Low levels of adherence with proton pump inhibitor therapy contribute to therapeutic failure in gastroesophageal reflux disease.

To assess adherence to proton pump inhibitor (PPI) treatment and associated variables in patients with gastroesophageal reflux disease (GERD). Cross-sectional and prospective comprising 240 consecutive adult patients, diagnosed with GERD for whom continuous use of standard or double dose of omeprazole had been prescribed. Patients were ranked as ne-GERD (162: 67.5%) or e-GERD classified according to the Los Angeles classification as A (48:20.0%), B (21:8.6%), C (1:0.5%), D (1:0.5%), and Barrett's esophagus (7:2.9%). The Morisky questionnaire was applied to assess adherence to therapy and a GERD questionnaire to assess symptoms and their impact. Adherence was correlated with demographics, cotherapies, comorbidities, treatment duration, symptoms scores, endoscopic findings, and patient awareness of their disease. 126 patients (52.5%) exhibited high level of adherence and 114 (47.5%) low level. Youngers (P= 0.002) or married (O.R. 2.41, P= 0.03 vs. widowers) patients had lower levels of adherence; symptomatic patients exhibited lower adherence (P= 0.02). All other variables studied had no influence on adherence. Patients with GERD attending a tertiary referral hospital in São Paulo exhibited a high rate of low adherence to the prescribed PPI therapy that may play a role in the therapy failure. Age <60 years, marital status and being symptomatic were risk factors for low adherence.

Oral cavity is not a reservoir for Helicobacter pylori in infected patients with functional dyspepsia.

INTRODUCTION: Helicobacter pylori infection is very prevalent in Brazil, infecting almost 65% of the population. The aim of this study was to evaluate the presence of this bacterium in the oral cavity of patients with functional dyspepsia (epigastric pain syndrome), establish the main sites of infection in the mouth, and assess the frequency of cagA and vacA genotypes of oral H. pylori. METHODS: All 43 outpatients with epigastric pain syndrome, who entered the study, were submitted to upper gastrointestinal endoscopy to rule out organic diseases. Helicobacter pylori infection in the stomach was confirmed by a rapid urease test and urea breath tests. Samples of saliva, the tongue dorsum and supragingival dental plaque were collected from the oral cavity of each subject and subgingival dental plaque samples were collected from the patients with periodontitis; H. pylori infection was verified by polymerase chain reaction using primers that amplify the DNA sequence of a species-specific antigen present in all H. pylori strains; primers that amplify a region of urease gene, and primers for cagA and vacA (m1, m2, s1a, s1b, s2) genotyping. RESULTS: Thirty patients harbored H. pylori in the stomach, but it was not possible to detect H. pylori in any oral samples using P1/P2 and Urease A/B. The genotype cagA was also negative in all samples and vacA genotype could not be characterized (s-m-). CONCLUSION: The oral cavity may not be a reservoir for H. pylori in patients with epigastric pain syndrome, the bacterium being detected exclusively in the stomach.

Factors affecting Helicobacter pylori eradication using a seven-day triple therapy with a proton pump inhibitor, tinidazole and clarithromycin, in Brazilian patients with peptic ulcer.

UNLABELLED: Triple therapy is accepted as the treatment of choice for H. pylori eradication. In industrialized countries, a proton pump inhibitor plus clarithromycin and amoxicillin or nitroimidazole have shown the best results. Our aims were: 1. To study the eradication rate of the association of a proton pump inhibitor plus tinidazole and clarithromycin on H. pylori infection in our population. 2. To determine if previous treatments, gender, age, tobacco, alcohol use, and non-steroidal anti-inflammatory drugs (NSAIDs) change the response to therapy. METHODS: Two hundred patients with peptic ulcer (upper endoscopy) and H. pylori infection (histology and rapid urease test - RUT) were included. A proton pump inhibitor (lanzoprazole 30 mg or omeprazole 20 mg), tinidazole 500 mg, and clarithromycin 250 mg were dispensed twice a day for a seven-day period. Eradication was assessed after 10 to 12 weeks of treatment through histology and RUT. RESULTS: The eradication rate of H. pylori per protocol was 65% (128/196 patients). This rate was 53% for previously treated patients, rising to 76% for not previously treated patients, with a statistical difference p<0.01. No significant difference was observed regarding sex, tobacco use, alcohol consumption, and NSAID use, but for elderly patients the difference was p = 0.05. Adherence to treatment was good, and side effects were mild. CONCLUSIONS: A proton pump inhibitor, tinidazole, and clarithromycin bid for seven days resulted in H. pylori eradication in 65% of the patients. Previous treatments were the main cause of treatment failure.

Hansen's disease and the digestive system: clinical symptoms and gastric secretory profile at baseline conditions and following maximum stimulation with pentagastrin.

