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D Y Graham

Publications and source records attributed to D Y Graham.

At least 181 records · Page 10Linked to original sources
PubMed1998

Lymphocytes in the human gastric mucosa during Helicobacter pylori have a T helper cell 1 phenotype.

BACKGROUND & AIMS: Studies have shown that gastric T cells are increased during Helicobacter pylori infection. The purpose of this study was to characterize the human gastric T-cell responses in the presence or absence of H. pylori. METHODS: T-cell surface antigens were examined by immunohistochemistry or after isolation for evaluation of surface antigens and cytoplasmic cytokines using flow cytometry. RESULTS: CD4+ and CD8+ T cells were increased in situ during infection with H. pylori. Freshly isolated gastric T cells expressed cytoplasmic interferon gamma (IFN-gamma) and interleukin (IL)-2 after a brief stimulation. Simultaneous four-color flow cytometry demonstrated that both CD8+ and CD4+ T cells expressed IFN-gamma. Because stimulation through CD30 favors the induction of IL-5 and Th2 cells, gastric and colonic T cells were examined for CD30 expression. Consistent with the notion that Th2 cells are found in the intestine, CD30 was evident throughout the lamina propria of the colon but was virtually absent in the stomach. Furthermore, freshly isolated gastric T cells produced little IL-4 and virtually no IL-5 or tumor necrosis factor beta. CONCLUSIONS: These observations show that gastric T cells resemble the Th1 type, which may explain their failure to induce immunity to H. pylori and their ability to contribute to the pathogenesis of gastric disease.

Adult↗
PubMed1998

Intestinal metaplasia with adherent Helicobacter pylori: a hybrid epithelium with both gastric and intestinal features.

Helicobacter pylori seem to avoid areas of intestinal metaplasia in the gastric mucosa, but attachment of these bacteria to epithelium with the appearance of incomplete intestinal metaplasia has been documented. To characterize the nature of the epithelium to which H pylori was attached, we carried out an immunohistochemical study using monoclonal antibodies against gastric surface mucous cell mucins (M1), blood group-related carbohydrates antigens (Le(a), sialyl Le(a), Le(b), type 1H, and type 2H) and sialyl Tn antigen. The results of this study suggest that these areas of H pylori attachment represent a hybrid epithelium whose cells share characteristics of both gastric surface mucous cells and intestinal metaplastic cells. Whether all areas of incomplete intestinal metaplasia represent an intermediate stage between the normal gastric epithelium and the fully developed complete type of metaplasia remains to be determined.

ABO Blood-Group System↗
PubMed1998

REP-PCR fragments as biomarkers for differentiating gastroduodenal disease-specific Helicobacter pylori strains.

We previously identified four potential putative gastroduodenal disease fragments by using the interspersed repetitive extragenic palindromic DNA sequence based PCR (REP-PCR) technique. We investigated these fragments with regard to their disease specificity. The putative disease-specific REP-PCR fragments were cloned, mapped by restriction enzymes, cross-hybridized, and confirmed by Southern hybridization. The four fragments were also used as probes against REP-PCR amplicons from H. pylori isolates obtained from gastritis (N = 20), duodenal ulcer (N = 30), and gastric cancer patients (N = 30). Three of these fragments (1.4- and 0.76-kb for gastritis; 1.35 kb for duodenal ulcer) were amplified without any discrimination between any disease-specific H. pylori isolates. However, amplification following hybridization with the fourth 0.81-kb fragment was observed only from gastritis (60%) and duodenal ulcer (52%) but with none (0%) of gastric cancer patients. Nucleotide sequence analysis of the 0.81-kb fragment revealed that it was an open reading frame of the hypothetical protein HP0373 matched to the position of 380,966 to 383,068 nucleotides of the H. pylori complete genome sequence. Hence, the REP-PCR sequence was not a extragenic palindromic DNA sequence. The hypothetical protein was also present in all the tested isolates. The REP-PCR fingerprinting technique is useful to differentiate disease-specific H. pylori strains based on the interspersed repetitive extragenic palindromic DNA sequences; however, it may not be useful to identify disease-specific virulence determinant(s) without being confirmed by DNA sequence analysis and functional studies.

