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D Y Graham

Publications and source records attributed to D Y Graham.

At least 289 records · Page 16Linked to original sources
PubMed1996

The interaction of pH, bile, and Helicobacter pylori may explain duodenal ulcer.

BACKGROUND: Inhibition of Helicobacter pylori growth by bile suggests that it should be difficult for H. pylori to colonize the duodenum and cause duodenal ulcer. To search for a common mechanism, we investigated the relationship between H. pylori strain (duodenal ulcer vs gastritis), type of bile acid conjugate, and inhibition of H. pylori growth. METHODS: H. pylori isolates from patients with duodenal ulcer and from volunteers with asymptomatic gastritis (six each) were grown in brain heart infusion broth medium containing mixtures of glycocholate, taurocholate, glycodeoxycholate, taurodeoxycholate, glycochenodeoxycholate, and taurochenodeoxycholate with and without lecithin. RESULTS: Synthetic human bile with or without lecithin inhibited H. pylori growth in a dose-dependent manner. There was no difference in inhibition between H. pylori gastritis and duodenal ulcer isolates. Glycine and mixed glycine and taurine-conjugated bile acids inhibited H. pylori more than taurine-conjugated bile acids (e.g., 51%, 67%, and 80% compared to 21%, 39%, and 46% for 1, 2, and 4 mM mixed conjugates compared with taurine conjugates, p < 0.05, respectively. CONCLUSIONS: The ability of H. pylori to grow in the presence of taurine-conjugated bile acids and the precipitation of glycine but not taurine bile acid conjugates by acid may provide one missing link among inhibition of H. pylori by bile, acid secretion, ability of antisecretory therapy to accelerate ulcer healing, and the ability of H. pylori to colonize the duodenal bulb of ulcer patients, leading to duodenal ulcer. These data also explain the disparate results of previous investigations of the effect of bile reflux in the stomach on the presence of H. pylori.

Bile↗
PubMed1996

Noninvasive detection of Helicobacter pylori infection in clinical practice: the 13C urea breath test.

OBJECTIVES: To validate the 13C urea breath test for the detection of Helicobacter pylori infection both before and after treatment. METHODS: 13C urea breath tests with 125-mg and 250-mg doses were carried out on each of 60 infected and 60 noninfected subjects. Results were compared with histological examination of gastric biopsies to establish detection limits. The best cut-off point was used in a clinical trial of the efficacy of the breath test in duodenal ulcer patients before and after antimicrobial therapy. The incremental increase (percentage, delta over baseline in U of delta/mil) in respiratory 13CO2 abundance was associated with histological evidence of H.pylori. Outpatient, tertiary care medical center, and secondary and primary care facilities were included. One hundred twenty healthy asymptomatic subjects and 465 patients with duodenal ulcer disease were studied. The test kit assessed repeatability of breath sample collection and storage and stability of stored samples. Test performance was analyzed by comparison of 125-mg and 250-mg 13C urea with measurements at 30 and 40 min postdose. The test was used to diagnose active H.pylori infection and gauge success of antimicrobial therapy. RESULTS: The test kit results were highly reproducible. The cut-off values were higher with 250-mg compared with 125-mg doses of 13C urea and 40 min compared with 30 min. Using a 125-mg 13C urea and test detection limit of 2.4% at 30 min, the accuracy was 94.8 (95% confidence interval = 92-97%) before antimicrobial therapy and 95.4% (95% confidence interval = 91-98%) after. An increase of 2.4% in the abundance of breath 13CO2 measured 30 min after a 125-mg dose of 13C urea reliably indicated the presence of active H.pylori infection either before or after antimicrobial therapy. The 13C urea breath test provides a simple and reliable and noninvasive method of assessing H.pylori status.

Anti-Bacterial Agents↗
PubMed1996

Allelic variation in the cagA gene of Helicobacter pylori obtained from Korea compared to the United States.

