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C O'Morain

Publications and source records attributed to C O'Morain.

At least 55 records · Page 3Linked to original sources
PubMed1999

Gastro-oesophageal reflux disease and Helicobacter pylori: an intricate relation.

Heartburn is a common symptom affecting 21-44% of the adult population on a monthly basis. Oesophagitis is less common, affecting 2% of individuals. Epidemiological studies have shown that patients with gastro-oesophageal reflux disease (GORD) have similar incidence rates of Helicobacter pylori infection as do controls. Some groups have reported that there is a lower incidence, deducing that infection does not cause, and in some way confers protection against GORD. Additional supportive evidence is available from reports of GORD development following successful H pylori eradication. The mechanisms involved are complicated. Individuals with H pylori induced pangastritis and subsequent hypochlorhydria may be protected whereas those with an antral predominant gastritis, as in duodenal ulcer disease, with an increased acid output may be prone to development of GORD. Recent evidence has linked H pylori infection with the development of inflammation of the gastric cardia---carditis. Reports are available which show that carditis is a frequent finding in patients with GORD. The incidence of both cardia and oesophageal carcinoma is increasing. The relation between GORD, carditis, intestinal metaplasia, and cardia carcinoma is unclear. Intestinal metaplasia may result from multifocal atrophic gastritis, linked to H pylori infection or from GORD and the development of Barrett's oesophagus. Long term follow up studies will be required to assess the malignant potential of these histological entities and whether or not H pylori infection has an aetiological role.

Gastritis↗
PubMed1998

Screening for Helicobacter pylori in young dyspeptic patients referred for investigation--endoscopy for those who test negative.

BACKGROUND: Studies in young dyspeptic patients have suggested that screening strategies based on non-invasive H. pylori testing can reduce endoscopy workload by 25-40%. Such strategies usually propose that only H. pylori-positive individuals should undergo endoscopy. This approach may fail to diagnose idiopathic ulcers, ulcers in patients whose screening test is falsely negative and reflux disease. AIM: To investigate a hypothetical screening strategy in which endoscopy is initially performed only in H. pylori-negative dyspeptics. METHODS: Seventy-two consecutive patients under 45 years of age undergoing investigation for 'ulcer-like' dyspepsia had invasive and non-invasive determination of H. pylori status. Individuals found to be H. pylori-positive at endoscopy received 1 week of proton pump inhibitor-based triple therapy. H. pylori-negative individuals received therapy tailored to their diagnosis. Endoscopy was repeated in the positive group to confirm successful eradication. Results were analysed according to our strategy, i.e. serologically-positive patients would have received eradication therapy without endoscopy, but patients found to be negative would have been referred for endoscopy. RESULTS: According to the serology test there were 39 positive and 33 negative results. Symptoms failed to resolve during follow-up in nine of the serological positives despite successful eradication. There were also five false positives who were deemed likely treatment failures. Thus according to our strategy, these 14 serologically-positive patients would ultimately have required an endoscopy and the other 25 serologically-positive patients would have avoided an endoscopy, resulting in a 35% reduction in endoscopy usage in this population. In the serologically-negative group there were three cases of peptic ulcer disease where the test was falsely negative, but they were detected by the strategy. No cases of gastric malignancy were detected at endoscopy. Thus our strategy would have reduced initial endoscopy referrals by 35% in this selected population. CONCLUSION: A strategy of empirical H. pylori eradication therapy can safely reduce the requirement for endoscopy in young dyspeptic patients without sinister symptoms.

Adult↗
PubMed1998

Incidence of duodenal ulcer healing after 1 week of proton pump inhibitor triple therapy for eradication of Helicobacter pylori. The Lansoprazole Helicobacter Study Group.