Amino Acid Sequence↗
PubMed1998

Search for putative virulence factors of Helicobacter pylori: the low-molecular-weight (33-35 K) antigen.

Early studies suggested that two Helicobacter pylori proteins, CagA and VacA, were virulence factors. Support for that hypothesis has been undermined by geographic differences in prevalence of these antigens. To identify other possible putative virulence factors by establishing a relationship between antigens and different H. pylori diseases, two commercial available immunoblot assay kits, HelicoBlot 2.0 (Genelabs Diagnostics, Singapore) and RIDA Blot Helicobacter (R-Biopharm GmbH, Darmstadt, Germany), were used to investigate the prevalence of various specific antigen seropositivity in 80 H. pylori-infected Japanese (20 each with gastritis, duodenal ulcer, gastric ulcer, or gastric cancer). The production of interleukin-8 (IL-8) in biopsy specimens was also measured by enzyme-linked immunosorbent assay (ELISA). Both assays had 100% sensitivity; specificity was 90% for HB2.0 and 80% for RIDA-BH. With the exception of the 33-35 K antigen, there was no relationship between antigens, endoscopic diagnoses, histological findings, or mucosal IL-8 levels. The 33-35 K antigen was present in 97.5% (39 of 40) patients with gastric or duodenal ulcer compared to 70% (14 of 20) those with chronic gastritis (P < 0.006). The mean IL-8 levels in the corpus was significantly higher in those with antibody to the 33-35 K antigen compared to those without (105.4+/-22 pg/mg vs 10.2+/-8.8 pg/mg) (P=0.015). There was no relationship between other antigens including CagA and production of IL-8. In conclusion, the low-molecular-weight 33-35 K antigen may play an important role in the pathogenesis of H. pylori-related disease.

Antibodies, Bacterial↗
PubMed1998

One-week triple therapy with lansoprazole, clarithromycin, and metronidazole to cure Helicobacter pylori infection in peptic ulcer disease in Korea.

The efficacy and acceptability of classical bismuth triple therapy may be limited by poor patient compliance and adverse effects. It is widely agreed that improved, simpler, and reliable therapies are needed to cure Helicobacter pylori infection and foster patient compliance. We evaluated the efficacy and side effects of a Bazzoli triple therapy substituting lansoprazole for omeprazole for H. pylori infection in active peptic ulcer in Korea (30 mg of lansoprazole, 250 mg of clarithromycin, and 400 mg of metronidazole, all twice daily). H. pylori status was evaluated by rapid urease test, histology, and culture at entry and four or more weeks after ending antimicrobial therapy. Fifty-eight patients (mean age: 43 years) with gastric (N = 30) or duodenal ulcer (N = 28) and H. pylori infection were studied. H. pylori was cured in 47 (81%, 95% CI = 69-90%). Mild side effects, including vomiting, diarrhea, and itching, were observed in four patients (7%). Compliance averaged 95%. Fifty-five ulcers (95%) were healed. Pretreatment pylorobulbar deformity was observed in 49 patients (85%), and in 43 (88%) the deformity disappeared after treatment. Pretreatment metronidazole and clarithromycin resistance was observed in 87% and 2% of patients, respectively. The cure rate of H. pylori infection was significantly higher in patients >50 years of age than those <50. Treatment with low-dose one-week lansoprazole, clarithromycin, and metronidazole resulted in a relatively low cure rate, but was well tolerated. Studies to define the optimal duration, dose, and dosing interval of this combination therapy in Korea are needed.

2-Pyridinylmethylsulfinylbenzimidazoles↗
PubMed1998

A randomized comparison of dilatation alone versus dilatation plus laser in patients receiving chemotherapy and external beam radiation for esophageal carcinoma.