OBJECTIVE: Helicobacter pylori is an important factor in the development of duodenal ulcer disease and has been implicated in the pathogenesis of gastric adenocarcinoma. It has been suggested that the cagA gene is a marker for more virulent strains of H. pylori. METHODS: We determined the prevalence of the cagA gene in 60 clinical isolates [34 from gastric carcinoma patients (CA), 26 from duodenal ulcer patients (DU)] from Korea, a country with a high incidence and mortality from gastric cancer. Genomic DNA was polymerase chain reaction-amplified by using two different primer sets for the cagA gene. The first cagA primer set amplifies a 297-bp product from the midregion of the cagA gene. The second primer set, which was previously established in a patient population from the Houston area (21 DU patients, 20 from individuals with asymptomatic gastritis) amplified a 1.4-kb region further downstream in the cagA gene. RESULTS: The expected 297 bp polymerase chain reaction amplicon for cagA was identified in 59/60 (98.3%) H. pylori isolates from Korea (33/34 CA, 26/26 DU), and in 36/41 (88%) isolates from the Houston area (20/21 DU, 16/20 asymptomatic gastritis) (NS). Using the second cagA primer set, the expected 1.4-kb product was found in only 1/60 (1.7%) H. pylori isolates from Korea (1/34 CA, 0/26 DU), and in 36/41 (88%) of isolates from the Houston area (20/21 DU, 16/20 GST) (p < 0.001). Western blot analysis showed that all Korean H. pylori isolates expressed cagA. CONCLUSIONS: The high prevalence of the cagA gene in H. pylori isolates from Korean patients with gastric adenocarcinoma or duodenal ulcers indicates that the cagA gene is common in H. pylori strains, and therefore, is not reliable as a single marker for the discrimination of H. pylori strains with respect to a specific disease. Our data further suggest that allelic variations in the genome of H. pylori strains may exist and that distinct H. pylori populations may circulate in different geographic regions.

Adenocarcinoma↗
PubMed1996

Proposal for use of a standard side effect scoring system in studies exploring Helicobacter pylori treatment regimens.

Many antibiotic regimens for treating Helicobacter pylori infection are currently used in clinical trials. The reported side-effect profiles of similar anti-Helicobacter therapies vary widely due to the use of different scoring systems. Therefore side-effect data from separate studies cannot be compared. Only randomized controlled trials will show how side-effect profiles and tolerability really differ between regimens, but few such studies are available. Therefore a choice of treatment based on side-effect profile is not possible at present. We seek standardization of side-effect registration among investigators and propose a side-effect questionnaire which, if generally accepted, would make it possible to compare data between trials.

Adverse Drug Reaction Reporting Systems↗
PubMed1996

Nonsteroidal anti-inflammatory drugs, Helicobacter pylori, and ulcers: where we stand.

BACKGROUND: Despite the progress in the diagnosis and treatment of Helicobacter pylori-related peptic ulcer disease, it has become apparent that we may be in the midst of an epidemic of nonsteroidal anti-inflammatory drug ulcers and ulcer complications. We also have almost no information about whether there is a link between ulcers in NSAID users and H. pylori infection or whether clinically significant interactions occur. METHODS: Current data regarding the diagnosis, prevention, and treatment of NSAID-induced ulcers and the possible relationship between H. pylori ulcers and NSAID use is reviewed. CONCLUSION: We need to rethink past conclusions about NSAIDs and gastroduodenal complications and also re-do many of the experiments, taking into account the H. pylori status of the patient (infected, uninfected, cured). It is predicted that the epidemic of NSAID complications will only get worse. Only the future will tell whether selective COX II inhibitors or NO-NSAIDs that incorporate a nitroxybutyl moiety will actually provide the same benefit at lower risk. Until then we must rely on more rational use of NSAIDs, and misoprostol to keep the number of complications at a minimum.

Adult↗
PubMed1996

Helicobacter pylori does not migrate from the antrum to the corpus in response to omeprazole.