The incidence of digestive symptoms in 100 patients with Hansen's disease was evaluated in this study, following a standardized questionnaire. A correlation between the frequency of symptoms, the form of the disease, and the length of treatment was investigated. Digestive symptoms were found in 31 patients (31%). No statistically significant difference was found between the presence of symptoms and the length of the disease or between the multibacillary and the paucibacillary form of the disease. However, a positive correlation between digestive symptoms and Hansen's disease was found in the multibacillary form of the disease only for patients treated for more than 12 months. Baseline and pentagastrin-stimulated gastric acid secretion was studied in 30 Hansen's disease patients and in 10 controls. A Iower basal acid output was observed in patients with Hansen's disease, but no statistical difference was found. Pentagastrin-stimulated gastric acid secretion was statistically different in Hansen's disease patients, as compared to controls. A Iower pentagastrin-stimulated acid secretion was found in Hansen's disease patients under treatment, as compared to untreated patients, but the difference was not statistically significant.

[Gastrointestinal damage in osteoarthritis patients]. / Lesão gastroduodenal assintomática em portadores de osteoartrose.

Seventy-seven patients with symptomatic osteoarthritis of the hip and/or knee, with clinical indication for nonsteroidal anti-inflammatory drugs were studied. However, no patient was submitted to any anti-inflammatory medication seven days, prior the beginning of the study and did not complain of any gastrointestinal disease. Shortly before starting the anti-inflammatory drug therapy all patients were submitted to gastroduodenal endoscopy. This diagnostic procedure revealed that 54.6% of the patients presented at least one gastroduodenal damage, 22.1%, hyperemia, 3.9%, petechias, 23.4%, erosions and 5.2%, peptic ulcers. There results permitted to conclude that to identify and/or exclude damage of the gastrointestinal tract, data obtained in the anamnese are not sufficient. For these patients the endoscopic examination is a need. Anti-inflammatory therapy must be careful associated with dietetic orientation and the prescription of drugs to protect the gastrointestinal mucosa.

Five day and ten day triple therapy (amoxicillin, furazolidone and metronidazole) in the treatment of duodenal ulcer.

This investigation aimed to compare bacterial eradication and healing in patients with active duodenal ulcer treated with a combination of furazolidone 600 mg/day and metronidazole 750 mg/day and amoxicillin 1.5 and g/day for 5 (TT5) or 10 (TT10) days. Fifty four (TT5 = 28 and TT10 = 26) patients were included in the study. Ulcer healing was observed in 77.8% of TT5 Group and in 75% of TT10 Group at week 4. H pylori eradication was observed in 51.9% and 65% respectively (p > 0.05). When all patients were grouped, a significantly healing rate was observed in those eradicated as compared to those not eradicated (p = 0.03). We concluded that extending the treatment to 10 days did not significantly influence the results of ulcer healing and eradication of Helicobacter pylori.

Helicobacter pylori and refractory duodenal ulcers: cross-over comparison of continued cimetidine with cimetidine plus antimicrobials.

OBJECTIVES: To determine the distribution of Helicobacter pylori in the antral and duodenal mucosa of patients with duodenal ulcers refractory to 12 wk of treatment with cimetidine and to evaluate the effect of adding antimicrobial agents to cimetidine on the healing of refractory duodenal ulcers. METHODS: A randomized crossover comparison of continued 800 mg of cimetidine at night for 4 wk with cimetidine plus 500 mg of amoxycillin three times a day for the first 2 wk and 250 mg of metronidazole three times a day for the second 2 wk. H. pylori status in the gastric antral and duodenal mucosa was evaluated by histology and bacterial culture before and at the end of each treatment period. RESULTS: Forty-eight patients were studied. Upon entry to the study, all patients had antral colonization with H. pylori. In the duodenum, active chronic duodenitis was present in 66%, duodenal gastric metaplasia in 33%, and H. pylori in 50%, similar proportions to patients with nonrefractory duodenal ulcers. Healing occurred in 70% (30 of 43) of patients during treatment with cimetidine plus antimicrobials but in only 21% (6 of 28) during treatment with cimetidine alone (p = 0.0003). In patients who received antimicrobials, neither clearance of H. pylori from the antrum (58% of patients) or duodenum (71% of colonized patients) nor eradication of H. pylori (33%) was significantly correlated with ulcer healing. CONCLUSIONS: The distribution of H. pylori in refractory duodenal ulcers is similar to nonrefractory ulcers, and the combination of amoxycillin and metronidazole with cimetidine increases the proportion of refractory duodenal ulcers, which heals.

Treatment of duodenal ulcer with omeprazole or ranitidine in a Brazilian population: a multicenter double-blind, parallel group study.