Most patients with carcinoma of the esophagus have advanced disease at presentation. Since cure is usually not possible, the goal of treatment is the palliation of dysphagia. Palliative modalities include bougies, balloons, stents, tumor probe, laser, surgery, chemotherapy, and radiation. In recent years, combined chemotherapy and radiation has shown promising results. However, the relief of dysphagia is slow and frequently incomplete. We compared the effectiveness of dilatation alone versus dilatation plus Nd-YAG laser therapy for the relief of dysphagia while assessing the role of chemotherapy and radiation as an adjunct to surgery. Fifteen patients with squamous cell carcinoma of esophagus who were deemed fit for intensive chemotherapy and radiation were randomized to receive either dilatation alone (N = 7) or dilatation plus laser (N = 8); the end-point for initial success was the passage of a 45 French Savary dilator, and the relief of dysphagia. At entry, 13 of these 15 patients were judged potentially resectable. However, after chemotherapy and radiation, only 3 of 13 (20%) patients could be offered surgery; the remainder were considered too poor a surgical risk. Follow-up was for 30 months, or until death. Further dilatations were performed as needed for relief of dysphagia. No difference was observed between the laser plus dilatation and the dilatation alone group with respect to the degree of dysphagia, weight record, quality of life index (Karnofsky score), or mortality rate. Our results indicate that in patients undergoing chemotherapy and radiation for esophageal carcinoma, dilatation alone provides adequate palliation of dysphagia, and in these patients, chemotherapy and radiation is a poor adjunct to surgical treatment.

Adult↗
PubMed1998

Microflora of gastric biopsies from patients with duodenal ulcer and gastric cancer: a comparative study of patients from Korea, Colombia, and the United States.

It remains unclear why the spectrum of H. pylori-related diseases differs among different geographic regions. We examined the non-H. pylori contamination rates of the stomach in patients with duodenal ulcer or gastric adenocarcinoma from three different regions with different spectra of H. pylori-related diseases. Gastric biopsies were cultured from patients with duodenal ulcer or histologically proven gastric cancer from Seoul, Korea; Bogota, Colombia; and Houston, Texas. The frequency of non-H. pylori contamination was tallied in relation to the clinical diagnosis. Cultures from 247 duodenal ulcer patients and 165 patients with gastric cancer had bacterial growth. H. pylori was isolated from 207 (73.7%) patients with duodenal ulcer and 90 (47.1%) patients with gastric cancer (P < 0.001). In patients with duodenal ulcer (DU) or gastric cancer (GC), the rate of positive cultures for H. pylori were not statistically different (P > 0.143 for DU, P > 0.190 for GC) between regions. The frequency of isolation ranged from 69% to 79% for DU patients and from 39% to 50% for gastric cancer patients. Non-H. pylori bacterial contamination was found more frequently (63%) in Colombian duodenal ulcer patients compared to 30% ulcer patients from the United States or Korea (P < 0.001). Non-H. pylori growth occurred in 50.8-75.5% of cancer patients and was significantly lower in US patients than in patients from either Colombia or Korea (P < 0.01). The geographic location as well as disease status affects the rate of H. pylori recovery and non-H. pylori contamination of the stomach and may play a role in the geographic differences in manifestation of H. pylori infection. The fact that the proportion of gastric cancer patients in the United States with non-H. pylori contamination was significantly less than that of Korea or Colombia shows that the notion of an almost universal increase in gastric microbial content in gastric adenocarcinoma should be reconsidered.

Adenocarcinoma↗
PubMed1998

Amoxycillin resistance is one reason for failure of amoxycillin-omeprazole treatment of Helicobacter pylori infection.

BACKGROUND: The efficacy of omeprazole and amoxycillin dual therapy to treat Helicobacter pylori infection has been inconsistent, suggesting the presence of host or bacterial factors influencing treatment success. The aim of this study was to assess the role of pre-treatment amoxycillin resistance in the efficacy of omeprazole and amoxycillin dual therapy. METHODS: We studied 43 consecutive dyspeptic patients with H. pylori infection. Pre-treatment H. pylori infection was established by the combination of positive rapid urease test, culture and histology. Amoxycillin susceptibility testing was performed by an Epsilometer test (E-test) method and amoxycillin resistance was defined as minimum inhibitory concentration greater than 8 microg/mL. Patients received 20 mg omeprazole twice daily for 28 days and amoxycillin 1000 mg twice daily for 2 weeks. Adverse effects were documented using a questionnaire. H. pylori status was reassessed 6-8 weeks after the end of treatment by rapid urease testing and histological examination of gastric biopsies. RESULTS: Forty-two dyspeptic patients completed the study, and one patient dropped out. H. pylori infection was cured in 2 3 of 42 patients (55%). The cure rate was higher in patients harbouring amoxycillin-sensitive organisms than in those with resistant strains: 66% (19/29) vs. 31% (4/13), respectively (P = 0.049). No significant differences in cure rates were evident in relation to age, sex, smoking habits or compliance. CONCLUSIONS: The effectiveness of amoxycillin-omeprazole dual therapy was greatly reduced in the presence of pre-treatment amoxycillin-resistant H. pylori. The success rate in patients with amoxycillin-sensitive H. pylori was only 66%, suggesting the presence of additional factors affecting the efficacy of this therapy.

