Does Helicobacter pylori eradication affect symptoms in nonulcer dyspepsia: a 5-year follow-up study.

The role of Helicobacter pylori infection in nonulcer dyspepsia remains controversial. To date studies exploring the effect of H. pylori eradication on symptoms have reported conflicting results. Randomised control trials employing validated outcome measures have also been difficult to interpret because of several important issues such as the large placebo response seen in patients with nonulcer dyspepsia and both the natural variability in symptoms and symptom severity with time. The association of symptom improvement with resolution of gastritis has meant that the length of follow up employed in most studies has been insufficient. We report the findings of a randomised placebo controlled trial (n = 100), using a validated symptom questionnaire and 5 year follow up to determine the effect of H. pylori eradication on symptoms in nonulcer dyspepsia. In all 64 that were reviewed at 5 years there was a significant difference between patients who were H. pylori negative and those who remained positive with regard to complete symptom resolution, consumption of relevant medications and peptic ulcer disease development, in favour of active treatment. There was a trend for gradual symptom improvement over time irrespective of H. pylori status, which may reflect the natural history of this condition. For those who remained symptomatic at 5 years, there was no difference in symptom severity based on H. pylori status. The findings of this study support the use of H. pylori eradication in symptomatic patients with nonulcer dyspepsia both to induce symptom resolution and to prevent disease progression.

Eradication of Helicobacter pylori affects symptoms in non-ulcer dyspepsia.

BACKGROUND: The relationship between Helicobacter pylori infection and non-ulcer dyspepsia is controversial. METHODS: In a prospective, long-term, double-blind study we randomized 100 patients with non-ulcer dyspepsia and H. pylori infection to receive either of two treatment regimens: 1) bismuth-based triple therapy (n = 50) or 2) bismuth + placebo (n = 50). RESULTS: Triple therapy: subjects who became H. pylori-negative (n = 42) showed a significant symptomatic response when interviewed at 8 weeks, 6 months, and 1 year (P < 0.01). This improvement was evident in the 'ulcer-like' dyspepsia group at all times (P < 0.01) but in the 'reflux-like' and 'motility-like' groups at 6 months only (P < 0.01). Those who remained H. pylori-positive showed no decrease in symptoms at 8 weeks, 6 months, and 1 year. Bismuth-placebo therapy: subjects who became H. pylori-negative (n = 7) showed an improvement in symptoms at 8 weeks, 6 months, and 1 year. Those who continued to harbour the infection after treatment (n = 42) showed an insignificant improvement in the motility and non-specific groups only. CONCLUSION: This study shows that eradication of H. pylori results in a significant long-term reduction in symptoms of non-ulcer dyspepsia.

Eradication of Helicobacter pylori: the results of a pilot study of 3, 5 & 7 day triple antibiotic regime with bismuth for one month.

In a prospective study designed to assess the effect of duration of antibiotic therapy on the helicobactericidal and ulcer healing efficacy of bismuth therapy, groups of patients, 10 in each group, with H. pylori-positive duodenal ulcer received a triple therapy regimen consisting of colloidal bismuth subcitrate 120 mg 4 times daily for 28 days with metronidazole 400 mg 3 times daily and tetracycline 500 mg 3 times daily for the first 3, 5 or 7 days of therapy. H. pylori infection was assessed by urease test, culture and histology performed before and 4 or more weeks after completion of therapy. Three patients (30 per cent) were H. pylori-negative after therapy in the 3 day compared with 5 (50 per cent) in the 5 day and 9 (90 per cent) in the 7 day treatment groups (3 vs 7, P = 0.01; 5 vs 7, P = 0.14). Healed ulcers were seen in 7 (70 per cent) of the 3 day, in 6 (60 per cent) of the 5 day, and in 10 (100 per cent) of the 7 day treatment groups (5 vs 7, P = 0.04). Bismuth triple therapy incorporating metronidazole and tetracycline for 7 days is associated with superior H. pylori eradication and ulcer healing rates than bismuth triple incorporating antibiotics for 3 or 5 days.

The safety and efficacy of ranitidine bismuth citrate in combination with antibiotics for the eradication of Helicobacter pylori.

BACKGROUND: Ranitidine bismuth citrate is a novel salt of ranitidine and a bismuth citrate complex. It has intrinsic antisecretory and anti-Helicobacter pylori activity, but monotherapy rarely eradicates H. pylori infection in man. AIM: A pilot study to investigate rates of H. pylori eradication achieved by co-prescription of ranitidine bismuth citrate with antibiotics, and to identify several regimens which would merit further investigation. METHOD: One hundred dyspeptic patients infected with H. pylori were randomly allocated to treatment with ranitidine bismuth citrate 800 mg b.d. plus either amoxycillin, metronidazole, clarithromycin, cefuroxime axetil, tetracycline, tetracycline plus metronidazole or clarithromycin plus tetracycline for 14 days. Eradication of infection was assessed using the 13C-urea breath test 4 weeks after the end of treatment. RESULTS: In a per protocol analysis eradication of H. pylori ranged between 22 and 100%; the intention-to-treat eradication rates ranged between 15 and 92%. No adverse events were specifically attributed to ranitidine bismuth citrate. CONCLUSION: Co-prescription therapy, using ranitidine bismuth citrate and one or more antibiotics, is suitable for further investigation in large-scale clinical trials in patients infected with H. pylori.

Do non-steroidal anti-inflammatory drugs have an effect on gastric cell turnover?