BACKGROUND: A number of clinical studies have assessed the efficacy of short-term twice-daily Helicobacter pylori eradication regimens but few have investigated the proportion of patients in whom duodenal ulcer disease was healed with these regimens. AIM: To compare the safety and efficacy of four 1-week H. pylori eradication regimens in the healing of H. pylori associated duodenal ulcer disease. METHODS: Following endoscopic confirmation of duodenal ulcer disease and a positive CLO test, patients underwent a 13C-urea breath test to confirm H. pylori status. Treatment with one of four regimens: LAC, LAM, LCM or OAM, where L is lansoprazole 30 mg b.d., A is amoxycillin 1 g b.d., M is metronidazole 400 mg b.d., C is clarithromycin 250 mg b.d., and O is omeprazole 20 mg b.d., was assigned randomly to those patients who were H. pylori positive, with 62 (LAC), 64 (LAM), 61 (LCM) and 75 (OAM) patients in each treatment group. Follow-up breath tests and endoscopies were performed at least 28 days after the end of treatment. RESULTS: Duodenal ulcer disease was healed 28 days after treatment in 53/62 (85.5%) patients who were treated with LAC, 52/64 (81.3%) of patients treated with LAM, 49/61 (80.3%) of patients treated with LCM and 60/75 (80.0%) of patients treated with OAM (intention-to-treat analysis, n = 262, assumed unhealed if no follow-up endoscopy was performed). All the treatments were of similar efficacy (P = 0.85, chi-squared test) with regard to the healing of duodenal ulcer disease. CONCLUSIONS: The four 1-week treatment regimens were equally effective in healing H. pylori associated duodenal ulcer disease.

2-Pyridinylmethylsulfinylbenzimidazoles↗
PubMed1998

Helicobacter pylori and gastric cancer.

Gastric cancer despite a declining incidence remains a significant cause of morbidity and mortality world wide. There is strong epidemiological and histological evidence to associate Helicobacter pylori infection with the subsequent development of gastric cancer. The exact pathophysiological mechanisms involved remain to be elucidated. There is evidence to relate Helicobacter pylori infection and subsequent inflammation with an increase in gastric epithelial cell proliferation and with the induction of apoptosis. Such alterations in cellular dynamics may promote the development of mitogenic cell lines by inducing DNA damage. Studies have shown that following successful treatment, proliferation rates return to normal. At what histological stage, eradication is of benefit is less clear. It is likely that following the development of atrophy or intestinal metaplasia eradication will only slow progression. It would, therefore, seem logical, that to establish any benefit for a population, treatment should be employed at an earlier stage. As yet, an at risk group has not been identified, and as such population screening cannot be advised, mainly as a result of financial implications and the risk of promoting the development of resistant strains. Recent studies have explored the rules of bacterial factors, CagA and VacA status, host factors, HLA type, and environmental factors as determinants of outcome. Results have been variable. The establishment of an at risk group would enable selective screening and treatment, and thus prevent the development of gastric carcinoma as a result of Helicobacter pylori infection in the long-term.

Adenocarcinoma↗
PubMed1997

Who should be treated for Helicobacter pylori infection? A review of consensus conferences and guidelines.

The publication of the National Institutes of Health Consensus Development Conference guidelines on management of Helicobacter pylori infection in 1994 set a precedence. At present, at least eight European countries have produced national guidelines, and, more recently, the European Helicobacter pylori Study Group also outlined guidelines based on the strength of available evidence. It is generally agreed that H. pylori should be eradicated in peptic ulcer disease. In nonsteroidal anti-inflammatory drug (NSAID)-related ulcers, most countries that considered the issue suggested discontinuing NSAIDs when possible and eradicating H. pylori. The prophylactic eradication of H. pylori was not recommended. A number of panels felt that there was not enough evidence available to recommend eradication of H. pylori in functional dyspepsia, whereas other groups felt that nonulcer dyspepsia, particularly after investigation and with severe or recurrent symptoms, was an indication for eradication therapy. Other conditions (i.e., gastroesophageal reflux disease [GERD] and mucosa-associated lymphoid tissue [MALT] lymphoma) have emerged in this short time as possible indications for H. pylori eradication. There is no evidence that H. pylori infection has a role in the pathogenesis of GERD, but there is evidence suggesting that patients with H. pylori infection who require long-term acid suppression may be at risk of developing atrophic gastritis. The European Helicobacter pylori Study Group has suggested that eradication therapy should be offered to infected family members of patients with gastric cancer. It also recommended that eradication therapy was "strongly recommended" on the basis of "supportive" evidence in gastritis with severe abnormalities and after early resection of early gastric cancer. An "uncertain" recommendation with "equivocal" evidence was given for asymptomatic subjects, extra-alimentary tract disease, the prevention of gastric cancer in the absence of risk factors, and in pediatric patients with recurrent abdominal pain. Despite considerable advances, further research studies are needed to provide definite direction for the treatment of many conditions.