BACKGROUND: Omeprazole is known to have an effect on Helicobacter pylori in vivo. One opinion is that H. pylori "migrates" from the antrum to the corpus in response to omeprazole therapy. METHODS: To determine whether H. pylori migrates in response to omeprazole, we assessed the presence of H. pylori in the antrum and corpus in duodenal ulcer patients receiving omeprazole for 4 wk. Culture and histological examination of antral biopsies (Genta stain) were performed before patients received omeprazole, at the end of therapy, and 4-6 wk later. The end points were presence or absence of H. pylori and the number of H. pylori colonies per biopsy. RESULTS: Seventy-two patients had H. pylori in both the antrum and corpus at entry and 4-6 wk after ending therapy. Three general patterns were prevalent at the end of omeprazole therapy: antrum- and corpus-positive (54%), antrum-negative and corpus-positive (24%), both antrum- and corpus-negative (21%), and one patient had antrum-positive with corpus-negative (1%). Evaluation of the number of colonies per biopsy in those who remained H. pylori-positive in both the antrum and corpus throughout showed that the number of H. pylori decreased in both the antrum and corpus during therapy (507 +/- 60 vs. 225 +/- 51, p < 0.01 and 415 +/- 58 vs. 290 +/- 46 0.1) for antrum and corpus, respectively, and tended to return to pre-therapy levels 4-6 wk later. The number of H. pylori in the corpus also decreased in the antrum-negative and corpus-positive group during therapy with omeprazole (433 +/- 87 vs. 185 +/- 61, p < 0.05). In most of the patients studied, the number of H. pylori in the corpus was less posttreatment than it was pretreatment. The decrease in H. pylori load was also reflected in the development of false-negative urea breath tests. CONCLUSIONS: Omeprazole is detrimental to H. pylori in both the antrum and the corpus; migration from the antrum to the corpus in response to omeprazole is a myth.

Anti-Ulcer Agents↗
PubMed1995

Misoprostol reduces serious gastrointestinal complications in patients with rheumatoid arthritis receiving nonsteroidal anti-inflammatory drugs. A randomized, double-blind, placebo-controlled trial.

OBJECTIVE: To investigate whether concurrent administration of misoprostol reduces the occurrence of serious upper gastrointestinal complications, such as perforation, gastric outlet obstruction, or bleeding, in patients with rheumatoid arthritis who are receiving nonsteroidal anti-inflammatory drugs (NSAIDs). DESIGN: 6-month randomized, double-blind, placebo-controlled trial. SETTING: 664 clinical practices of family medicine, internal medicine, or rheumatology in the United States and Canada. PATIENTS: 8843 men and women (mean age, 68 years) receiving continuous therapy with any of 10 specified NSAIDs for control of symptoms of rheumatoid arthritis. Patients were enrolled between July 1991 and August 1993. INTERVENTION: Patients were randomly assigned to receive 200 micrograms of misoprostol or placebo four times a day. MEASUREMENTS: Development of serious upper gastrointestinal complications detected by clinical symptoms or findings (not by scheduled endoscopy). RESULTS: Serious upper gastrointestinal complications were reduced by 40% (odds ratio, 0.598 [95% CI, 0.364 to 0.982; P = 0.049]) among patients receiving misoprostol (25 of 4404 patients) compared with those receiving placebo (42 of 4439 patients). During the first month, more patients receiving misoprostol (20%) than placebo (15%) withdrew from the study, primarily because of diarrhea and related problems (P < 0.001). Risk factors for serious upper gastrointestinal complications were increasing age, history of peptic ulcer or bleeding, and cardiovascular disease. Patients with all four risk factors would have a 9% risk for a major complication in 6 months. CONCLUSIONS: In older patients with rheumatoid arthritis, misoprostol reduced serious NSAID-induced upper gastrointestinal complications by 40% compared with placebo.

Aged↗
PubMed1995

[13C]Aminopyrine breath test detects altered liver metabolism caused by low-dose oral contraceptives.

