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      Alcohol intake andHelicobacter pyloriinfection: a dose–response meta-analysis of observational studies

      , , , , ,
      Infectious Diseases
      Informa UK Limited

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          Abstract

          Background Alcohol intake has been suggested to have an impact on the development of many chronic diseases. How alcohol intake may modulate risk of Helicobacter pylori (H. pylori) infection, however, remains a subject open for investigation. A dose-response meta-analysis was performed of epidemiological studies to better quantify this relationship. Materials and methods Twelve observational articles were identified. The summary odds ratio (OR) and confidence intervals (CI) were calculated for alcohol drinkers vs non-drinkers. The summary OR estimates were obtained using the random-effects model and dose-response meta-analysis. Sub-group and sensitivity analysis were also conducted. Results The summary OR was 0.78 (95% CI = 0.69-0.89). The dose-response analysis demonstrated that for drinkers of 10, 15, 30, 60 and 96 g/day alcohol intake, the estimated ORs were 0.80 (95% CI = 0.76-0.85), 0.79 (95% CI = 0.75-0.84), 0.83 (95% CI = 0.78-0.87), 0.85 (95% CI = 0.78-0.93) and 0.87 (95% CI = 0.70-1.06), respectively, compared to non-drinkers. The inverse relationship between alcohol intake and H. pylori infection was consistent, regardless of sex, age, geographic areas, detection methods or beverage types.

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          Facilitating meta-analyses by deriving relative effect and precision estimates for alternative comparisons from a set of estimates presented by exposure level or disease category.

          Epidemiological studies relating a particular exposure to a specified disease may present their results in a variety of ways. Often, results are presented as estimated odds ratios (or relative risks) and confidence intervals (CIs) for a number of categories of exposure, for example, by duration or level of exposure, compared with a single reference category, often the unexposed. For systematic literature review, and particularly meta-analysis, estimates for an alternative comparison of the categories, such as any exposure versus none, may be required. Obtaining these alternative comparisons is not straightforward, as the initial set of estimates is correlated. This paper describes a method for estimating these alternative comparisons based on the ideas originally put forward by Greenland and Longnecker, and provides implementations of the method, developed using Microsoft Excel and SAS. Examples of the method based on studies of smoking and cancer are given. The method also deals with results given by categories of disease (such as histological types of a cancer). The method allows the use of a more consistent comparison when summarizing published evidence, thus potentially improving the reliability of a meta-analysis. Copyright (c) 2007 John Wiley & Sons, Ltd.
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            Helicobacter pylori and autoimmune disease: cause or bystander.

            Helicobacter pylori (H. pylori) is the main cause of chronic gastritis and a major risk factor for gastric cancer. This pathogen has also been considered a potential trigger of gastric autoimmunity, and in particular of autoimmune gastritis. However, a considerable number of reports have attempted to link H. pylori infection with the development of extra-gastrointestinal autoimmune disorders, affecting organs not immediately relevant to the stomach. This review discusses the current evidence in support or against the role of H. pylori as a potential trigger of autoimmune rheumatic and skin diseases, as well as organ specific autoimmune diseases. We discuss epidemiological, serological, immunological and experimental evidence associating this pathogen with autoimmune diseases. Although over one hundred autoimmune diseases have been investigated in relation to H. pylori, we discuss a select number of papers with a larger literature base, and include Sjögrens syndrome, rheumatoid arthritis, systemic lupus erythematosus, vasculitides, autoimmune skin conditions, idiopathic thrombocytopenic purpura, autoimmune thyroid disease, multiple sclerosis, neuromyelitis optica and autoimmune liver diseases. Specific mention is given to those studies reporting an association of anti-H. pylori antibodies with the presence of autoimmune disease-specific clinical parameters, as well as those failing to find such associations. We also provide helpful hints for future research.
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              Relationship between Helicobacter pylori infection and smoking and drinking habits.

              Helicobacter pylori is a major cause of various gastroduodenal diseases. Some risk factors related to H. pylori infection have been reported; however, studies on the relationship between H. pylori infection and smoking or drinking habits have given conflicting results. In the present study, these relationships were investigated by collecting sera and information from 8837 subjects. Serum H. pylori immunoglobulin G antibody was measured by an enzyme-linked immunoassay. In addition to sex and age, information on smoking and drinking habits was collected by questionnaire. Age- and sex-adjusted odds ratios (95% confidence interval) of smoking and alcohol consumption were calculated for H. pylori seropositivity using logistic regression models. Current smokers had a 0.82 (0.74-0.91)-fold greater risk of H. pylori seropositivity than those who had never smoked. Current cigarette consumption showed a dose-dependently negative association with H. pylori seropositivity, and the association between smoking and H. pylori infection was strong in younger subjects. Current drinkers had a 0.88 (0.79-0.98)-fold greater risk of H. pylori seropositivity than those who had never drunk alcohol. The volume of alcohol consumed showed a negative association with H. pylori seropositivity. In the current study, smoking was negatively associated with H. pylori infection. The risk of H. pylori seropositivity decreased linearly with cigarette consumption per day. Increased gastric acidity in the stomach through smoking may be a cause of the dose-dependently negative association between H. pylori and smoking. Drinking was negatively and dose-dependently associated with H. pylori positivity, although the effect of drinking was weaker than that of smoking.
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                Author and article information

                Journal
                Infectious Diseases
                Infectious Diseases
                Informa UK Limited
                2374-4235
                2374-4243
                December 2015
                November 20 2015
                April 02 2016
                : 48
                : 4
                : 303-309
                Article
                10.3109/23744235.2015.1113556
                26585858
                c8aefd86-4d13-425e-a082-0ade90fc19ba
                © 2016
                History

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