Helicobacter pylori infection and peptic ulcer disease in children.
Explore the source record for details and available documents.
Adolescent↗
Biomedical subjects
P Sherman
Publications and source records attributed to P Sherman.
Supplementary enteral nutrition maintains remission in paediatric Crohn's disease.
BACKGROUND: Liquid diets given enterally combined with "bowel rest' are efficacious in the treatment of active Crohn's disease, but rapid recrudescence of gastrointestinal symptoms after resumption of a normal diet is common. AIMS: This study examined whether continuation of enteral nutrition as a nocturnal supplement to an ad libitum daytime intake of a normal diet increased the length of remission of Crohn's disease in children. PATIENTS AND METHODS: Children and adolescents with active Crohn's disease treated successfully with exclusive enteral nutrition were classified retrospectively according to whether they continued supplementary enteral nutrition or not. Time to relapse and linear growth were compared between the two cohorts. RESULTS: Between January 1986 and December 1992, 65 patients aged 7-17 years (mean (SD) 13.6 (2.1) years) (36 males, 29 females) with Crohn's disease in exacerbation were treated for > or = four weeks by bowel rest and nasogastric tube feeding of an oligopeptide or amino acid based formula. At first follow up visit, remission (fall in Paediatric Crohn's Disease Activity Index, PCDAI to < or = 20) was achieved in 47 of 65 (72%) patients. Subsequently, 20 of these 47 (43%) relapsed by six months and 28 of 47 (60%) by 12 months. Patients who continued nasogastric supplementary feeding (n = 28) after resumption of an otherwise normal diet remained well longer than those who discontinued nocturnal supplements completely (n = 19) (p < 0.02). Furthermore, continued use of nasogastric supplements before completion of puberty was associated with improved linear growth. CONCLUSION: After successful treatment of active Crohn's disease by exclusive enteral nutrition, supplementary enteral nutrition without restriction of normal diet is associated with prolongation of remission and improved linear growth in children and adolescents.
Adolescent↗
Expression of interleukin 8 and CD54 by human gastric epithelium after Helicobacter pylori infection in vitro.
BACKGROUND/AIMS: Helicobacter pylori is associated with neutrophil infiltrates, although the mechanism of their recruitment is only partially defined. The aim of the study was to determine if Kato III, a human gastric epithelial cell line, expressed cytokines and the intercellular adhesion molecule 1 (ICAM-1), which could contribute to the initiation of inflammation during infection with H. pylori. METHODS: Kato III cells were stimulated with H. pylori and were examined for evidence of infection, cytokine production, and the expression of ICAM-1. RESULTS: The expression of interleukin 8 messenger RNA and immunoreactive protein by Kato III cells was significantly increased over constitutive levels within 3 hours of infection with H. pylori. Infected Kato III supernatants activated neutrophils as evidenced by increased CD11b/CD18 and decreased L-selectin that could be blocked by anti-interleukin 8. In contrast, Campylobacter jejuni, lipopolysaccharide, killed H. pylori, and supernatants from cultures of H. pylori did not increase interleukin 8. Interleukins 2 and 6; interferons alfa, beta, and gamma; and tumor necrosis factor were not produced by resting or H. pylori-stimulated Kato III cells. In addition to producing interleukin 8, Kato III constitutively expressed surface ICAM-1, which acts as an intercellular adhesion molecule for neutrophils. CONCLUSIONS: Our results indicate that H. pylori stimulates the gastric epithelium to initiate inflammation and neutrophil recruitment and activation.
Base Sequence↗
Synthesis, in vivo biodistribution and dosimetry of [11C]N-methylpiperidyl benzilate ([11C]NMPB), a muscarinic acetylcholine receptor antagonist.
4-N-Methylpiperidyl benzilate (NMPB), a high affinity antagonist for the muscarinic cholinergic receptor, has been synthesized in carbon-11-labeled form through the N-[11C]methylation of 4-piperidylbenzilate. The product was isolated by HPLC, and obtained in yields (> 100 mCi) and specific activities (500-3000 Ci/mmol) sufficient for in vivo evaluation in small animals. Time-dependent regional brain distributions in rats and mice showed high radiotracer uptake and retention in striatum and cortex, and low in cerebellum, consistent with muscarinic cholinergic receptor distributions. Radiotracer retention in tissues could be significantly reduced by pretreatment of animals with a large dose of a competing antagonist, quiniclidinyl benzilate. Whole body biodistribution in rats was used to calculate the expected human internal radiation dosimetry for this new radiopharmaceutical. These animal experiments formed the basis for subsequent introduction of [11C]NMPB into human use with positron emission tomography.
Animals↗
Cell-to-cell spread of Shigella flexneri: exploitation of the host cytoskeleton.