Consensus Statements as Topic↗
PubMed1997

Consensus or confusion: a review of existing national guidelines on Helicobacter pylori-related disease.

Since the discovery of Helicobacter pylori, a considerable amount of progress has been made in our understanding of H. pylori-related conditions. However, considerable confusion exists in relation to the optimal application of these findings to clinical practice, particularly at a primary care setting. In the USA the National Institutes of Health published guidelines outlining the role of H. pylori in peptic ulcer disease in 1994. Since then at least eight European countries have issued guidelines. The differences that exist between these documents reflect the rapid evolution of opinion on how the diagnosis and treatment of H. pylori should influence the traditional management of conditions presenting with dyspepsia. It is clear that little controversy surrounds the approach to duodenal and gastric ulceration. Patients with gastric mucosa-associated lymphoid tissue lymphoma need careful follow-up. The greatest level of disagreement exists in relation to the management of non-ulcer dyspepsia and dyspepsia in the community. These areas, in addition to the role of H. pylori eradication when non-steroidal antiinflammatory drugs or long-term acid suppressor are considered, need further evaluation. Most countries now recommend proton pump-based triple therapy regimes as first-line treatment for the eradication of H. pylori.

Consensus Development Conferences, NIH as Topic↗
PubMed1997

Monozygotic twins with Crohn's disease and ulcerative colitis: a unique case report.

BACKGROUND: A large number of monozygotic and dizygotic twin pairs with inflammatory bowel disease have been reported. To date no twin pair has developed phenotypically discordant inflammatory bowel disease. This case report is the first documented occurrence of discordant inflammatory bowel disease occurring in monozygotic twins. CASE REPORT: Twenty two year old identical male twins presented within three months of each other with inflammatory bowel disease that proved to be discordant in overall disease type, disease distribution, clinical course, and histopathological findings. Twin 1 developed a severe pancolitis necessitating total colectomy while twin 2 developed a predominantly distal patchy colitis with frequent granulomas, controlled by aminosalicylates. Twin 1 was antineutrophil cytoplasmic antibody (ANCA) negative at the time of testing while twin 2 (Crohn's disease) was ANCA positive. Significantly, the twins possessed the HLA type DR3-DR52-DQ2 previously associated with extensive colitis. CONCLUSION: This case report confirms the important role played by genetic factors in the development of inflammatory bowel disease. It also highlights the crucial role of undetermined environmental agents in dictating disease expression and phenotype.

Adult↗
PubMed1997

One week triple therapy for Helicobacter pylori: a multicentre comparative study. Lansoprazole Helicobacter Study Group.

BACKGROUND: Eradication of Helicobacter pylori cures and prevents the relapse of duodenal ulceration and also results in histological resolution of chronic active gastritis. AIM: To compare four treatment regimens lasting seven days of a proton pump inhibitor and two antibiotics in the eradication of H pylori. PATIENTS: Men or women with H pylori positive duodenal ulceration or gastritis, or both. METHODS: A single blind, prospectively randomised, parallel group, comparative, multicentre study. After a positive CLO test, patients underwent histology, H pylori culture, and a 13C urea breath test to confirm H pylori status. Treatment with one of four regimens: LAC, LAM, LCM, or OAM, where L is 30 mg of lansoprazole twice daily, A is 1 g of amoxycillin twice daily, M is 400 mg of metronidazole twice daily, C is 250 mg of clarithromycin twice daily, and O is 20 mg of omeprazole twice daily, was assigned randomly. A follow up breath test was done at least 28 days after completing treatment. RESULTS: H pylori eradication (intention to treat) was 104/121 (86.0%) with LAC, 87/131 (66.4%) with LAM, 103/118 (87.3%) with LCM, and 94/126 (74.6%) with OAM. There was a significant difference (p < 0.001) in the proportion of patients in whom eradication was successful between LAC and LCM when compared with LAM, but no significant difference (p = 0.15) between LAM and OAM. Metronidazole resistance before treatment was identified as a significant prognostic factor with regard to eradication of H pylori. The regimens which contained metronidazole were significantly less effective than those without metronidazole in the presence of pretreatment resistant H pylori. There was no difference among the treatment groups with regard to the incidence and severity of adverse events reported. CONCLUSIONS: All four treatment regimens were safe and effective in eradicating H pylori in the patient population studied. LAC was the most efficacious treatment in patients with pretreatment metronidazole resistant H pylori, and was significantly better than LAM and OAM in this group of patients.

