Immune responses to Helicobacter pylori infection in children with intellectual disabilities.Res Dev Disabil. 2012 Mar-Apr; 33(2):663-9.RD
Infection with Helicobacter pylori was assessed through serum H. pylori IgG antibody in children with intellectual disabilities (ID). The sero-status of cytotoxin-associated gene A (CagA) was determined as a risk determinant for severe H. pylori-associated diseases. In total, 210 children with ID were included who were permanent resident of three institutes in Tehran. Medical history and demographic data were collected by reviewing the medical file records. The anti H. pylori IgG antibody was detected in serum of 74.8% of children using ELISA. Significant correlations were found between the rate of infection and age (P = 0.001) and duration of institutionalization (P = 0.018). The likelihood of H. pylori IgG positive response increased with age with the highest response in 15-18 years age group (OR = 6.66, 95% CI: 2.14-20.17; P = 0.001). Similarly, the average titers of H. pylori IgG antibody were increased with age. The institutionalization duration of more than 49 months affected the likelihood of H. pylori IgG positive response (OR = 2.437, 95% CI: 1.12-5.26; P = 0.023). Anti-CagA titers were higher than 5arbU/ml in 92 (58.6%) children, indicating a positive response against CagA protein. The titer of H. pylori IgG was significantly higher in CagA-positive (mean ± SE = 51.04 ± 3.41) than in CagA-negative children (38.07 ± 4.18; P = 0.017). In contrast to total H. pylori IgG titers, anti-CagA antibody had non-regular trend of alterations with age. The seropositivity rate of H. pylori infection in ID children was higher than other reports in healthy children from various regions of the country. The risk of H. pylori infection is increased with age and duration of institutionalization. The serostatus of CagA in children with IDs has not been reported so far. The regular monitoring of the CagA-positive carriers is recommended; since CagA positive cases carry the risk of progression of infection toward severe H. pylori associated sequels such as gastric cancer and duodenal ulcers.