Explore the source record for details and available documents.
Animals↗
Physical and genetic map of the genome of Campylobacter upsaliensis.
A physical map of Campylobacter upsaliensis ATCC 43954 was constructed from DNA fragments generated by SalI (5' G/TCGAC), NarI (5' GG/CGCC) and BssHII (5' G/CGCGC) restriction digests separated using pulsed-field gel electrophoresis. The size of the C. upsaliensis genome was approximately 2000 kb, providing evidence of the largest Campylobacter genome sized to date. Twenty-one fragments created from these restriction digests were assembled into a physical map using a combination of complementary methods including cross-Southern hybridization, hybridization fingerprint analysis and hybridization with homologous and heterologous (from Campylobacter jejuni) gene probes. The position of ten genetic loci, including that of the iron-uptake regulatory (fur) gene, were localized to the physical map. A genomic library of C. upsaliensis ATCC 43954 was constructed in lambda Gem-11 vector. Fifty thousand recombinants with an average size of 16 kb represent a library about 200 times the size of the genome. Using C. jejuni DNA probes, clones representing C. upsaliensis flaA, fur and ftsZ genes were isolated and localized to the physical map.
Blotting, Southern↗
Helicobacter pylori infection in children. Is there specific symptomatology?
Helicobacter pylori is an established cause of chronic-active gastritis in both adults and children. However, it is unclear whether H. pylori causes specific clinical symptoms. Therefore, the spectrum of clinical symptoms associated with H. pylori infection was studied in consecutive symptomatic children undergoing diagnostic endoscopy at two pediatric centers, using a structured questionnaire. In Toronto, Canada, 86 of 97 eligible children were enrolled into the study and in Limerick, Ireland, 24 of 29 were enrolled. The frequency of biopsy-confirmed H. pylori infection in Limerick, 16 of 24 (67%), was fivefold higher than in Toronto, 11 of 86 (13%, P = 0.0001). The two study populations were comparable in clinical presentation and duration of symptomatology and did not differ in age (11.9 +/- 3.5 and 11.6 +/- 2.0 years, respectively). Within both study populations H. pylori infection was not associated with specific clinical symptomatology, including duration of abdominal pain, location of pain, and history of melena or vomiting. H. pylori was positively associated with hematemesis in the Limerick group. These findings demonstrate that H. pylori infection in children is not associated with specific clinical symptomatology across varying geographical locations.
Adolescent↗
Hypercarotenemia and transaminitis in female adolescents with eating disorders: a prospective, controlled study.
PURPOSE: Hypercarotenemia and transaminitis are reported as laboratory features of anorexia nervosa. However, the specificity and sensitivity of an elevation in serum carotene and transaminase are not known. Therefore, a prospective study was undertaken to determine the clinical utility of these serum markers. METHODS: Serum carotene was measured in 46 female adolescents between 13 years and 18 years of age (21 anorexia nervosa, 17 bulimia nervosa, 8 unclassified eating disorders). Findings were compared to levels of carotene in serum samples obtained from similarly aged females with either chronic inflammatory bowel disease (22 Crohn disease, 11 ulcerative colitis) or acute medical symptoms not associated with undernutrition or intestinal inflammation (N = 26), and 21 children of either sex with dyspeptic symptoms. RESULTS: Serum carotene was elevated in 6/46 (13.0%) females with eating disorders compared with only 2/80 (2.5%) children in the three comparison groups (p < 0.01). Hypercarotenemia was present in 4/21 girls with anorexia nervosa compared with 0/17 females with bulimia nervosa (p = 0.11). Transaminitis was present in 38.5% (AST) and 7.7% (ALT) of eating disorder patients. Liver enzyme abnormalities, however, did not correlate with hypercarotenemia. Transaminitis was also not specific for eating disorders since transaminitis was observed with comparable frequency in the three comparison groups. CONCLUSIONS: These findings confirm that hypercarotenemia is a laboratory feature in some subjects with eating disorders, in particular, anorexia nervosa. The low sensitivity (13.0%) does not provide justification for its use as a screening test. However, in complicated diagnostic settings a serum carotene determination could prove useful because the specificity (97.5%), positive predictive value (75.0%), and negative predictive value (66.1%) of an elevated carotene were high. These data also show that elevated carotene levels are not associated with hepatic abnormalities. Although transaminitis is reported as a laboratory feature of eating disorders, the prevalence of such abnormalities in this study was not higher than in age-matched comparison groups.
Adolescent↗
Peptic ulcer disease: what is the role for Helicobacter pylori?
Explore the source record for details and available documents.
Adult↗
The apple will drop when it is ripe....
Explore the source record for details and available documents.
Female↗
Seroprevalence of Helicobacter pylori infection is not increased in pediatric inflammatory arthritides.