The [13C]aminopyrine breath test measures hepatic mixed function oxidase activity. The cumulative percent dose recovered over 2 hr is a sensitive indicator of hepatic dysfunction; values < or = 7.0% have been shown to indicate severe liver disease. Previous studies have suggested that the test results may be influenced by the use of oral contraceptives steroids. We compared the results from five non-oral contraceptive-using women with those from 31 women whose duration of oral contraceptive steroid usage ranged from 4 to 204 months. The women were taking one of four oral contraceptive formulations that differed in the amounts of estrogen (20, 35, or 50 micrograms with 1 mg progesterone) and progesterone (35 micrograms estrogen with stepped levels of progesterone of 0.5, 0.75, and 1.0 mg). The [13C]aminopyrine breath test was performed on days 21 and 28 of the menstrual cycle. Cumulative percent dose recovery values among the normal menstrual cycle of non-oral contraceptive steroid-using women were 12.1 +/- 1.6 and 11.8 +/- 1.5% (mean +/- SD). In contrast, oral contraceptive steroid users showed a marked reduction in cumulative percent dose recovery at 21 days, averaging 6.1 +/- 2.3% (P < 0.001), and returned to normal values (10.2 +/- 3.5%) at 28 days in most women(seven days after oral contraceptive steroid usage was paused). The adverse impact on hepatic mixed function oxidase by oral contraceptive formulations did not differ on the basis of estrogen or progesterone content. The adverse impact of oral contraceptive usage on the mixed function oxidase activity measured by the [13C]aminopyrine breath test must be considered for women of childbearing potential.

Adult↗
PubMed1995

Determination of Helicobacter pylori status by reverse transcription-polymerase chain reaction. Comparison with urea breath test.

We previously reported the development and the possible application of reverse transcription-polymerase chain reaction (RT-PCR) assay for the detection of H. pylori in gastric mucosal biopsy specimens. In this communication, the application of this assay was assessed by comparing its results from 79 gastric biopsy specimens obtained from 68 patients with the more traditional [13C]urea breath test. When the amplified products were examined, the specificity and sensitivity of this RT-PCR assay were 100% and 47% on agarose gels and 80% and 91% by Southern hybridization, respectively. The specificity and sensitivity of urea breath test were 91% and 96% and were generally superior to RT-PCR (negative predictive value of 94% for UBT and 59-76% for RT-PCR). Although our RT-PCR results compare favorably with other PCR assays applied to gastric biopsy specimens for the detection of H. pylori, the use of this method did not add significantly to currently available noninvasive diagnostic methods.

Adult↗
PubMed1995

Transport and storage of Helicobacter pylori from gastric mucosal biopsies and clinical isolates.

Various transport and storage conditions for the recovery of Helicobacter pylori from gastric biopsies were evaluated. Gastric mucosal biopsies from 16 Helicobacter pylori-infected patients were stored in cysteine-Albimi medium containing 20% glycerol in a refrigerator (4 degrees C) for 1 and 2 weeks and in a -20 degrees C laboratory freezer for 4 and 12 weeks. Two clinical isolates were stored in saline, Stuart's transport media, cysteine-Albimi broth with 20% glycerol, brucella broth with 20% glycerol and skim milk with 17% glycerol at room temperature, 4 degrees C, -20 degrees C and -70 degrees C. Storage at 4 degrees C for 1 and 2 weeks resulted in Helicobacter pylori recovery from 81% and 19% of biopsies, respectively. Storage at -20 degrees C yielded Helicobacter pylori recovery in 100% and 57% after 4 and 12 weeks, respectively. At room temperature after 6 h, the Helicobacter pylori titer was reduced. The best storage media for frozen isolates were skim milk/glycerol, brucella broth/glycerol and cysteine-Albimi/glycerol (in descending order). Recovery was better at -70 degrees C than -20 degrees C.

Biopsy↗
PubMed1995

Prospective validation of the Baylor bleeding score for predicting the likelihood of rebleeding after endoscopic hemostasis of peptic ulcers.

