Helicobacter pylori infection affects about half of the world's population and is usually acquired in childhood. The infection has been associated with chronic gastritis, peptic ulcer, and stomach cancer in adulthood. Little is known, however, about its consequences on child health. We examined the effect of H. pylori infection on growth among school-age children in the Colombian Andes by comparing growth velocity in the presence and absence of H. pylori infection.
Children who were 4–8 years old in 2004 were followed up in a community where infected children received anti-H. pylori treatment (n = 165) and a comparison community (n = 161) for a mean of 2.5 years. Anthropometry measurements were made every 3 months and H. pylori status ascertained by urea breath test every 6 months. Growth velocities (cm/month) were compared across person-time with and without infection, using mixed models for repeated measures.
In the untreated community, 83% were H. pylori-positive at baseline and 89% were -positive at study end. The corresponding prevalences were 74% and 46%, respectively, in the treated community. Growth velocity in the pretreatment interval was 0.44 (standard deviation [SD] = 0.13) cm/month. Models that adjusted for age, sex, and height estimated that H. pylori-positive children grew on average 0.022 cm/month (95% confidence interval = 0.008 to 0.035) slower than H. pylori-negative children, a result that was not appreciably altered by adjustment for socioenvironmental covariates.
This study suggests that chronic H. pylori infection is accompanied by slowed growth in school-age Andean children.
From the aDivision of Gastroenterology, Department of Medicine, University of Alberta, Edmonton, Alberta, Canada; bDepartment of Public Health Sciences, University of Alberta, Edmonton, Alberta, Canada; cDivision of Gastroenterology, Hepatology and Nutrition, Vanderbilt University Medical Center, Nashville, TN; dCentro de Estudios en Salud, Universidad de Nariño, Pasto, Colombia; eUniversity of Texas School of Public Health, Houston, Texas; and fDepartamento de Patología, Facultad de Medicina, Universidad del Valle, Cali, Colombia.
Submitted 18 November 2009; accepted 9 August 2010; posted 10 November 2010.
Supported by the National Cancer Institute (PO1CA028842).
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Correspondence: Karen J. Goodman, Division of Gastroenterology, 7–142 Katz Building, University of Alberta, Edmonton, Alberta, Canada T6G 2E1. E-mail: firstname.lastname@example.org.