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Biomedical subjects

David Y Graham

Publications and source records attributed to David Y Graham.

At least 19 recordsLinked to original sources
PubMed2004

Schatzki's ring: to cut or break an unresolved problem.

Symptom assessment has been proven to be less reliable than barium pill testing for success of dilation of peptic strictures. Schatzki's ring also has a high recurrence rate. Our aim here was to compare the efficacy of single dilatation with a 54-F Savary dilator and electrosurgical ring incision for symptomatic Schatzki's rings. Schatzki's ring patients who failed to pass a 12.7-mm barium pill were randomized to dilatation with a 54-F Savary dilator or four quadrant incisions with a needle knife. All received lansoprazole (30 mg) for 30 days posttreatment. Follow-up at 1, 3, 6, and 12 months used the pill test and a dysphagia score. Eleven patients (mean age, 62; median, 64) were randomized and received therapy, six with dilatation and five with incision. The ring diameter pretherapy was 9.8 +/- 1.3 mm. One patient with dilatation had a procedure-related esophageal perforation. The dysphagia score decreased (from 2.7 +/- 1.1 predilatation and 3.0 +/- 0.4 preincision) to 0 after treatment, suggesting that both therapies were equally successful. In contrast, using objective measurements with the barium pill showed that the pill failed to pass the ring in 60% at 1 month after therapy. The failure rate by 1 year was 100%. Use of an objective measure of effectiveness of treatment of symptomatic Schatzki's rings showed that neither single large-dilator dilatation nor four quadrant ring incision was a reliable and effective therapy. In the future studies, repeated dilatation may be needed to define success before long-term outcome can be accurately assessed.

2-Pyridinylmethylsulfinylbenzimidazoles↗
PubMed2004

Role of interferon-stimulated responsive element-like element in interleukin-8 promoter in Helicobacter pylori infection.

BACKGROUND & AIMS: Gastric mucosal interleukin (IL)-8 levels are related to the presence of both the cag pathogenicity island (PAI) and OipA. We investigated the regions of the IL-8 promoter and the upstream signaling involved in IL-8 gene transcription. METHODS: We cocultured parental Helicobacter pylori and isogenic oipA, hopZ, or cagE gene knockout mutants with gastric cancer cells. The regulatory sites in the IL-8 promoter were examined by luciferase reporter gene assay, electrophoretic mobility shift assays, and immunoblot analyses. Phosphorylated signal transducers and activators of transcription 1 (STAT1) levels in the antral gastric mucosa were measured by enzyme-linked immunosorbent assay. RESULTS: Maximal H. pylori -induced IL-8 gene transcription required the presence of the interferon-stimulated responsive element (ISRE)-like element, nuclear factor (NF)-kappa B and activator protein (AP)-1 binding sites. In vitro studies showed that OipA and the cag PAI were involved in inducing interferon regulatory factor (IRF)-1 to bind and activate the ISRE-like element and that the cag PAI, but not OipA, was involved in activating AP-1 and NF-kappa B. Both in vitro and in vivo studies showed that OipA, but not the cag PAI, was involved in STAT1 phosphorylation, as upstream signaling of IRF-1. CONCLUSIONS: OipA and the cag PAI are both necessary for full activation of the IL-8 promoter but act via different pathways that diverge upstream of IRF-1 where only OipA is involved in the STAT1-IRF1-ISRE pathway. The mucosal inflammatory response to H. pylori infection is complex and involves different pathways converging on the IL-8 promoter.

Antigens, Bacterial↗
PubMed2004

Gastroesophageal reflux among different racial groups in the United States.