Adult↗
PubMed1998

An alternative non-macrolide, non-imidazole treatment regimen for curing Helicobacter pylori and duodenal ulcers: ranitidine bismuth citrate plus amoxicillin. The RBC H. pylori Study Group.

BACKGROUND: Because patients who fail to be cured of H. pylori infection following macrolide or imidazole therapy are difficult to treat, there is a clear need for a reasonably effective and simple second-line treatment regimen. The purpose of these two studies was to evaluate the efficacy of ranitidine bismuth citrate (RBC) plus amoxicillin for the cure of H. pylori infection and for healing duodenal ulcers and preventing ulcer relapse. MATERIALS AND METHODS: Two identically designed randomized, double-blind, double-dummy studies were conducted in patients with an H. pylori-associated duodenal ulcer. Patients were treated with either RBC 400 mg bid for 4 weeks plus amoxicillin 500 mg qid for 2 weeks, RBC 400 mg bid for 4 weeks and placebo qid for 2 weeks, placebo bid for 4 weeks and amoxicillin 500 mg qid for 2 weeks, or placebo bid for 4 weeks and placebo qid for 2 weeks. Patients with healed ulcers after 4 weeks of treatment were eligible for entry into a 24-week observation phase for the assessment of H. pylori status (culture, histology, and CLOtest) and ulcer relapse. RESULTS: A total of 229 patients with confirmed H. pylori infection at baseline were evaluated. Of these, 132 whose ulcers had healed entered the 24-week posttreatment observation phase. The combination of RBC plus amoxicillin resulted in higher H. pylori cure rates (55%) and higher duodenal ulcer healing (74%) than did either treatment alone. All treatment were well tolerated. CONCLUSIONS: The combination of ranitidine bismuth citrate plus amoxicillin cures H. pylori infection in more than half of the patients treated. This treatment regimen shows promise as the basis for future non-macrolide, non-imidazole triple therapy regimens for curing H. pylori infection. Such regimens may be appropriate second-line treatment for patients who are resistant to or who are unable to tolerate macrolide- or imidazole-containing therapies.

Adolescent↗
PubMed1998

Effect of H. pylori infection and CagA status on leukocyte counts and liver function tests: extra-gastric manifestations of H. pylori infection.

BACKGROUND: It has been suggested that H. pylori infection is associated with abnormalities in total leukocyte count as well as the number of basophils and lymphocytes. In addition, CagA seropositivity has been associated with an increase in serum transaminase (SGOT) values. The aim of this study was to confirm the findings of previous subgroup analyses in patients before and after treatment for H. pylori infection and to ascertain whether the abnormalities reversed following successful treatment. METHODS: Blood counts and serum transaminase levels were obtained prior to and following treatment of H. pylori infection of H. pylori-infected duodenal ulcer patients. CagA status was assessed by Western blot of the H. pylori isolates obtained from the patients. RESULTS: Ninety-four ulcer patients were studied, including 77 with CagA-positive H. pylori isolates (82%) and 17 with CagA-negative H. pylori isolates. All study parameters remained within normal limits both before and after therapy. There were no significant changes in any study parameter in those who failed therapy. Successful therapy resulted in a significant fall in total white cell count (7413 +/- 520 cmm to 6738 +/- 410 cmm, for pretreatment vs. cured, respectively, p = 0.04) and was almost entirely accounted for by a reduction in the number of circulating polymorphonuclear leukocytes (4595 +/- 370 cmm to 3855 +/- 270 cmm for pretreatment vs. cured, respectively, p = 0.015). The pretreatment SGOT and basophil count were significantly higher in those with CagA-positive H. pylori (SGOT = 23 +/- 1 vs. 18.5 +/- 1 U). Successful or failed therapy with follow-up for 3 months post therapy did not result in a significant change of SGOT levels. CONCLUSIONS: We confirmed an increase in total leukocyte count and number of polymorphonuclear leukocytes in those with H. pylori infection. We also confirmed higher SGOT levels with CagA-positive H. pylori infection, but the failure to resolve within 3 months of cure of the infection makes it unlikely to be a direct result of the H. pylori infection.

