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“Background and Aim:  The present study was designed to determine the eradication rate of 10 day sequential therapy in genotypic clarithromycin-resistant Helicobacter pylori group identified by molecular polymerase chain reaction (PCR) detection in Thai patients. Methods:  Between May 2007 and June 2010, patients who had undergone gastroscopic examination at the King Chulalongkorn Memorial

Hospital, for dyspeptic symptoms were recruited. Two biopsy samples from gastric antrum were obtained, one for rapid urease test and another for PCR. PCR-sequencing was performed to determine point mutations in 23S rRNA gene. Patients received 10 day sequential therapy consisting of lanzoprazole 30 mg and amoxicillin 1 g twice daily for 5 days followed by lanzoprazole 30 mg, clarithromycin 500 mg and nitroimidazole 500 mg twice daily for the remaining this website 5 days. Urea breath test (UBT) was performed to assess www.selleckchem.com/products/LDE225(NVP-LDE225).html eradication therapy. Results:  A total of 151 patients (mean age 52.7 years, 75 males and 76 females) were recruited in this study. All patients completed sequential therapy without significant side effects. Point mutations at A2143G and A2142G were detected in 17 patients (11.3%). Overall eradication rate was 94%. The eradication rate in the group with point mutation was significantly lower than the eradication

rate in the group without point mutation (64.7% vs 97.8%; odds ratio = 19.6 and 95% confidence interval = 4.3–88.8; P < 0.0001). Conclusion:  Genotypic clarithromycin resistance was detected in only 11.3% of H. pylori infections in Thailand.

Sequential therapy is highly effective Sitaxentan in clarithromycin-sensitive but is less effective in clarithromycin-resistant H. pylori. PCR-molecular test could be a useful tool to identify antimicrobial resistance for optimizing an eradication regimen. “
“We read with interest the article by Clifford and colleagues in HEPATOLOGY.1 This well-designed study identified genetic factors associated with hepatocellular carcinoma (HCC) or liver cirrhosis (LC). Their analysis isolated a single-nucleotide polymorphism (SNP) for the TPTE2 gene, a PTEN (phosphatase and tensin) homolog encoded by chromosome 13, that differentiates HCC and LC. As for ourselves, we identified sequences near the TPTE2 gene that are replicated in the genome, flawing the interpretation of a genome-wide association study. We have inputted the flanking sequence of the aforementioned SNP rs2880301 (CTTTGCAGCAATCCAG [C/T] CTAAAAGCCTAAAAGC) in the Basic Local Alignment Search Tool (BLAST) from the National Center for Biotechnology Information website. Strikingly, we found total homology with a nucleotide sequence located both on chromosome 13 and the Y chromosome. To rule out that the association found by Clifford et al.