AIM: To study the effect of non-steroidal anti-inflammatory drugs (NSAIDs) on gastric cell turnover using an in vitro immunohistochemical method of bromodeoxyuridine (BrDU) uptake. METHODS: Thirty patients undergoing routine upper gastrointestinal endoscopy were studied. Sixteen had taken NSAIDs daily for more than 3 months and there were 14 age-matched controls. Endoscopic gastric antral biopsies were obtained and stained immediately using the BrDU technique. Cell proliferation was expressed as a labelling index percentage (LI%) defined as the number of BrDU-labelled nuclei in 10 gastric glands, expressed as a percentage of the total cells in the gastric gland. RESULTS: Gastric infection with Helicobacter pylori was excluded in all patients. Of the 16 patients on NSAIDs, four had gastritis, four had erosions or ulceration and eight had a normal examination. Endoscopy was normal in all patients in the control group. The LI% (mean +/- S.E.M.) in the entire NSAID group was 4.09 +/- 0.29 and in the control group 3.57 +/- 0.29. No significant difference was observed. In the NSAID patients with gastritis and erosions or ulceration, the LI% was 4.99 +/- 0.61 and 3.07 +/- 0.32, respectively. There was no significant difference in LI% between the endoscopic subgroups of patients on NSAIDs or between patients on NSAIDs who had normal endoscopy and the control patients. CONCLUSION: These results provide evidence that refutes the hypothesis that the prevalence of NSAID gastropathy is due to an effect on gastric cell turnover.

Recrudescence of Helicobacter pylori infection in patients with healed duodenal ulcer after treatment with different regimens.

OBJECTIVE: To determine the 12-month posttherapy recurrence (recrudescence) of Helicobacter pylori in patients with healed duodenal ulcer after apparent eradication of the organism with anti-H. pylori treatment. The influence of original anti-H. pylori treatment regimens on the recrudescence was also evaluated. METHODS: One hundred and ninety patients who had duodenal ulcer healed and H. pylori eradicated (as assessed by four routine techniques 4 wk after the end of anti-H. pylori therapy) with one of five regimens were studied. The five regimens were: 1) colloidal bismuth subcitrate (CBS) 120 mg; 2) CBS plus amoxicillin (500 mg); 3) CBS plus metronidazole (400 mg); 4) CBS plus metronidazole and amoxicillin; and 5) CBS plus metronidazole and tetracycline (500 mg). CBS was taken four times daily for 4 wk, and antibiotics were taken three times daily for the first week. The patients were re-endoscoped, and the status of H. pylori, duodenal ulcer, and gastritis was assessed after a period of follow-up (mean 14 months after commencement of treatment). RESULTS: H. pylori infection recurred in 36 (18.9%) of these patients. Recrudescence rate with monotherapy was 47.1%, with dual therapy 29.2-35% and with triple therapy 9.2-14.3%. Nineteen (52.7%) of the 36 patients with recrudescent infection had ulcer relapse, and the rate for H. pylori-negative patients was 3.2% (5/154). CONCLUSION: Recrudescence of H. pylori infection after apparent eradication can occur, but it could be that the treatment was only suppressing the organism. The definition of eradication of H. pylori infection may need to be revised, and more sensitive techniques to assess eradication of H. pylori are required.

Percutaneous endoscopic gastrostomy--its application in patients with neurological disease.

We performed percutaneous endoscopic gastrostomy (PEG) in 30 patients with prolonged swallowing difficulty (> 4 weeks duration). The average procedure time was 25 minutes. PEG insertion was done on an outpatient basis in four patients. The complication rate was 10% and included failed insertion, peristomal infection and herniation of the gastric mucosa at the gastrostomy exist site. At follow-up, the PEG tube continued to function in 18/22 of the surviving patients with a median in-use time of 85 days. Seven patients died from their original disease. Over a 28-day period, the weight gain among the patients ranged from 3kg to 7kg (mean 4.5kg) and average serum albumin increased from 29g/dl to 35g/dl. This confirms that PEG is a safe, easy and effective method of long-term enteral feeding in patients with neurological disease.

Eradication of Helicobacter pylori in patients with non-ulcer dyspepsia.

Non-ulcer dyspepsia is an unsatisfactory term, as it describes a spectrum of conditions. The term is used for patients who have a normal upper endoscopy, macroscopically, but who have persistent upper gastrointestinal symptoms. Patients with non-ulcer dyspepsia respond to a wide variety of treatments, and there is a strong placebo response. Fifty per cent of these patients are shown to have Helicobacter pylori present if biopsy specimens are taken at endoscopy. Previous studies suggest that H. pylori eradication improves patients' symptoms. In a study from our unit we have shown that, in the short term, patients' symptoms improved with treatment, independent of H. pylori status. However, at 1-year follow-up, prolonged improvement of symptoms was observed only in patients in whom the organism had been eradicated.

Good outcome in anti-glomerular basement membrane nephritis.

We report a 6-year-old boy with anti-glomerular basement membrane nephritis (Goodpasture's syndrome). Intensive treatment with plasmapheresis and immunosuppression resulted in clearance of antibody and good recovery of renal function.

Short report: sedation for upper gastrointestinal endoscopy--diazepam versus midazolam.

Intravenously injected midazolam was associated with a greater degree of sedation, as assessed by 24-h retrograde amnesia, than the longer acting benzodiazepine, diazepam. No differences in the frequency of pain on injection or the occurrence of venous sequelae were noted between the two preparations.

Severe haemolysis associated with hepatitis A and normal glucose-6-phosphate dehydrogenase status.

We report massive acute haemolysis associated with hepatitis A in a 36 year old Irish woman. Although mild anaemia is not uncommon during viral hepatitis, haemolysis of the severity observed in this patient has previously been reported only in patients with glucose-6-phosphate dehydrogenase deficiency.

The non-effect of pirenzepine in dietary resistant irritable bowel syndrome.

No subjective or objective evidence of beneficial effect was observed from the use of Pirenzepine in irritable bowel syndrome (IBS) patients who had not responded to a high fibre diet.