BACKGROUND & AIMS: White people in the United States are several-fold more affected by esophageal adenocarcinoma than black people. It remains unknown whether this racial discrepancy reflects a higher prevalence of gastroesophageal reflux disease (GERD) symptoms or a higher degree of esophageal damage. METHODS: A cross-sectional survey followed by endoscopy was performed among employees at a VA medical center. The association between race and GERD symptoms and erosive esophagitis was analyzed in logistic regression analyses controlling for demographic, clinical, and histologic variables. RESULTS: A total of 496 of 915 people (54%) returned interpretable questionnaires, and endoscopy was performed in 215 participants. The mean age was 45 years, and 336 (68%) were women. Racial distribution was 43% black, 34% white, and 23% other races. Heartburn occurring at least weekly was reported in 27%, 23%, and 24% of these racial groups, respectively. The age-adjusted prevalence of heartburn or regurgitation was not significantly different among the groups. Erosive esophagitis was found in 50 of 215 participants (23%); 31 of these cases were mild. Only one person had Barrett's esophagus (0.4%). For weekly heartburn or regurgitation, black participants had significantly less frequent erosive esophagitis than white participants (24% vs. 50%; P = 0.03). With multiple adjustments, black participants had a persistently lower risk of esophagitis (adjusted odds ratio, 0.22-0.46; P < 0.001). CONCLUSIONS: White and black people in the United States have a similarly high prevalence of GERD symptoms. However, black people have a lower prevalence of esophagitis for the same frequency of GERD symptoms. Barrett's esophagus was rare in this study, even among those with frequent symptoms.

Adolescent↗
PubMed2004

False negative urea breath tests with H2-receptor antagonists: interactions between Helicobacter pylori density and pH.

BACKGROUND: We studied the effects of famotidine, sodium bicarbonate, and citric acid on the 13C-urea breath test (UBT). METHODS: Helicobacter pylori-infected volunteers received a UBT, 40 mg of famotidine at bedtime, and a second UBT (pudding test meal, 648 mg NaHCO3 tablet then 125 mg of urea in 200 ml of water containing 650 mg of NaHCO3). Experiment 2 consisted of four UBTs. Two were standard citric acid UBTs with 75 mg of urea and 2 g citric acid and two were sequential bicarbonate-citric acid UBTs. Sequential UBTs consisted of administration of a 648 mg bicarbonate tablet with 50 g of Polycose in 200 ml of water. Five minutes later, 125 mg of 13C-urea was given in 75 ml of water containing 650 mg of NaHCO3. Breath samples were collected after 15 minutes. Then, to acutely acidify the stomach, 4 g of citric acid was given in 200 ml of water. A second breath sample was collected 15 minutes after the citric acid. The standard UBTs were done before and after 6 days of famotidine (40 mg b.i.d.). Sequential UBTs were done after 1 and 6 days of famotidine therapy. Gastric biopsies for histology, culture, and mucosal cytokines were assessed before and after 6 days of famotidine. RESULTS: Eighteen subjects participated, 10 in each experiment; seven had endoscopy with biopsy. Famotidine/ bicarbonate resulted an approximately 50% fall in UBT values (p = .021) with 10% becoming negative. The gastric pH increased from 5.1 +/- 0.5 to 6.7 +/- 0.2 (p = .03) although no pH value predicted the occurrence of false negative results. Under famotidine acid suppression, NaHCO3 reduced the delta over baseline (DOB) by 63% (p = .021). This was reversed with citric acid. Histology showed a H2-receptor antagonist-associated increase in the depth of gastric corpus inflammation. CONCLUSIONS: H2-receptor antagonists differ from proton pump inhibitors as high intragastric pH may cause a reduction in urease activity, unrelated to a reduced bacterial load and reversed by citric acid.

Adolescent↗
PubMed2004

Molecular epidemiology and outcome of Helicobacter pylori infection in Thailand: a cultural cross roads.

ABSTRACT Background. Thailand is at the cultural cross roads between East and South Asia. It has been suggested that this is also the region where the predominant Helicobacter pylori (H. pylori) genotype changes from East Asian to South Asian. Methods. We compared the molecular epidemiology and outcome of H. pylori infections among different ethnic groups in Thailand (Thai, Thai-Chinese and Chinese). H. pylori isolates were genotyped by polymerase chain reaction based on cagA, cag right end junction and vacA genotypes. Results. Ninety-eight isolates from 38 ethnic Thai, 20 ethnic Chinese and 40 Thai-Chinese were categorized into East Asian (45%), South/Central Asian (26%), Western (1%) or mixed type (29%). The East Asian genotype was the most common among Chinese (85%) and Thai-Chinese (55%) (p <.01 compared to ethnic Thai). The ethnicity of the mother among mixed Thai-Chinese marriages predicted the genotype of the child's H. pylori (e.g. when the mother was Chinese, 84% had East Asian type vs. 29% when the mother was Thai) (p <.001). Gastric cancer was common among ethnic Chinese with East Asian genotype (e.g. all Chinese with gastric cancer or peptic ulcer disease had East Asian genotype, whereas only 40% of Chinese with gastritis had this genotype). Conclusions. Immigration, intermarriage and the variety of H. pylori genotypes in Thailand suggest that Thailand is an ideal site for epidemiological studies attempting to relate H. pylori genotypes and host factors to outcome. Our data also support the hypothesis that the primary caretaker of the children is most likely the source of the infection.