OBJECTIVE: To determine the seroprevalence of H. pylori infection among children with inflammatory arthritides receiving antiinflammatory drug therapy. METHODS: An enzyme linked immunosorbent assay (ELISA) was used to detect H. pylori specific immunoglobulin G antibody in 95 children with inflammatory arthritides, 53 children with chronic inflammatory bowel diseases and 47 parents of children with inflammatory arthritis. RESULTS: The frequency of seropositivity in children with arthritis (9/95, 9.5%) was not significantly higher than in children with chronic inflammatory bowel diseases (1/53, 1.9%; p = 0.16). Serum samples from parents were positive in 16 of 47 (34%), including 4 parents with children who also demonstrated a positive immune response. CONCLUSION: These data do not provide evidence for an increased frequency of H. pylori infection among children with inflammatory arthritides. The therapeutic use of ulcerogenic medications is likely to be an independent risk factor predisposing to dyspeptic symptoms and gastritis in this patient population.
Adolescent↗
Helicobacter pylori infection in adolescents with eating disorders and dyspeptic symptoms.
The potential role of Helicobacter pylori infection of the antrum as a cause of symptoms of dyspepsia in patients with eating disorders was evaluated with an assay to detect H. pylori-specific IgG in serum. H. pylori-specific optical-density readings were comparable for adolescents with eating disorders (0.133 +/- 0.063, mean +/- SD) and for two comparison groups, and were lower than readings for children with documented H. pylori infection. Symptoms referable to the gastrointestinal tract did not correlate with H. pylori status in the teenagers with eating disorders.
Adolescent↗
Therapeutics used to alleviate peptic ulcers inhibit H. pylori receptor binding in vitro.
Treatment with bismuth-containing remedies has been long associated with the alleviation of minor gastric ailments. Bismuth salts have a potent antimicrobial activity, and are part of the current standard regime used to treat Helicobacter pylori infection. H. pylori is considered to be the major etiological factor in the development of peptic ulcer disease. Earlier efficacious treatments for peptic ulcer included the oral administration of Tween detergents. We have found that these agents have an inhibitory effect on H. pylori adhesion to the lipid species phosphatidylethanolamine (PE) and gangliotetraosylceramide (Gg4) shown previously to be receptors for H. pylori binding in vitro. H. pylori binding to PE and Gg4 was inhibited after a thirty minute preincubation with different bismuth compounds: bismuth subsalicylate > bismuth subgallate > bismuth carbonate > colloidal bismuth subcitrate > tripotassium dicitrato bismuthate. No inhibitory effect on H. pylori binding was observed when bismuth salts were added directly into the binding assay. No changes in bacterial morphology and motility were observed after the thirty minute incubation. Pretreatment with Tween detergents also inhibited H. pylori receptor binding by up to 80% at concentrations as low as 0.0001%. These results suggest that inhibition of H. pylori/host cell adhesion might play a role in efficacious treatment for this infection.
Anti-Ulcer Agents↗
Slow-release 5-aminosalicylic acid therapy in children with small intestinal Crohn's disease.
Pharmacologic agents effective in the treatment of Crohn's disease confined to the small intestine are limited. The therapeutic efficacy of oral mesalazine in small bowel inflammation, although theoretically promising, remains unproven. In an open-labeled initial trial, timed-release 5-aminosalicylic acid (5-ASA), administered at a daily dosage of 30.6 +/- 9.0 mg/kg (mean +/- SEM) to children with active Crohn's disease involving the small intestine, was associated with improvement on the Harvey index in six of 12 patients treated for 8.1 +/- 3.9 weeks. In a subsequent prospective, double-blind study 14 children, ages 9.3 to 16.1 years, with active Crohn's disease limited radiologically in the small intestine were randomized to receive either timed-release 5-ASA [50 mg/kg/day (maximum 3 g/day)] or placebo for 8 weeks. Following a 4-week washout period, patients crossed over to receive the other study drug for a further 8 weeks. Six children completed the entire 20-week trial. The van Hees index improved among patients receiving 5-ASA for 8 weeks (delta = -18 +/- 6.4) but deteriorated among patients given placebo (delta = +14 +/- 4.1) (p < 0.05). Mean Crohn's Disease Activity Index (CDAI) decreased marginally after 8 weeks of 5-ASA treatment (delta = -48 +/- 38.2) but not with placebo (delta = -3.0 +/- 7.9) (p = 0.31). Of the eight noncompleters, more patients dropped out of the study because of lack of therapeutic response to placebo (n = 5) than to 5-ASA (n = 2).(ABSTRACT TRUNCATED AT 250 WORDS)
Adolescent↗
Asymptomatic uveitis in children with chronic inflammatory bowel diseases.