Anti-Bacterial Agents↗
PubMed1998

How do practicing clinicians manage Helicobacter pylori-related gastrointestinal diseases in Germany? A survey of gastroenterologists and family practitioners.

BACKGROUND: Since the bacterium H. pylori was identified in 1982, overwhelming evidence has implicated it as the causal factor in the occurrence and relapse of peptic ulcer disease. The major objective of this study was to examine the extent to which physicians recognize H. pylori as a causal agent in peptic ulcer disease or as potential cofactor in other gastrointestinal diseases, and the extent to which this knowledge has influenced diagnostic and therapeutic practices. MATERIALS AND METHODS: Using a national mail survey in Germany in September 1995, 1197 family practitioners and 1197 gastroenterologists were selected for the study. RESULTS: Of the surveyed physicians, 756 (32%) responded. Family practitioners treated almost 50% of their patients with initial presentation of suspected ulcer disease without ordering further diagnostic tests. More than 25% of the family practitioners and 14% of the gastroenterologists reported that they do not treat diagnosed H. pylori infection in the first presentation of duodenal ulcer. At the time we conducted the study, 22% of responding family practitioners and 5% of responding gastroenterologists treated the first presentation of H. pylori-positive ulcer disease with regimens determined to be ineffective according to the available literature. CONCLUSIONS: Gastroenterologists preferred to treat H. pylori infection when the associated disease was one for which a causal relationship had been more clearly established, while family practitioners showed less discrimination. In order to provide optimal therapy aimed at minimizing the course and consequences of H. pylori-related diseases, researchers in the field must ensure continuous dissemination of current knowledge.

Clinical Competence↗
PubMed1998

H. pylori and cagA: relationships with gastric cancer, duodenal ulcer, and reflux esophagitis and its complications.

BACKGROUND: Helicobacter pylori infection is accepted to be associated with two mutually exclusive diseases: duodenal ulcer and gastric cancer. Attention has recently focused on possible relationships between H. pylori and gastroesophageal reflux disease and its complications such as adenocarcinoma of the gastric cardia. The aim of this study was to provide a framework for explaining the seemingly paradoxical associations between H. pylori and various gastrointestinal diseases. METHODS: Available data regarding H. pylori infection, cagA, acid secretion, corpus gastritis, and gastroesophageal reflux disease (GERD) and its complications are reviewed, and testable hypotheses are presented. RESULTS: Linking the type of H. pylori (cagA-positive vs. cagA-negative), the pattern and intensity of inflammation, and acid secretion explains the apparent paradoxes in the associations between H. pylori and gastric cancer, duodenal ulcer, and GERD. Although H. pylori is inhibited by bile, a duodenal acid load sufficient to lower the average pH to precipitate bile acids overcomes that inhibition. H. pylori that contain a functional cag pathogenicity island produce a vigorous inflammatory response. The severity of mucosal inflammation predicts likelihood of different outcomes (e.g., in the bulb with likelihood of developing duodenal ulcer, and in the corpus with the degree of reduction in acid secretion and the rate of development of multifocal atrophic gastritis). Development of H. pylori corpus gastritis is promoted by profound inhibition of acid secretion (e.g., childhood infections or a high level of antisecretory therapy). The CagA protein, or the cagA gene, is a marker for enhanced inflammation, but CagA is not directly involved in the pathogenesis of gastric cancer or duodenal ulcer disease, nor is it a reliable indicator of the presence of a functional cag pathogenicity island. CONCLUSION: The relationship between the type of H. pylori infection, presence or absence of a functional cag pathogenicity island, corpus inflammation, and acid secretion explains the duodenal ulcer/gastric cancer paradox and the relationship between H. pylori infection and the complications of GERD. The predicted rank order for the presence of GERD and its complications (peptic stricture, Barrett's esophagus, and adenocarcinoma of the gastric cardia) is highest in the population without H. pylori infection, less in those with H. pylori infection, and least in those infected with cagA-positive H. pylori. Controversy and confusing epidemiological observations will continue unless future studies provide data on the gastric corpus histology (or acid secretion) as well as regarding the presence or absence of a functional and intact cag pathogenicity island of the infecting organism.

