Malnutrition was associated with active H. pylori infection. Helicobacter pylori (H. pylori) is a gram-negative, curved-shaped bacterium, classified in Group I carcinogen, clinically associated with gastritis, peptic ulcer disease

and selleck inhibitor gastric cancer [1, 2]. In developing countries, more than 80% of adults and 50% of children are colonized by H. pylori compared to 30% of adults and 10% of children in developed countries [3]. In Mexico, in 1988 a seroepidemilogical survey estimated H. pylori prevalence of 66% [4, 5]. Twenty percent of infants of 1 year and younger were colonized by H. pylori, and colonization had reached 50% in children before they reached 10 years of age [6]. In a study carried out in 2001 in boarding schools of the National Indigenous Institute of Hidalgo State in Mexico, prevalence of active H. pylori infection was 52% [7]. In a population study, in Mexico City, 38% of school children had active H. pylori. Children with H. pylori infection ZD1839 averaged 1.32 cm (CI 95% −2.22 to −0.42) less in height than children without infection [8]. In the same population, the colonization by H. pylori was a dynamic phenomenon, with an incidence rate of 64 new cases/year/1000 school children and a spontaneous infection clearance rate of 47 cases/year/1000 school children [9]. There are different

H. pylori strains with genetic variability. Bacterial characteristics, host characteristics, and environmental factors determine the degree of damage that the infection can cause in the gastric mucosa [10]. H. pylori displays factors that determine its virulence; one of them is the cytotoxin-associated gene A (cagA) [11]. In Carnitine palmitoyltransferase II most populations, approximately 50% of H. pylori strains have this virulence

factor. The cagA island encodes a bacterial type IV secretion system that translocates CagA into host cells. Intracellular CagA affects multiple pathways that alter host cell morphology, signaling, and inflammatory responses [11]. H. pylori infection with this virulence factor has been associated with the development of severe diseases such as gastric and duodenal ulcer, gastric atrophy, and gastric cancer [12-14]. The infection by H. pylori in children has also been associated with extra-gastric manifestations such as lower growth rate and iron deficiency (ID) or iron deficiency anemia (IDA) [15-21]. Some authors suggest that a chronic infection is a prerequisite for the development of diseases such as symptomatic gastritis, gastric and duodenal ulcers, gastric cancer [22], ID or IDA [23, 24]. Studies on the effect of active infection on the speed of child growth have shown that there is a greater negative effect in the months after the onset of the infection. This effect is maintained and affects infected children’s growth cumulatively throughout time [18, 19, 21]. The majority of H. pylori-infected people remain asymptomatic; thus, the infection is not detected in the acute phase.