Purpose: Histologic assessment of high-risk gastritis for the development of gastric cancer is not well defined. The identification of tissue markers together with the integration of histologic features will be required for this assessment.Experimental Design: Matched tumor/nontumor adjacent mucosa (NTAM) of 91 early gastric cancer and 148 chronic gastritis cases were evaluated for histologic characteristics (atrophy, intestinal metaplasia, chronic inflammation, polymorphonuclear infiltration, and Helicobacter pylori) by the Sydney System. Atrophy risk assessment was also evaluated by the Operative Link on Gastritis Assessment (OLGA) staging system. Eight tissue markers (BRCA1, HSP90, STAT1, FHIT, EGFR, p73, p53, p16INK4a) and EBV were also evaluated by tissue microarray/immunohistochemistry/in situ hybridization platform. Data were analyzed by contingency tables (2 × 2) using Fisher's exact two-tailed test (P < 0.001) and integrated by Significance Analysis of Microarrays (SAM) and clustering analysis.Results: Histologically, NTAM have severe intestinal metaplasia/chronic inflammation and severe atrophy assessed by Sydney and OLGA staging systems. H. pylori infection was similar in both groups, and EBV was found only in 5.5% of the tumor samples. Overexpression of p73 was higher in NTAM (50.5%) than in chronic gastritis (10.8%; P < 0.0001). Integration of histologic features and tissue markers showed that overexpression of p73, severe atrophy, and OLGA stage 4 were the most relevant features in NTAM. Clustering analysis correctly assigned NTAM and control cases (P < 0.0001).Conclusions: Overexpression of p73 should be considered for the assessment of high-risk chronic gastritis. SAM allows the integration of histology and tissue markers for this assessment.

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Children with special health care needs: prevalence in a pediatric hospital and associated risks p < 0.01), nosocomial infections (RR 2.28; p < 0.001) and prolonged hospitalization (RR 1.99; p < 0.001). Conclusions: One in fi ve hospitalized children met CSHCN-3 defi nition. These patients had an increased risk of adverse events during their hospitalization compared to non-CSHCN. (Rev Med Chile 2012; 140: 458-465).

IntroductionPhenylketonuria (PKU) is an autosomal recessive disorder characterized by a deficiency in phenylalanine (Phe) hydroxylase activity. Early diagnosis and continuous treatment with a low Phe diet prevents severe neurological and cognitive impairment.Aims1. Analyze how treatment adherence evolves through infancy, childhood, and early adolescence in individuals with PKU. 2. Identify early signs of treatment discontinuation.MethodologyThis longitudinal, retrospective study included 75 children diagnosed through newborn screening, ages 7 to 13 years. Data on blood Phe concentration, number of blood samples sent, proportion of samples with Phe concentrations over the recommended range, and number of visits to the metabolism clinic were recorded. Logistic regression analysis was used to identify the variables that predict treatment discontinuation before 13 years of age.ResultsA progressive increase in mean blood Phe concentrations with age was identified. The greatest increase occurred between the first and second years of life. By age ten, mean Phe blood concentration of the group was above the recommended range. The proportion of samples with Phe concentrations over the recommended range also increased with age, from an average of 13% during the first year of life to 67% in early adolescence. Sixty-eight percent of the children attended the outpatient clinic and sent samples from birth to the time of the study. Individuals who discontinued follow-up showed significantly higher mean blood Phe concentrations (360 vs. 220.9 μmol/L; p = 0.004) and the proportion of samples over the recommended range (37% vs. 12% p = 0.002) was significantly higher during the second year of life. Mean age for children who discontinued treatment was 5.5 years of age. Blood Phe concentration values at 12 to 23 months of age and at 6 to 8 years of age significantly predicted treatment discontinuation before 13 years of age.ConclusionTreatment adherence in PKU diminishes with age. Early signs of treatment discontinuation can be identified during the second year of life, allowing preventive interventions in high risk groups.