Endoscopic therapy is effective in securing hemostasis for bleeding ulcers, but bleeding recurs in 10% to 30% of patients. Prospective identification of patients at increased risk for rebleeding is requisite to reducing rebleeding rates. We previously developed a three-component scoring system that identifies patients at increased risk for rebleeding. In the present study, we prospectively validated our scoring system. Forty-seven men ranging in age from 23 to 95 years in whom endoscopic therapy for bleeding ulcers was successful were studied. Patients with pre-endoscopy scores greater than 5 or postendoscopy scores greater than 10 were stratified as high-risk, and patients with pre-endoscopy scores of 5 or less and post-endoscopy scores of 10 or less as low-risk. Twenty-six patients were categorized as high-risk and 19 as low-risk. All patients were followed until discharged from the hospital. The rebleeding rate for high-risk patients was 31% (8 of 26), compared with 0 for low-risk patients (p < .05). We conclude that our scoring system accurately predicts patients at increased risk for rebleeding after successful endoscopic therapy of bleeding ulcers.

Adult↗
PubMed1995

Prospective randomized comparison of polyvinyl bougies and through-the-scope balloons for dilation of peptic strictures of the esophagus.

We prospectively compared the efficacy of polyvinyl bougies (Savary type) passed over a guide wire and through-the-scope balloons for the dilation of peptic esophageal strictures in a randomized study. Thirty-four patients, 17 in each treatment arm, were studied. At entry, dysphagia was assessed according to a six-point scale (0, unable to swallow; 5, normal). The end-point for dilation was to size 45F or 15 mm. Discomfort during the procedure was graded on a four-point scale (0, no discomfort; 1, mild; 2, moderate; 3, severe discomfort). Follow-up visits were at 1 week, 1 month, 3 months, and every 3 months thereafter for 2 years. At the 1-week visit, the size of esophageal lumen was measured by 8-, 10-, and 12-mm pills. Both devices effectively relieved dysphagia. By life-table analysis, stricture recurrence during the first year of follow-up was similar in both groups, but during the second year, the risk of recurrence was significantly lower in patients whose strictures were dilated with balloons. Other advantages of balloons included the need for fewer treatment sessions to achieve the defined end-diameter for dilation (1.1 + 0.1 versus 1.7 + 0.2, p < .05), and less procedural discomfort (p < .05). The differences in luminal size after dilation, measured by the barium pill test, were not significant. Ability to pass the 12-mm pill and absence of dysphagia were correlated. Our results indicate that both devices are effective in relieving dysphagia, but balloons may have a long-term advantage.

Adult↗
PubMed1995

Helicobacter pylori in the oral cavity. A critical review of the literature.

Helicobacter pylori is now generally accepted as a key etiologic agent in peptic ulcer disease as well as in gastric cancer. Dental plaque has been implicated as a possible source of H. pylori by studies that used culture, biochemical, nucleic acid, and immunologic analyses. Variation in the sensitivities of detection by these different reported assays may reflect the methods used, technical difficulties, microbiota complexes, geographic distribution, and host response. The finding of H. pylori in dental plaque also suggested that dental workers may be at increased risk of acquiring H. pylori infection from occupational exposure. We review the available data concerning the presence of this important pathogen in the oral cavity and its potential to be acquired by dental workers. Knowledge of this organism's route of transmission may aid in the development of therapeutic procedures to stop its potential spread.

Dental Plaque↗
PubMed1995

Protean manifestation of gastrointestinal tuberculosis: report on 130 patients.

Over the past 8 years, 820 patients with tuberculosis were seen at the Armed Forces Hospital, Riyadh, Kingdom of Saudi Arabia. A total of 292 of these patients (35.6%) had pulmonary tuberculosis, and 130 patients (15.8%) had alimentary tract tuberculosis, making this the second commonest site of involvement. In these 130 patients, the disease was located in the upper gastrointestinal tract in 11 patients (8.5%), small bowel 44 patients (33.8%), large bowel 29 patients (22.3%), peritoneum 40 patients (30.7%), and liver 19 patients (14.6%). The diagnosis in most patients was made by specimens from endoscopy or laparoscopy, or liver or surgical specimens. Gastrointestinal tuberculosis is not uncommon in developing countries, and its incidence is increasing in developed countries due to immigration and in patients with AIDS or those receiving immunosuppressive therapy. It can mimic any diseases affecting the gastrointestinal tract and may present with very different symptoms, so a high index of suspicion is required.