Antigens, Bacterial↗
PubMed1998

Relationship of vacA genotypes of Helicobacter pylori to cagA status, cytotoxin production, and clinical outcome.

BACKGROUND: Mosaicism in vacA alleles with three distinct families of vacA signal sequences (s1a, s1b and s2) and two distinct families of middle region alleles (m1 and m2) has been reported. It was suggested that the vacA s1a genotype was closely associated with duodenal ulcer disease and with high cytotoxin production. The aim of this study was to evaluate the role of vacA genotyping with respect to gastric inflammation and injury, cytotoxin activity, and clinical presentation. METHODS: H. pylori from patients with gastritis, peptic ulcer disease, or gastric cancer were characterized by vacA typing by polymerase chain reaction (PCR) and DNA sequencing. In vitro cytotoxin activity was assessed by vacuolation assay using Vero cells as well as with Hela cells. RESULTS: Four hundred ninety-one strains were tested. vacA genotype s1a/m1 was present in more than 95% of strains independent of presentation with gastritis, peptic ulcer, or gastric cancer. No vacA genotype was associated with high average cytotoxin activity. The s2/m2 isolates had low or absent cytotoxin activity. All cagA negative strains (n = 18) were s1a strains and both s2/m2 strains were cagA positive. One strain that was a recombinant of m1 and m2 strains was identified and had low cytotoxin activity. The nucleotide and amino acid sequences between original m1 strains and Japanese m1 strains (new m1 strains) were about 85% and 81%, respectively. Strains with the new m1 genotype had nucleotide and amino acid sequences similarity of more than 96%. There was no difference in cytotoxin activity between strains with the Western type m1 and the new type m1 genotype. CONCLUSION: In this as in other reported studies ( approximately 1500 patients overall) vacA genotype was strongly but not exclusively associated with the presence of cagA. Overall, the studies did not support a role for vacA genotyping in relation to cytotoxin activity, virulence, histologic finding, or risk of a particular H. pylori disease. vacA genotype s1 is likely to be a surrogate marker for the presence of the cag pathogenicity island.

Adult↗
PubMed1998

Failure to confirm association of vac A gene mosaicism with duodenal ulcer disease.

BACKGROUND: Mosaicism of the Helicobacter pylori vac A gene comprises two families of allelic variations of the signal sequence region (s1, s2) and of the mid-region (m1, m2). Initial studies suggested that peptic ulcer disease correlated with the s1 subtype of vac A. We compared the prevalence of various vac A genotypes of H. pylori isolates obtained from duodenal ulcer (DU) patients and subjects with simple gastritis. Those isolates with s1 type were further examined to determine whether the specific vac A s1 (s1a versus s1b) genotype enabled prediction of gastroduodenal disease. METHODS: H. pylori isolates were obtained from 38 patients with endoscopically documented DU and 39 individuals with asymptomatic H. pylori gastritis from Houston, Texas. The vac A genotype of each isolate was determined by polymerase chain reaction (PCR) amplification of genomic DNA for specific regions of the vac A gene. Those isolates with s1 vac A subtype were further examined to determine whether they had s1a or s1b mosaicism. RESULTS: There was no difference in frequency of the s1 genotype of isolates obtained from patients with duodenal ulcer or asymptomatic H. pylori gastritis in this sample (84% versus 79%, respectively; P = 0.77). The s1/m1 vac A genotype was detected in isolates from 16 duodenal ulcer patients versus 15 with H. pylori gastritis (P = 0.82). Detailed analysis of the s1 region failed to show a correlation of either s1a or s1b with duodenal ulcer. Both s1a and s1b genotypes were detected in 24 strains, and both m1 and m2 mid-gene PCR amplicons were seen in 16 strains. CONCLUSIONS: We were unable to use H. pylori vac A genotyping to predict type of gastroduodenal disease in our patient sample. This failure to confirm an association of vac A genotype and duodenal ulcer disease differs from samples from other regions. This most likely represents an example of differences in H. pylori strains infecting host populations in different geographic regions. This study confirms the importance of establishing statistical associations with isolates from widely separate geographic regions before concluding that disease-related associations exist.

