood donors (group II) were recruited. Samples found to be positive for HBV DNA were further studied. A nested PCR was used for the detection of HBV DNA. The 1896 precore mutation was detected using PCR-restriction fragment length polymorphism (RFLP). Nucleotide sequencing was performed on representative samples to confirm PCR-RFLP findings. The study population was stratified comprising: group IA: 17 HBeAg-positive CH-B patients; group IB: 105 HBeAg-negative CH-B patients; group IIA: 12 HBeAg-positive blood donors; and group IIB: 55 HBeAg-negative blood donors. RESULTS: There was no significant difference in the HBeAg-positive status between groups I and II. Significantly higher levels of alanine transaminase (ALT) were seen in groups IA and IB than in groups IIA and IIB, respectively (p = 0.033; p = 0.004). A significantly higher proportion of CH-B patients (32.7%) were positive for anti-HBc IgM compared with the blood donor groups (10.4%; p = 0.0006). Among the HBeAg-negative subjects, 69% of the CH-B patients and 65% of the blood donors showed evidence of 1896 precore mutant. This infection included the 1896 mutant exclusively or mixed infection involving the 1896 mutant and 1896 wild-type. DISCUSSION: The absence of detectable HBeAg in most of the viremic blood donors and patients emphasizes the need for HBV DNA testing irrespective of HBeAg status. Mixed infection was detected in a higher proportion (42.6%) of CH-B patients than in blood donors (26.8%; p = 0.031). Among those with mixed infection, a significant proportion (44.2%) of CH-B patients, had ALT levels greater than the upper limit of normal (ULN), as compared with the blood donor groups (16.6%; p = 0.036). CONCLUSIONS: The majority of CH-B patients and blood donors were negative for HBeAg despite their positive HIV DNA status. About two-thirds of the HBsAg-positive blood donors were viremic. Mixed infection was detected more frequently in CH-B patients and appears to be associated with more pronounced liver damage, as indicated by increased ALT levels.
AIM: Hepatitis B virus (HBV) e antigen (HBeAg)-negative variants are reported to harbor 1896 precore mutants, and predict a worse clinical outcome. The aim of this study was to estimate the incidence of a precore mutation (1896) in both patients with chronic hepatitis B (CH-B) infection and blood donors in a tertiary care hospital in south India. METHODS: One hundred and twenty-two consecutive HBV DNA-positive CH-B patients (group I) and 102 HBsAg-positive 'healthy' blood donors (group II) were recruited. Samples found to be positive for HBV DNA were further studied. A nested PCR was used for the detection of HBV DNA. The 1896 precore mutation was detected using PCR-restriction fragment length polymorphism (RFLP). Nucleotide sequencing was performed on representative samples to confirm PCR-RFLP findings. The study population was stratified comprising: group IA: 17 HBeAg-positive CH-B patients; group IB: 105 HBeAg-negative CH-B patients; group IIA: 12 HBeAg-positive blood donors; and group IIB: 55 HBeAg-negative blood donors. RESULTS: There was no significant difference in the HBeAg-positive status between groups I and II. Significantly higher levels of alanine transaminase (ALT) were seen in groups IA and IB than in groups IIA and IIB, respectively (p = 0.033; p = 0.004). A significantly higher proportion of CH-B patients (32.7%) were positive for anti-HBc IgM compared with the blood donor groups (10.4%; p = 0.0006). Among the HBeAg-negative subjects, 69% of the CH-B patients and 65% of the blood donors showed evidence of 1896 precore mutant. This infection included the 1896 mutant exclusively or mixed infection involving the 1896 mutant and 1896 wild-type. DISCUSSION: The absence of detectable HBeAg in most of the viremic blood donors and patients emphasizes the need for HBV DNA testing irrespective of HBeAg status. Mixed infection was detected in a higher proportion (42.6%) of CH-B patients than in blood donors (26.8%; p = 0.031). Among those with mixed infection, a significant proportion (44.2%) of CH-B patients, had ALT levels greater than the upper limit of normal (ULN), as compared with the blood donor groups (16.6%; p = 0.036). CONCLUSIONS: The majority of CH-B patients and blood donors were negative for HBeAg despite their positive HIV DNA status. About two-thirds of the HBsAg-positive blood donors were viremic. Mixed infection was detected more frequently in CH-B patients and appears to be associated with more pronounced liver damage, as indicated by increased ALT levels.
Authors: M R Brunetto; M Giarin; G Saracco; F Oliveri; P Calvo; G Capra; A Randone; M L Abate; P Manzini; M Capalbo Journal: Gastroenterology Date: 1993-09 Impact factor: 22.682
Authors: Abdul Malik; Deepak Kumar; Abdul Arif Khan; Azmat Ali Khan; Anis Ahmad Chaudhary; Syed Akhtar Husain; P Kar Journal: Saudi J Biol Sci Date: 2016-05-10 Impact factor: 4.219