Antigens, Bacterial↗
PubMed2004

Correlation between Helicobacter pylori OipA protein expression and oipA gene switch status.

Polyclonal antisera to either a synthetic OipA peptide or a recombinant OipA protein detected OipA expression in Helicobacter pylori and correlated with functional oipA status determined by PCR sequence (sensitivity and specificity of >94%). Immunoblotting is a simple and accurate method for detecting expression of the important virulence factor OipA.

Amino Acid Sequence↗
PubMed2004

Alanine-threonine polymorphism of Helicobacter pylori RpoB is correlated with differential induction of interleukin-8 in MKN45 cells.

Geographical differences in the genetic diversity of Helicobacter pylori isolates were examined by analyzing rpoB sequences. An extremely high level of allelic diversity among H. pylori strains was found. The rpoB sequences of Asian and non-Asian (North and South American, European, and South African) strains were found to differ. An amino acid polymorphism (alanine and threonine RpoB types) was found at the 497th residue by deduced amino acid analysis. RpoB with a threonine residue (RpoB(Thr)) was uniquely present in East Asian countries, and two-thirds of the H. pylori isolate population in this region was RpoB(Thr); however, this type was rare or absent in Western countries, where RpoB(Ala) predominated. RpoB(Thr) strains induced a much larger amount of interleukin-8, a chemokine that plays an important role in chronic inflammation, than RpoB(Ala) strains in cultured MKN45 cells.

Alanine↗
PubMed2003

Seroepidemiology of Helicobacter pylori and hepatitis A virus and the mode of transmission of infection: a 9-year cohort study in rural Japan.

We compared the seroepidemiologic patterns of Helicobacter pylori and hepatitis A virus (HAV) infections among participants in 2 independent cross-sectional studies conducted in Japan in 1986 and 1994. Subgroups were monitored with successive blood sampling. H. pylori and HAV infection status was defined by results of enzyme-linked immunosorbent assay. In 1986, the prevalence of H. pylori infection and HAV infection, respectively, were 80% and 70% among adults and 31% and 5% among children. The prevalence of both infections increased with age. Concordant infections were found in 74.5% of adults (kappa=0.2) versus 2% of children (kappa=0.05). During the 9-year study period, the incidence of H. pylori infection was 1.1% among adults and 2% among children. The seroprevalence of HAV remained constant. The disparity between the increase in prevalence of H. pylori and HAV infection with age is likely associated with improvements in hygienic practices. The discordance between the presence of the infections among younger persons is evidence against a common source and/or vehicle for transmission.

Adolescent↗
PubMed2003

Traces of human migrations in Helicobacter pylori populations.

Helicobacter pylori, a chronic gastric pathogen of human beings, can be divided into seven populations and subpopulations with distinct geographical distributions. These modern populations derive their gene pools from ancestral populations that arose in Africa, Central Asia, and East Asia. Subsequent spread can be attributed to human migratory fluxes such as the prehistoric colonization of Polynesia and the Americas, the neolithic introduction of farming to Europe, the Bantu expansion within Africa, and the slave trade.

Africa↗
PubMed2003

Enterococcus gastritis.

Helicobacter pylori infection is the most common cause of gastritis with its associated sequelae. Gastritis secondary to other bacteria is rare. This report describes Enterococcus-associated gastritis in a 59-year-old diabetic man. Nine months after receiving treatment for H. pylori-associated gastritis, he underwent endoscopy to confirm H. pylori eradication and to evaluate the status of previously seen ulcers. Mucosal biopsy specimens revealed severe active but focal gastritis adjacent to gram-positive coccobacilli in short to long chains with no H. pylori. Culture grew an Enterococcus similar to E. hirae and E. durans. No treatment was given, and endoscopy done 2 months later showed complete resolution of the gastritis and absence of H. pylori or enterococci. Our patient's gastritis represents a previously undescribed manifestation of Enterococcus infection. It is possible that the presence of NSAID gastric mucosal injury and diabetes predisposed this individual to the development of transient Enterococcus gastritis.

