Browsing by Author "Duarte, I."

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    CagA antibodies as a marker of virulence in Chilean patients with Helicobacter pylori infection
    (2003) Harris, Paul R.; Godoy, A.; Arenillas, S.; Riera, F.; Garcia, D.; Einisman, H.; Pena, A.; Rollan, T.; Duarte, I.; Guiraldes, E.; Perez-Perez, G.
    Background: The bacterial and host factors that influence the clinical outcomes of the Helicobacter pylori infection have not been fully identified. Cytotoxin-associated gene product (CagA), one of the virulence factors, has been associated with a more aggressive form of infection. The authors studied the relationship between CagA status and clinical outcome in Chilean children and adults with H. pylori infection. Methods: One hundred eighty consecutive patients undergoing upper gastrointestinal endoscopic analysis were enrolled after informed consent was obtained. Rapid urease test and histologic analysis were used to detect H. pylori infection. IgA and IgG antibodies to H. pylori whole cell antigen preparation and IgG antibodies to CagA were measured by enzyme-linked immunosorbent assay (ELISA). Results: H. pylori infection was detected in 42% of the patients by biopsy or urease test and in 38% and 20% of patients by IgG and IgA antibodies, respectively. The prevalence of H. Pylori either by the invasive or the serologic tests was directly related to patient age. Among patients with H. pylori, there was no significant association between age and prevalence of CagA. Nearly 70% of the patients with H. pylori and peptic ulcer disease had CagA-positive strains. In contrast, only 49% of the patients with chronic gastritis alone had CagA-positive strains (P < 0.05). Conclusions: In Chile, patients infected with H. pylori have a proportion of CagA-positive strains similar to that reported in developed countries. CagA prevalence was not significantly different in adults and children infected with H. pylori, suggesting that variations in clinical outcome may be related to host immune or environmental factors.
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    Characterization of the gastric lesions in Chilean children with sysptomatic Helicobacter pylori associated gastritis
    (1999) Guiraldes, E.; Pena, A.; Duarte, I.; Trivino, X.; Schultz, M.; Larrain, F.; Espinosa, M.N.; Harris, Paul R.
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    Congenital hepatic fibrosis. Report of five cases.
    (2004) Harris, Paul R.; Fodor, D.; Cavagnaro, F.; Di Egidio, M.; Duarte, I.; Fava, M.
    Background. Congenital hepatic fibrosis (CHF) is an autosomic dominant disease that has been associated with polycystic kidney disease. Aim: To describe the medical management of 5 children with CHF and to evaluate the presence and extension of the associated renal disease. Patients and methods: Retrospective review of the medical charts of 5 children with CHF, aged 2 to 14 years. Results: Three children presented autosomic recessive polycystic kidney disease, which was diagnosed before the appearance of liver disease manifestations. They presented a more severe liver damage, with a more aggressive clinical course requiring use of transjugular intrahepatic porto-systemic shunts (TIPS) or surgical porto-systemic shunts to control portal hypertension. The other two children, in whom the diagnosed was based on asymptomatic hepatomegaly, had normal renal function and structure with a more benign clinical course. Conclusions: The diagnosis of CHF should be suspected not only in children with polycystic kidney disease but in those children with persistent, hard consistency, left lobe predominance hepatomegaly.
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    Helicobacter pylori Gastritis in Children Is Associated With a Regulatory T-Cell Response
    (2008) Harris, P.R.; Wright, S.W.; Serrano, C.; Riera, F.; Duarte, I.; Torres, J.; Peña, A.; Rollán, A.; Viviani, P.; Guiraldes, E.; Schmitz, J.M.; Lorenz, R.G.; Novak, L.; Smythies, L.E.; Smith, P.D.
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    Helicobacter pylori-associated hypochlorhydria in children relates to the development of iron deficiency
    (2010) Harris, Paul R.; Villagran, A.; Serrano, C.; Duarte, I.; Windle, H. J.; Crabtree, J. E.
    Introduction Acute H pylori infection is associated with transient hypochlorhydria of variable duration. Hypochlorhydria in H pylori-associated atrophy has a role in iron deficiency (ID) through changes in the physiology of iron absorption. The role of hypochlorhydria in H pylori-associated ID in childhood has not been investigated. The aims were to evaluate the association between H pylori-associated hypochlorhydria and ID in children. Methods A total of 123 children were prospectively enrolled in the study. Any child with peptic ulceration, or who received antacids, PPIs, H2 antagonists, and antibiotics in the previous 4 weeks was excluded. Blood was taken for complete blood count and iron profile. Gastric biopsies were taken for H. pylori determination by histology and rapid urease test. H pylori status was defined as +ve if either test was positive. Gastric juice was obtained at the beginning of the endoscopy avoiding water insufflation. Duodenal biopsies were taken for exclusion of coeliac disease (CD). Stool samples were collected for parasitology/microbiology. Of the 123 children, 2 with CD, 8 with non-specific duodenal inflammation (DI), 5 with lost blood analysis and 9 with parasitic infections (2 with DI) were excluded. Results Of the remaining 101 children 31 were H pylori +ve and 10 were hypochlorhydric (pH>4). There were no differences in demographic characteristics with regard to infection status, or gastric pH. In H pylori +ve children with pH >4 (n=6) serum iron (median (IQR): 60.2 (45–66) μg/dl) and transferrin saturation levels percentage (16.6 (15–19)) were significantly lower (p<0.01) than H pylori positive children (n=25) with pH≤4 (iron 113.2 (91–132); transferrin saturation 32.6 (24–38)). No differences in ferritin or TIBC were observed. In H pylori negative children with pH>4 (n=4) both iron (119 (101–137)), and transferrin saturation (36.4 (31–41)), were not significantly different from children with pH≤4 (n=66) (iron 98.7 (80–122); transferrin saturation 32.2 (25–40)). Conclusion: Low serum iron and transferrin in childhood H pylori infection is associated with hypochlorhydria. In uninfected children, hypochlorhydria was not associated with altered serum iron parameters, indicating a combination of H pylori infection and/or inflammation and hypochlorhydria has a role in the aetiology of iron deficiency. Even though H pylori-associated hypochlorhydria may reflect a transient period during acute gastritis, it alters iron homeostasis with clinical impact in developing countries with a high H pylori prevalence. Funded by EU CONTENT Project (INCO-CT-2006-032136) and CONICYT/BM (RUE #29).