2-Pyridinylmethylsulfinylbenzimidazoles↗
PubMed1996

Double-blind, multicenter, placebo-controlled evaluation of clarithromycin and omeprazole for Helicobacter pylori-associated duodenal ulcer.

BACKGROUND: Eradication of Helicobacter pylori leads to faster ulcer healing and a significant decrease in ulcer recurrence. Clarithromycin is the most effective monotherapy for eradicating H. pylori from the gastric mucosa, and omeprazole frequently is used for the treatment of duodenal ulcer disease, prompting the interest to investigate rigorously the combination of clarithromycin and omeprazole for eradicating H. pylori. MATERIALS AND METHODS: The aim of this double-blind, randomized, multicenter (n = 30), multinational (n = 10) study was to compare clarithromycin and omeprazole with omeprazole monotherapy for the eradication of H. pylori from the gastric mucosa, endoscopic healing, and reduction of symptoms and ulcer recurrence in patients with active duodenal ulcer. Patients with active duodenal ulcer associated with H. pylori infection were randomized to receive omeprazole, 40 mg every morning for 14 days, with either clarithromycin, 500 mg, or placebo three times daily, which was followed by omeprazole, 20 mg every morning for 14 days. Patients underwent endoscopy before enrolling in the study, immediately after finishing treatment, and at 4- to 6-week and 6-month follow-up evaluations or at the recurrence of symptoms. RESULTS: Two hundred and eight patients with active duodenal ulcer associated with confirmed H. pylori infection were randomized to treatment with either clarithromycin and omeprazole (n = 102) or omeprazole and placebo (n = 106). Four to six weeks after treatment was completed, H. pylori was eradicated in 74% (95% confidence interval, 63.0%-82.4%) of patients receiving clarithromycin and omeprazole, compared with 1% (0.0%-6.2%) of patients receiving omeprazole monotherapy (p < .001). Clarithromycin resistance developed in eight patients treated with clarithromycin and omeprazole and in none given omeprazole and placebo. Ulcers, which were healed following treatment in more than 95% of study patients, recurred by the 6-month follow-up visit in 10% (5%-19%) of dual therapy recipients, compared with 50% (39%-61%) of those who took omeprazole alone (p < .001). CONCLUSION: Clarithromycin and omeprazole dual therapy is simple and well-tolerated and leads to consistently high eradication rates for patients with duodenal ulcer associated with H. pylori infection.

Adult↗
PubMed1996

Eradication of Helicobacter pylori using one-week triple therapies combining omeprazole with two antimicrobials: the MACH I Study.

BACKGROUND: Eradication of Helicobacter pylori provides potential cure in the majority of patients with peptic ulcer disease, and eradication rates of more than 90% have been reported, using omeprazole in combination with two antimicrobials. The choice of antimicrobials, dose regimen and duration of treatment have varied between studies, however, and an optimal treatment still has to be established. MATERIALS AND METHODS: We conducted an international, randomized, double-blind, placebo-controlled study involving more than 100 patients in each of six treatment groups in 43 hospital gastrointestinal units in Canada, Germany, Ireland, Sweden, and the United Kingdom. Patients (n = 787) with proved duodenal ulcer disease were randomized to treatment twice daily for 1 week with omeprazole, 20 mg (O), plus either placebo (P) or combinations of two of the following antimicrobials: amoxicillin, 1 gm (A), clarithromycin, 250 or 500 mg (C250, C500), or metronidazole, 400 mg (M). Eradication of H. pylori was evaluated by 13C-UBT, performed before and 4 weeks after treatment cessation. RESULTS: The eradication rates for the all-patients-treated analysis were 96%, OAC500; 95%, OMC250; 90%, OMC500; 84%, OAC250; 79%, OAM; and 1%, OP. OAC500 and OMC250 achieved eradication rates with lower 95% confidence interval limits exceeding 90%. All regimens were well-tolerated, 96% of patients complied with their dose regimen, and 2.3% of the patients discontinued treatment owing to adverse events. CONCLUSIONS: Omeprazole triple therapies given twice daily for 1 week produce high eradication rates, are well-tolerated, and are associated with high patient compliance. The two most effective therapies were those combining omeprazole, 20 mg, with either amoxicillin, 1 gm, plus clarithromycin, 500 mg, or metronidazole, 400 mg, plus clarithromycin, 250 mg, all given twice daily.

