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1.
Indian J Med Microbiol ; 2018 Jun; 36(2): 217-223
Article | IMSEAR | ID: sea-198757

ABSTRACT

Background: Combination of tenofovir disoproxil fumarate (TDF), lamivudine (3TC) and efavirenz (EFV) is preferred in the treatment of HIV/hepatitis B virus (HBV) coinfection. We postulated that a HBV active nucleoside reverse transcriptase (RT) inhibitor/nucleotide RT inhibitor backbone of adefovir dipivoxil (ADV) +3TC would be as effective as TDF +3TC for the Indian population. Objective: ADV + 3TC could be an alternative option for these HIV/HBV coinfected individuals, preserving the dually active TDF + 3TC as second-line nucleoside backbone following failure of the first-line ART. Materials and Methods: This randomised control trial (CTRI/2012/03/002471) was carried out at the ART Centre of Calcutta School of Tropical Medicine, India. Seventy-eight (39 on each arm) treatment-naïve HIV/HBV coinfected patients were randomised to receive either the combination of lamivudine + tenofovir + EFV or lamivudine + adefovir + zidovudine + EFV and followed up for 120 weeks. Results: Median age of the study participants was 36 years (21–62), majority were male (61/78; 78.2%) and heterosexually (39/78; 50%) infected. Baseline characteristics were identical in both arms. There was no statistically significant difference in median aspartate aminotransferase (37 vs. 29.5 U/L), alanine aminotransferase (ALT) (36 vs. 34.5 U/L), ALT normalisation rate (80 vs. 70%), AST to platelet ratio index (0.45 vs. 0.33), CD4 count (508 vs. 427 cells/mm3), HBV DNA suppression (81.8 vs. 70%), hepatitis B e antigen loss (9 vs. 5%), hepatitis B surface antigen seroclearance rate (6.06 vs. 18.75%) and death (3 vs. 3) at 120 weeks between TDF (n = 33) and ADV (n = 32), respectively. Conclusions: Adefovir plus lamivudine is an effective alternative of tenofovir plus lamivudine in long-term HBV treatment outcome in HIV/HBV coinfected patients.

2.
Article in English | IMSEAR | ID: sea-24645

ABSTRACT

This study was undertaken in rats to ascertain the role of zinc as an antiulcerogenic agent employing its more bioavailable gluconate derivative. Pretreatment with zinc gluconate 10 mg/kg body wt orally for three consecutive days, protected against alcohol induced gastric epithelial damage and also significantly prevented non-steroidal anti-inflammatory drugs (NSAID) induced gastric ulcer in rats. The enhanced levels of mucus, and hexosamine and decreased acid output in the gastric secretion of zinc treated rats, increased the gastric mucosal barrier. Studies on the mechanism of action suggested the involvement of -SH groups in producing gastric antisecretory effect. Thus, zinc gluconate at > > 100 microM concentrations inhibited H(+)-ion transport which could be reversed by incorporating beta-mercaptoethanol in the secretory solution (luminal side). On the other hand, beta-mercaptoethanol added from the nutrient side showed no effect on the inhibition of H(+)-transport indicting that the implication of -SH groups may not be the sole factor. Zinc appeared to play a vital and multifaceted protective role in chemically induced gastric ulcer disorders.


Subject(s)
Animals , Anti-Inflammatory Agents, Non-Steroidal/adverse effects , Biological Availability , Biological Transport , Ethanol , Gastric Mucosa/pathology , Gluconates/pharmacokinetics , Indomethacin/adverse effects , Male , Ranidae , Rats , Stomach Ulcer/chemically induced , Zinc/pharmacokinetics
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