Adult↗
PubMed1995

Metronidazole, omeprazole and clarithromycin: an effective combination therapy for Helicobacter pylori infection.

BACKGROUND: Successful treatment of Helicobacter pylori infection results in cure of peptic ulcer disease. Multi-drug regimens are needed to cure this infection. We studied the effectiveness and side effect profile of two antibiotics active against Helicobacter pylori, metronidazole and clarithromycin, combined with omeprazole. METHODS: We evaluated a combination therapy for H. pylori infection consisting of metronidazole (500 mg b.d.), omeprazole (20 mg b.d.), and clarithromycin (250 mg b.d.) for 2 weeks, followed by ranitidine 300 mg daily for 4 weeks. RESULTS: Thirty-three patients with documented H. pylori infection were studied. Twenty had previously failed antimicrobial therapy, including one with metronidazole-based triple therapy and eight with macrolide-based therapy (five with clarithromycin-based therapy), and 11 with amoxycillin, tetracycline, and bismuth. H. pylori status was determined by histopathology using the Genta stain and by culture. H. pylori status was determined at entry and 4 weeks after completing antimicrobial therapy. The H. pylori infection was cured in 88% (95% CI = 72%-96%) including 90% of those who had failed previous anti-H. pylori therapies. Mild side effects were reported by 18%. CONCLUSION: We conclude that the combination of metronidazole, omeprazole and clarithromycin is an effective treatment for H. pylori infection.

Adult↗
PubMed1995

Nucleotide sequence analysis and seroreactivities of the 65K heat shock protein from Mycobacterium paratuberculosis.

Mycobacterium paratuberculosis is the causative agent of Johne's disease, a chronic enteritis in ruminants. It has also been implicated as a possible cause of Crohn's disease, an inflammatory bowel disease of unknown etiology. The mycobacterial 65K heat shock proteins (hsp-65K) are among the most extensively studied mycobacterial proteins, and their immunogenic characteristics have been suggested to be the basis for autoimmunization in chronic inflammatory diseases. In this context, we isolated and sequenced the hsp-65K-encoding gene from our M. paratuberculosis PTB65K genomic library. A high degree of identity was found between the open reading frame (ORF) of the PTB65K gene and those of Mycobacterium tuberculosis (89.6%), Mycobacterium leprae (86.6%), and Mycobacterium avium 18 (98.8%). The amino acid sequence alignment of the PTB65K protein with the hsp-65K homologs revealed that the M. tuberculosis and M. leprae proteins each differed by 36 amino acid residues and that the M. avium 18 protein differed by 8 residues. We also investigated the humoral immune responses of animals with Johne's disease and patients with Crohn's disease against the recombinant PTB65K antigen. Immunoblot analysis showed that sera from only 3 of 10 clinically ill and 5 of 25 subclinically ill cows reacted with PTB65K. In addition, sera from two of two sheep and one of two goats with clinical symptoms of Johne's disease also reacted with PTB65K; 0 samples from 10 normal cows reacted. In humans, sera from 7 of 13 patients with Crohn's disease, 3 of 4 with tuberculosis, 5 of 6 with leprosy, 5 of 12 with non-inflammatory bowel disease, and 0 of 4 with ulcerative colitis reacted with the recombinant PTB65K antigen. These results indicate that this PTB65K heat shock protein is uninformative when used for serodiagnosis of Johne's disease in animals. However, in humans, the high intensity of antibody reactions of some sera from Crohn's disease patients compared with that from noninflammatory bowel disease patients showed a positive correlation with mycobacterial diseases.

Animals↗