The effect of antioxidants on Helicobacter pylori eradication: A systematic review with meta-analysis.

BACKGROUND: The efficacy and safety of the addition of antioxidants to triple or quadruple therapy were unclear. MATERIALS AND METHODS: This systematic review was performed in accordance with the PRISMA 2009 guidelines. A systematic search of PubMed, EMBASE, and the Cochrane Library databases was conducted to identify potentially relevant publications using the following keywords: ([Helicobacter pylori] or [H. pylori] or [Hp]) and ([antioxidant] or [vitamin] or [N-acetylcysteine] or [curcumin] or [cranberry]). The primary end-point of this study was to evaluate the efficacy of the addition of antioxidants to triple or quadruple therapy according to ITT and PP analysis. The second end-points were side effects and the comparative efficacy in terms of H. pylori eradication according to different antioxidant and antibiotic combinations. RESULTS: We included 9 studies with 1260 participants. The total eradication rate of H. pylori in the group combining eradication therapy with antioxidants was not superior to that without antioxidants according to the ITT (pooled RR [95% CI] = 1.17 [0.99-1.38]; P = 0.07) and PP analysis (pooled RR [95% CI] = 1.15 [0.99-1.34; P = 0.07]. There were no differences regarding side effects between the two groups (pooled RR [95% CI], 1.36 [0.81-2.28]; P = 0.24). However, the eradication regimen with vitamin supplementation (1400 mg/day) showed a significant, superior efficacy in eradication relative to those without supplementation (pooled RR [95% CI] = 1.57 [1.35, 1.84]; P < 0.01). In particular, in the amoxicillin-clarithromycin-based subgroup, the crude H. pylori eradication rate determined by ITT analysis was 81.3% and 68.6% for eradication therapy with and without antioxidant supplementation, respectively, which was a statistically significant difference (pooled RR [95% CI] = 1.23 [1.02-1.49]; P = 0.03). CONCLUSIONS: The addition of antioxidants (vitamin, N-acetylcysteine, curcumin, cranberry) to amoxicillin-clarithromycin-based therapy could improve the eradication rate, and vitamin supplementation might be effective at a high dosage. However, antioxidant supplements have no impact on improving side effects.

Analysis of key genes and signaling pathways involved in Helicobacter pylori-associated gastric cancer based on The Cancer Genome Atlas database and RNA sequencing data.

BACKGROUND: Helicobacter pylori (H. pylori) infection is associated with the development of gastric cancer, although the mechanism is unclear. Herein, this study aimed to clarify the key genes and signaling pathways involved in H. pylori pathogenesis based on The Cancer Genome Atlas (TCGA) database and RNA sequencing analysis. MATERIALS AND METHODS: Forty-nine gastric cancer samples (16 with H. pylori and 33 without H. pylori) and 35 cancer-adjacent normal samples from TCGA database were analyzed by bioinformatics. The differentially expressed genes between H. pylori-positive and H. pylori-negative patients were verified in 18 gastric cancer (GC) samples (9 with H. pylori and 9 without H. pylori), which were analyzed using RNA sequencing. Survival analysis was carried out to explore associations between the differentially expressed genes and prognosis. Bioinformatics analysis was performed to determine the signaling pathways associated with H. pylori. RESULTS: The baseline level of clinical features from TCGA database and RNA sequencing showed no differences between the H. pylori-positive and H. pylori-negative GC groups (P > 0.05). TP53 was shown to be upregulated in the H. pylori-positive group in both TCGA database and RNA sequencing data, which also showed higher expression in the GC tissues than in adjacent normal tissues (P < 0.05). CCDC151, CHRNB2, GMPR2, HDGFRP2, and VSTM2L were shown to be downregulated in the H. pylori-positive group by both TCGA database and RNA sequencing, which also showed lower expression in the GC tissues than in adjacent normal tissues (P < 0.05). GC patients with low expression levels of HDGFRP2 had a poor prognosis (P < 0.05). Thirty-three signaling pathways and 10 biological processes were found to be positively associated with H. pylori infection (P < 0.05, FDR < 0.05). CONCLUSIONS: These results indicate that some genes (TP53, CCDC151, CHRNB2, GMPR2, HDGFRP2, VSTM2L) and previously unidentified signaling pathways (eg, the Hippo signaling pathway) might play an important role in H. pylori-associated GC.