A Case-Control Study of Association of Helicobacter Pylori Infection with Morbid Obesity in Taiwan
Resource
ARCHIVES OF INTERNAL MEDICINE v.165 n.13 pp.1552-1555
Journal
ARCHIVES OF INTERNAL MEDICINE
Journal Volume
v.165
Journal Issue
n.13
Pages
1552-1555
Date Issued
2005
Date
2005
Author(s)
LIN, JAW-TOWN
WANG, HSIH-HSI
LEE, WEI-JEI
WU, MING-SHIANG
Abstract
Background Obesity is an increasing health problem in developed countries, where the prevalence of Helicobacter pylori infection is decreasing. Recent studies suggested colonization of the stomach by H pylori might affect gastric expression of appetite- and satiety-related hormone and patients cured of H pylori infection gained weight. It was hypothesized that H pylori could be a contributing pathogenic factor in childhood and adult obesity. Methods To determine whether H pylori infection is linked to obesity , a case-control study composed of 414 patients with morbid obesity (a body mass index [calculated as weight in kilograms divided by the square of height in meters] of 35 with serious comorbidity or a body mass index of 40) and 683 control subjects (a body mass index of <25) with a comparable socioeconomic status was conducted. Immunoglobulin G antibodies against H pylori were measured from frozen serum samples by an enzyme-linked immunosorbent assay. Logistic regression was used to calculate the odds ratio (OR) and 95% confidence interval (CI ). Results The overall seropositivity was significantly lower in obese patients (181 [43.7%] of 414) than controls (410 [60.0%] of 683) (OR, 0.50 ; 95% CI, 0.39-0.65; P<.001). Differences in the estimated risk of the presence of H pylori were more pronounced in younger age groups, with ORs of 0.32 (95% CI, 0.10-1.00; P = .05) in those aged 10 to 19 years, 0.55 ( 95% CI, 0.34-0.89; P = .01) in those aged 20 to 29 years, 0.49 ( 95% CI, 0 .30-0.80; P = .007) in those aged 30 to 39 years, and 0.58 (95% CI, 0.33-1 .00; P = .05) in those aged 40 years or older. Conclusions Our data indicated an inverse relationship between morbid obesity and H pylori seropositivity. These findings raise the hypothesis that a lack of H pylori infection, especially during childhood, might enhance the risk of the development of morbid obesity.
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