Adult↗
PubMed1998

Demonstration of unexpected antibiotic resistance of genotypically identical Helicobacter pylori isolates.

With use of multiple- and single-colony expansion procedures, the results of susceptibility testing of Helicobacter pylori isolates from patients with duodenal ulcer were assessed by Etest. The H. pylori genotype was assessed by repetitive extragenic palindrome-based polymerase chain reaction (REP-PCR). There was a high degree of genotypic heterogeneity between different patients, but a single REP-PCR pattern was found for 92% of patients. In contrast, a high degree of phenotypic heterogeneity was shown among the isolated colonies. Antibiogram susceptibility patterns differed only with respect to metronidazole but not with respect to clarithromycin or amoxicillin. The 42% rate of resistance to metronidazole determined with use of the conventional multiple-strains expansion method was increased to 92% when the single-colony expansion method was used. Similarly, dual clarithromycin/metronidazole resistance was increased from 8% to 42% with single-colony expansion. Despite evidence of a single genotype in most patients, single-colony expansion shows that routine susceptibility testing may greatly underestimate the frequency of metronidazole resistance.

Amoxicillin↗
PubMed1998

Acquisition versus loss of Helicobacter pylori infection in Japan: results from an 8-year birth cohort study.

Studies of the pattern of change in the epidemiology of Helicobacter pylori infection are scarce. A longitudinal cohort study consisted of 644 children and adults, and two independent cross-sectional surveys were conducted in rural Japan between 1986 and 1994. The anti-H. pylori IgG seroconversion rates were 1.1% and 1% per year for children and adults, respectively. The seroreversion rate per year was 1.8% for children and 1.5% for adults. The cohort study was confirmed by the two cross-sectional studies. H. pylori prevalence fell in all age groups in both children (odds ratio [OR] = 0.5, 95% confidence interval [CI] = 0.2-1.0, P = .05) and adults (OR = 0.4, 95% CI = 0.3-0.6, P = .001). The rate of loss of H. pylori infection was greater than the acquisition. Data regarding acquisition and loss of H. pylori infection are critical to understanding the epidemiology of the infection and to developing treatment and vaccination strategies.

Adolescent↗
PubMed1998

How do clinicians practicing in the U.S. manage Helicobacter pylori-related gastrointestinal diseases? A comparison of primary care and specialist physicians.

OBJECTIVES: We sought to examine the extent to which physicians recognize H. pylori as a causal agent in peptic ulcer disease or as a potential cofactor in other gastrointestinal diseases, and to observe how this knowledge has influenced diagnostic and therapeutic practices. METHODS: We used a national mail survey in the U.S. between February and May of 1996, querying 5994 U.S. physicians (family/general practitioners [FPs], internists [IMs], and gastroenterologists) selected at random from three different membership databases of professional associations. RESULTS: The response rate was 52%. More than 95% of physicians who treat symptoms empirically would prescribe acid suppressant therapy rather than anti-H. pylori therapy. Between 43% and 66% of physicians, varying in frequency by medical specialty, would treat the infection in H. pylori-positive patients with nonulcer dyspepsia. In confirmed peptic ulcer disease, between 88% and 100% of physicians would treat the H. pylori infection, depending on the physician group and whether or not the presentation of an ulcer was recurrent. Although 103 distinct anti-H. pylori regimens were reported, 89% of the gastroenterologists and 70% of the primary care physicians (PCPs) used combinations of antimicrobials with reported cure rates of at least 80%. CONCLUSIONS: General knowledge regarding H. pylori-associated diseases was widespread among primary care physicians and gastroenterologists. However, anti-H. pylori therapies judged ineffective were reported as the first choice regimen by 5% of gastroenterologists and 18% of primary care physicians. Gastroenterologists appear to implement the latest scientific developments in the field rapidly whereas PCPs manifest a delayed response, due to either insufficient knowledge or to other factors influencing their approach to treatment.

Gastroenterology↗