Amoxicillin↗
PubMed1996

Gastric epithelial cell kinetics in the progression from normal mucosa to gastric carcinoma.

Increased epithelial cell proliferation is associated with an increased risk of adenocarcinoma and is associated with Helicobacter pylori infection. The aim of this study was to assess both gastric epithelial cell proliferation and the influence of H pylori infection on cell kinetics in the progression from normal mucosa to gastric carcinoma. One hundred and forty four subjects were assigned to study groups based on diagnosis and H pylori status: microscopically normal mucosa and H pylori negative (n = 28); chronic active gastritis and H pylori positive (n = 83); atrophic gastritis (n = 9); intestinal metaplasia (n = 19); gastric carcinoma (n = 12). Gastric antral epithelial cell proliferation was assessed using the in vitro bromodeoxyuridine immunohistochemical technique and expressed as the labelling index per cent (LI%). Subjects with chronic atrophic gastritis, intestinal metaplasia or gastric cancer have increased gastric epithelial cell proliferation compared with normal mucosa (LI% mean (SEM): 5.14 (0.6), 4.68 (0.3), 6.50 (0.5) v 3.08 (0.2), p < 0.001). This increase in gastric epithelial cell proliferation was not influenced by H pylori status. Gastritis associated with H pylori had an increased LI% compared with normal controls or subjects with H pylori negative gastritis (4.98 (0.2) v 3.08 (0.2), 3.83 (0.2), p < 0.01). H pylori infection although associated with an increased epithelial cell proliferation in subjects with chronic gastritis, does not influence the increased epithelial cell proliferation seen in subjects with precancerous lesions or gastric carcinoma. This is further evidence that H pylori may be an initiating step in gastric carcinogenesis.

Adenocarcinoma↗
PubMed1996

Duodeno-jejunal adenocarcinoma as a first presentation of coeliac disease.

Long standing coeliac disease is associated with an increased risk of malignancy, not only of intestinal lymphoma but also small intestinal adenocarcinoma. Two patients whose initial presentation was adenocarcinoma of the small bowel, but who were subsequently found to have coeliac disease after Whipple's resection, are described. The diagnosis was made early in the postoperative period in the first patient after close histological examination of the tumour-free mucosal margins. This patient was placed on a gluten-free diet and had an uncomplicated postoperative recovery with rapid weight gain. Diagnosis and dietary intervention in the second patient was very delayed and resulted in the development of severe malabsorption and weight loss. This illustrates the importance of ruling out coeliac disease prior to surgery in patients with small intestinal malignancies.

Adenocarcinoma↗
PubMed1996

Helicobacter pylori and dyspepsia.

Non-ulcer dyspepsia (NUD) is a common condition that often goes unrecognized. Although approximately 50% of patients with NUD are infected with Helicobacter pylori, attempts to establish a link between this organism and the pathogenesis of NUD have yielded conflicting results. Recent studies have shown that eradication of H. pylori leads to improvements in symptoms in patients with NUD, and have highlighted the importance of long-term follow-up in this condition. It is possible that patients with NUD and H. pylori infection have a discrete condition that forms part of a spectrum of peptic ulcer disease. Hence, it may soon be possible to recommend H. pylori eradication treatment for patients with NUD.

Dyspepsia↗