Enterococcus↗
PubMed2003

Detection of Chlamydiae pneumoniae but not Helicobacter pylori DNA in atherosclerosis plaques.

Chronic infections have been associated with cardiovascular disease. We used bacterial culture, polymerase chain reaction (PCR), and immunohistochemical staining with anti-vacA and anticagA antibodies to search for Helicobacter pylori and Chlamydiae pneumoniae in atherosclerotic plaques obtained at endarterectomy. Serum IgG antibodies to H. pylori and C. pneumoniae were also determined. Thirty-two patients were enrolled. Anti-H. pylori and anti-C. pneumoniae IgG were present in 72% and 81%, respectively. Culture and PCR for H. pylori of vessel walls and plaques were negative. Atherosclerotic plaque and normal vessel sections from H. pylori-negative and- positive patients showed reactivity with anti-vacA and anti-cagA antibodies. C. pneumoniae DNA was amplified in three atherosclerotic lesions. These findings suggest that the association between H. pylori infection and atherosclerosis does not result from continuing direct effects of H. pylori antigens in the vessel walls. Antigens within vessel atherosclerotic plaques cross-react with H. pylori virulence factors and could act as cofactors in determining instability for the atherosclerotic plaques.

Aged↗
PubMed2003

Cyclooxygenase expression during Helicobacter pylori infection in Mongolian gerbils.

We investigated the expression of cyclooxygenase-2 (COX-2) and COX-1 mRNAs during longterm Helicobacter pylori infection of the Mongolian gerbil (18 months) as well as the effect of eradication therapy and the cag pathogenicity island on COX mRNA expression. COX mRNA levels were determined by reverse transcription-polymerase chain reaction. Pyloric channel ulcers were noted in one of 10 gerbils (10%) at 3 months, 33% at 6 months, 50% at 9 months, 17% at 10 months, 40% at 12 months and 25% at 18 months after inoculation of parental strains. Nineteen of 21 gerbils had successful H. pylori eradication and showed significant reduction of inflammation and no ulcerations. There were no significant differences in COX-1 mRNA expression between the groups. COX-2 mRNA expression was significantly increased 1 and 3 months after inoculation and then decreased to basal levels. In control animals, COX-2 mRNA expression was significantly higher at 12 and 18 months compared to younger animals. cagE knockout mutants did not induce gastric inflammation and induced significantly lower COX-2 mRNA expression compared to parental strains. COX-2 mRNA was induced early in H. pylori infection and then declined. COX-2 mRNA expression was also induced with aging.

Animals↗
PubMed2003

Interleukin-6 genetic polymorphisms are not related to Helicobacter pylori-associated gastroduodenal diseases.

BACKGROUND: Polymorphisms in the promoter region of the proinflammatory cytokine, interleukin (IL)-6 have been related to several chronic inflammatory diseases. Inter-individual variation in the severity of gastric inflammation may be important in determining the clinical outcome of an Helicobacter pylori infection and relate to polymorphisms in this region. MATERIALS AND METHODS: We studied H. pylori-infected patients with duodenal ulcer or gastric cancer. In addition six gastric cancer cell lines, AGS, SNU-668, MKN-1, MKN-7, MKN28 and KATOIII, were cocultured with both cag pathogenicity island-positive and -negative H. pylori. Single nucleotide polymorphisms at positions -174, -572, and -597 in the IL-6 promoter region were identified by PCR-RFLP. The IL-6 production from the cancer cells was determined by ELISA. RESULTS: Sixty patients with gastric cancer and 60 with duodenal ulcer were studied. The alleles at positions -174 and -597 were closely linked (-174G/-597G or -174C/-597A) regardless of the ethnic group or disease presentation. There was no difference in the allele frequency at any of the sites among patient groups. H. pylori-induced IL-6 production from the gastric cancer cell lines was also independent of the IL-6 polymorphisms or the presence of the cag pathogenicity island. CONCLUSIONS: The genetic polymorphisms in IL-6 can be attributable to ethnicity and appear to be independent of the clinical outcome of an H. pylori infection.

Adult↗