Change in insulin resistance according to virological response during antiviral treatment for hepatitis C virus infection

SummaryBackgroundHepatitis C virus (HCV) infection can lead to increased insulin resistance, but the dynamics of insulin resistance in HCV-infected patients receiving pegylated interferon plus ribavirin remain elusive.MethodsThis prospective study enrolled HCV-infected patients who received pegylated interferon plus ribavirin. Patients were classified according to the attainment of sustained virological response (SVR). Insulin resistance was measured using homeostatic model assessment-insulin resistance (HOMA-IR). The change in HOMA-IR at baseline, the end of treatment, and 24 weeks after the end of treatment was compared in patients who achieved SVR and those who did not.ResultsA total of 65 patients participated in this study, of which 46 (71%) achieved SVR. Overall, The HOMA-IR changed significantly during antiviral therapy, with the median values [interquartile range (IQR)] of 3.7 (1.6–10.0) prior to the treatment, 1.5 (0.8–2.9) at the end, and 1.6 (0.9–3.1) at 24 weeks after completion of therapy. However, only patients who achieved SVR had significant off-therapy reduction of HOMA-IR, with median values of 1.3 (IQR, 0.7–2.6) at 24 weeks off therapy and 3.6 (IQR, 1.5–9.9) at baseline (p < 0.0001). In those without SVR, the HOMA-IR measured 24 weeks after treatment completion (median, 2.2; IQR, 1.9–4.7) did not differ from baseline values (median, 3.9; IQR, 2.2–10.0; p = 0.5).ConclusionDual therapy with pegylated interferon plus ribavirin ameliorated IR in HCV-infected patients, but the off-therapy improvement of IR was limited to those who attained SVR

Endoscopic Submucosal Dissection for Gastric Epithelial Tumors: A Multicenter Study in Taiwan

Background/PurposeEndoscopic submucosal dissection (ESD) is an advanced endoscopic procedure to resect early gastric cancer (EGC). The purpose of this study was to determine the effectiveness and complications of ESD for gastric epithelial tumors in Taiwan.MethodsWe retrospectively analyzed the efficacy and outcome of ESD in patients who received ESD for gastric epithelial tumors between June 2004 and August 2007.ResultsA total of 70 patients with gastric epithelial tumors were treated by ESD. The mean age was 66.5 ±12.9 years (range, 35–84 years). The mean size of the gastric epithelial tumors was 1.85 ± 0.81 cm. The mean size of resected specimens was 3.26 ± 1.39 cm. The one-piece resection rate was 91.4% (64/70). The median operation time was 92.4 minutes. The complicating bleeding and perforation rates were 5.7% (4/70) and 4.3% (3/70), respectively. Emergency surgery was performed for three patients with perforations. The local recurrence rate of gastric cancer was 2.8%. Except for one patient who died of congestive heart failure and another who died of stroke, the remaining 68 patients (97.1%) survived.ConclusionESD is a promising local curative treatment option for EGC in Taiwan but it still carries risks of perforation and bleeding. The education and learning curve of endoscopists will improve the outcome of this procedure

Induction of cyclooxygenase-2 overexpression in human gastric epithelial cells by Helicobacter pylori involves TLR2/TLR9 and c-Srcdependent nuclear factor-

ABSTRACT Gastric epithelial cells were incubated with a panel of clinical isolates of Helicobacter pylori, including nonulcer dyspepsia with gastritis (HS, n ϭ 20), gastric ulcer (HU, n ϭ 20), duodenal ulcer (HD, n ϭ 21), and gastric cancer (HC, n ϭ 20). HC strains induced a higher cyclooxygenase-2 (COX-2) expression than those from HS, HD, and HU. The bacterial virulence factors and the host cellular pathways were investigated. Virulence genes of iceA, vacA, babA2, cagA 3Ј repeat region, and hrgA failed to show any association with the disease status and COX-2 expression. Methylation-specific polymerase chain reaction revealed HC strains not affecting the methylation status of COX-2 promoter. Nuclear factor (NF)-B, NF-interleukin 6, and cAMP response element were found to be involved in COX-2 induction. We explored a novel NF-B activation pathway. The mutants of TLR2 and TLR9, but not TLR4, inhibited H. pyloriinduced COX-2 promoter activity, and neutralizing antibodies for TLR2 and TLR9 abolished H. pylori-induced COX-2 expression