Uveitis may be an asymptomatic ocular process when it occurs in association with chronic inflammatory bowel disease (IBD). However, the frequency of uveitis in pediatric IBD is not known, as few patients have eye examinations on a routine basis. Experience with a child with Crohn's disease, who had asymptomatic uveitis identified by routine screening initiated because of associated arthritis, prompted us to undertake this evaluation. The purpose of this cross-sectional prospective study was to ascertain the point-prevalence of uveitis in pediatric IBD patients, including 97 with Crohn's disease and 50 with ulcerative colitis. Each child underwent an ophthalmologic assessment, including slit-lamp examination. In Crohn's disease, inflammatory cells and/or flare were observed in the anterior chamber of six (6.2%) patients. These changes were mild in all six patients and required no treatment. In the group with ulcerative colitis, there were no cases of asymptomatic uveitis. There was a higher frequency of asymptomatic transient uveitis in patients with Crohn's colitis (four of 22, 18.2%) than in those of other anatomic subgroups (two of 75, 2.7%; p < 0.05). Frequency of uveitis was also higher in IBD patients having other extraintestinal manifestations (15.0%) than in those without (3.1%; p < 0.10). There was no relationship observed between the activity of bowel disease and presence of ocular inflammation.
Adolescent↗
Expression and characterization of the eaeA gene product of Escherichia coli serotype O157:H7.
In enteropathogenic Escherichia coli, the eaeA gene produces a 94-kDa outer membrane protein called intimin which has been shown to be necessary but not sufficient to produce the attaching-and-effacing lesion. The purpose of this study was to characterize the intimin specified by the eaeA allele of the enterohemorrhagic E. coli (EHEC) serotype O157:H7 strain CL8 and to determine its role in adherence. The carboxyl-terminal 266 amino acids of the CL8 intimin were expressed as a protein fusion with glutathione S-transferase, which was used to raise antiserum in rabbits. The antiserum reacted in Western immunoblots with a 97-kDa outer membrane protein of EHEC strains of serogroups O5, O26, O111, and O157 and enteropathogenic E. coli strains of serogroups O55 and O127. Surface labelling of CL8 with 125I showed that intimin was surface exposed. An eaeA insertional inactivation mutant of CL8 was produced and was designated CL8-KO1. Total adherence of CL8-KO1 to HEp-2 cells was not significantly different from that of CL8, but CL8-KO1 gave a negative result in the fluorescent actin staining test. The eaeA gene expressed alone in E. coli HB101 also gave a negative fluorescent actin staining test result. The eaeA gene of CL8 was able to complement the eaeA deletion mutation in CVD206. We conclude that the product of the EHEC eaeA gene is a 97-kDa surface-exposed protein and propose that it be designated intiminO157. Sherman et al. described a 94-kDa outer membrane protein which played an important role in adherence of E. coli O157:H7 (Infect. Immun. 59:890-899, 1991). Western immunoblotting and indirect fluorescent antibody studies showed that the protein described by Sherman et al. is not intimin.
Actin Cytoskeleton↗
Comparison of Helicobacter pylori and attaching-effacing Escherichia coli adhesion to eukaryotic cells.
Adhesion of Helicobacter pylori was reported previously to be morphologically identical to "attaching and effacing" Escherichia coli. Therefore, the aim of the present study was to define the adhesion phenotype of H. pylori LC-11 to HEp-2, KATO-III, HEL, and CHO tissue culture cells. By using both staining of F-actin with fluorescein-labeled phalloidin and ultrastructural analysis, diffuse bacterial adhesion to discrete microvillus-denuded regions of the plasma membrane was observed in each of the infected cell lines. However, strain LC-11 did not induce formation of F-actin adhesion pedestals on the eukaryotic cells. H. pylori was negative by colony blot hybridization with an E. coli attaching and effacing gene probe. Elevations in inositol triphosphates followed infection of HEp-2 cells with H. pylori (405% of control values +/- 147%; P < 0.05). To correlate the observed histopathology with expression of the H. pylori phosphatidylethanolamine receptor, a thin-layer chromatography overlay-binding assay was used to identify receptors in each of the cell lines. H. pylori adhered to eukaryotic cells regardless of the presence (HEp-2, KATO-III, and CHO cells) or absence (HEL cells) of the lipid receptor as detected under the assay conditions. However, in comparison to cell lines that possess the phosphatidylethanolamine receptor, HEL cells demonstrated less quantitative H. pylori binding. These findings suggest that mechanisms distinct from E. coli enteropathogens underlie the adhesion of H. pylori to mucosal surfaces. In addition to the phosphatidylethanolamine H. pylori receptor, another host factor(s) likely mediates the attachment of H. pylori to human eukaryotic cells.
Animals↗