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      Association between Helicobacter pylori and end-stage renal disease: A meta-analysis

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          Abstract

          AIM

          To investigate the prevalence and association of Helicobacter pylori ( H. pylori) with end-stage renal disease (ESRD).

          METHODS

          SA comprehensive literature search was completed from inception until October 2016. Studies that reported prevalence, relative risks, odd ratios, hazard ratios or standardized incidence ratio of H. pylori among ESRD patients were included. Participants without H. pylori were used as comparators to assess the association between H. pylori infection and ESRD. Pooled risk ratios and 95%CI was calculated using a random-effect model. Adjusted point estimates from each study were combined by the generic inverse variance method of DerSimonian and Laird.

          RESULTS

          Of 4546 relevant studies, thirty-seven observational studies met all inclusion criteria. Thirty-five cross-sectional studies were included in the analyses to assess the prevalence and association of H. pylori with ESRD. The estimated prevalence of H. pylori among ESRD patients was 44% (95%CI: 40%-49%). The pooled RR of H. pylori in patients with ESRD was 0.77 (95%CI: 0.59-1.00) when compared with the patients without ESRD. Subgroup analysis showed significantly reduced risk of H. pylori in adult ESRD patients with pooled RR of 0.71 (95%CI: 0.55-0.94). The data on the risk of ESRD in patients with H. pylori were limited. Two cohort studies were included to assess the risk of ESRD in patients with H. pylori. The pooled risk RR of ESRD in patients with H. pylori was 0.61 (95%CI: 0.03-12.20).

          CONCLUSION

          The estimated prevalence of H. pylori in ESRD patients is 44%. Our meta-analysis demonstrates a decreased risk of H. pylori in adult ESRD patients.

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          Most cited references53

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          Effect of interleukin 1 polymorphisms on gastric mucosal interleukin 1beta production in Helicobacter pylori infection.

          Although epidemiological studies suggest that interleukin (IL)-1 genetic polymorphisms are involved in Helicobacter pylori-related gastric carcinogenesis, the data are conflicting regarding the effects of these polymorphisms on IL-1beta production. IL-1B-511 polymorphism was genotyped by polymerase chain reaction (PCR)-restriction fragment length polymorphism, and IL-1RN variable number of tandem repeats was determined by PCR. Mucosal IL-1beta levels were measured by enzyme-linked immunosorbent assay. To determine which factors influence mucosal IL-1beta levels, gastric inflammation, and atrophy, multiple regression analyses were performed. We studied 117 H. pylori-infected Japanese patients. Carriers of the IL-1B-511T/T genotype or IL-1RN*2 allele had higher mucosal IL-1beta levels than noncarriers (partial regression coefficient [PRC] +/- SE), TT versus CC: 37.6 +/- 6 [antrum] and 32.1 +/- 6 [corpus] pg/mg protein (P < 0.001 for each), *1/*2 versus *1/*1: 24 +/- 8 [antrum] (P <0.01) and 36.5 +/- 7 [corpus] (P <0.001). Simultaneous carriers of IL-1B-511T/T genotype and IL-1RN*2 allele had the highest IL-1beta levels (82.9 +/- 12 [antrum] and 87.2 +/- 11 [corpus]) and showed a synergistic effect between 2 loci. The *1/*2 carriers were closely related to atrophy (PRC +/- SE; 0.87 +/- 0.4 [antrum] and 0.93 +/- 0.4 [corpus], P < 0.05), whereas being a carrier of the -511T/T genotype was related to severe gastric inflammation. IL-1 genetic polymorphisms influenced H. pylori-related gastric mucosal IL-1beta levels and were related to gastric inflammation and atrophy, factors thought to be important in gastric carcinogenesis.
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            Transmission and epidemiology of Helicobacter pylori.

            Kyle Cave (1996)
            Helicobacter pylori is one of the most common bacterial infections worldwide. However, the majority of those infected do not develop clinical manifestations of disease. This review discusses the epidemiology of the organism in terms of incidence and prevalence, the presumed means of transmission from person to person, and how typing of the organism has helped the epidemiologist. The epidemiology of disorders that are associated with H. pylori is also discussed.
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              Association between Helicobacter pylori infection and metabolic syndrome: a systematic review and meta-analysis.

              To systematically review and quantify the effect of Helicobacter pylori (H. pylori) infection on the risk of metabolic syndrome (MS) and metabolic parameters in individuals with H. pylori infection.
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                Author and article information

                Journal
                World J Gastroenterol
                World J. Gastroenterol
                WJG
                World Journal of Gastroenterology
                Baishideng Publishing Group Inc
                1007-9327
                2219-2840
                28 February 2017
                28 February 2017
                : 23
                : 8
                : 1497-1506
                Affiliations
                Karn Wijarnpreecha, Charat Thongprayoon, Ridhmi Rajapakse, Department of Internal Medicine, Bassett Medical Center, Cooperstown, NY 13326, United States
                Pitchaphon Nissaisorakarn, Department of Internal Medicine, Jacobi Medical Center, Albert Einstein College of Medicine, Bronx, NY 10461, United States
                Natasorn Lekuthai, Department of Medicine, Faculty of Medicine Siriraj Hospital, Mahidol University, Bangkok 10700, Thailand
                Veeravich Jaruvongvanich, Department of Medicine, University of Hawaii, Honolulu, HI 96822, United States
                Kiran Nakkala, Cape Fear Center for Digestive Diseases, P.A., Fayetteville, NC 28312, United States
                Wisit Cheungpasitporn, Division of Nephrology, Department of Internal Medicine, Mayo Clinic, Rochester, MN 55905, United States
                Author notes

                Author contributions: Cheungpasitporn W contributed to conception and design of the study, and critical revision; Wijarnpreecha K, Thongprayoon C, Nissaisorakarn P and Jaruvongvanich V contributed to acquisition of data, Wijarnpreecha K, Nissaisorakarn P, Lekuthai N, Jaruvongvanich V, Nakkala K and Rajapakse R interpreted the data; Wijarnpreecha K and Thongprayoon C drafted the article; Lekuthai N, Nakkala K and Rajapakse R revised the article; all authors approved the final version.

                Correspondence to: Wisit Cheungpasitporn, MD, Division of Nephrology, Department of Internal Medicine, Mayo Clinic, 200 First street SW, Rochester, MN 55905, United States. wcheungpasitporn@ 123456gmail.com

                Telephone: +1-507-2848450 Fax: +1-507-2667891

                Article
                jWJG.v23.i8.pg1497
                10.3748/wjg.v23.i8.1497
                5330835
                28293097
                1fc6c598-acff-41a1-bc7b-4b0297d7606b
                ©The Author(s) 2017. Published by Baishideng Publishing Group Inc. All rights reserved.

                This article is an open-access article which was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial.

                History
                : 30 October 2016
                : 9 December 2016
                : 18 January 2017
                Categories
                Meta-Analysis

                helicobacter pylori,kidney failure,renal disease,renal insufficiency,end stage kidney disease,meta-analysis

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