Two hundred and forty-one patients with at least one ulcer at stage A1 or A2, measuring at least 5 mm in its larger diameter, were included in this Brazilian double-blind randomized study. Patients received omeprazole 20 mg in the morning (n = 120) or ranitidine 300 mg at night (n = 121) for 2 wk; unhealed ulcers were treated for an additional 2 wk. At the end of 4 wk, unhealed ulcers were treated openly with omeprazole 20 mg o.m. for 4 wk. Healing rates at 2 and 4 wk were 67.3% and 92.9% for omeprazole and 39.8% and 82.0% for ranitidine (per protocol analysis). Results were similar when analyzed as intention to treat (p significant in favor of omeprazole). Epigastric day-time pain was the most common of all symptoms (89.2%), but only heartburn at day 15 showed a significantly better response to omeprazole than to ranitidine. A multivariate analysis (logit analysis) showed that the odds in favor of healing were greater for small ulcers, nonsmokers, and omeprazole treatment.

Coffee drinking in patients with duodenal ulcer and a control population.

The ingestion of plain coffee was compared in 150 duodenal ulcer patients (DU) and 100 control subjects without digestive complaints (C). The DU and C groups were registered in accordance with their daily consumption of coffee: none, 1-100 ml, 101-300 ml, 301-500 ml, and more than 500 ml. Fifty millilitres of coffee as prepared in Brazil contain around 50 mg of a caffeine, which is 2.8 times more than in an equal volume of coffee in the United States. Patients with DU stopped drinking coffee or reduced the volume significantly after symptoms started. There was a significant change in coffee intake at all volume levels except at 1-100 ml. The main reason for the reduction of coffee ingestion was the relationship observed by the patients between the consumption of coffee and dyspeptic complaints. Our results suggest a close correlation between the ulcer-like symptoms and the amount of coffee ingested by patients with duodenal ulcer.

[Treatment of gastric ulcer with ranitidine: comparison of a single 300 mg dose at night with 150 mg twice a day]. / Tratamento da úlcera gástrica com ranitidina: comparação da dose única noturna de 300 mg com a de 150 mg duas vezes ao dia.

Twenty five patients with endoscopically diagnosed gastric ulcer, were randomly allocated to treatment with ranitidine 300 mg at night or ranitidine 150 mg twice daily. After six weeks, ulcer healing was observed in 7 out of 14 patients (50%) treated with ranitidine 300 mg nocte and in 7 out of 11 (63.6%) receiving 150 mg bid. Cumulative healing rates at 12 weeks were 64.2% and 81.8%, respectively. There was no statistically significant difference between these two groups. No adverse events were reported by any patient. Ranitidine 300 mg administered at night was effective and a safe regimen for the treatment of gastric ulcer.

Is the inhibition of nocturnal gastric acid secretion the most important factor in duodenal ulcer treatment? A comparison between the effectiveness of single morning and nocte doses of ranitidine 300 mg.

Fifty-five patients with an endoscopically confirmed duodenal ulcer were randomly allocated to receive ranitidine 300 mg either in a single morning or a single nocte dose (26 and 29 patients respectively). They were endoscopically examined at the end of the second week and when the ulcer was still active, the patient was treated for another two weeks, when endoscopy was repeated. Patients with ulcers still active at four weeks were considered treatment failures. The healing rate observed when ranitidine 300 mg was given in the morning was 10/26 (38%) at the end of the second week and 17/26 (65%) at the end of the fourth week. The healing rates after the 300 mg nocte treatment was 12/29 (41%) at the end of the second week and 20/29 (68%) at the end of the fourth week. No side effects were observed in any of the 55 patients, although one patient in the morning regimen bled at the end of the second week and was withdrawn from the study. Our results showed that ranitidine 300 mg in a single morning dose is as effective as when given in a single night dose. This finding is suggestive that reduction of nocturnal gastric acid secretion is important, but not essential for the healing of duodenal ulcer.

Famotidine in the short and long-term treatment of duodenal ulcer.

Famotidine was compared to ranitidine in a short-term study on the treatment of duodenal ulcer. Famotidine 20 mg. b.i.d., 40 mg. b.i.d. and 40 mg. nocte heal as many ulcer as ranitidine (90.9%, 91.7%, 83.3% and 100% respectively). A single 20 mg. bedtime dose shows to be effective on preventing ulcer recurrence for as long as 48 weeks; the 38% recurrence rate observed with famotidine was statistically different from the 78% observed with placebo. Diarrhoea was the most common complain observed during the short-term trial, followed by sleepiness and headache. The few and small biochemical alterations during the long-term treatment (increase in transaminases, alkaline phosphatase, glucose, BUN) could in no instance be directly related to the substances on use.

Famotidine in the short and long-term treatment of duodenal ulcer.

Famotidine was compared to ranitidine in a short-term study on the treatment of duodenal ulcer. Famotidine 20 mg. b.i.d., 40 mg. b.i.d. and 40 mg. nocte heal as many ulcer as ranitidine (90.9

, 91.7

, 83.3

and 100

respectively). A single 20 mg. bedtime dose shows to be effective on preventing ulcer recurrence for as long as 48 weeks; the 38

recurrence rate observed with famotidine was statistically different from the 78

observed with placebo. Diarrhoea was the most common complain observed during the short-term trial, followed by sleepiness and headache. The few and small biochemical alterations during the long-term treatment (increase in transaminases, alkaline phosphatase, glucose, BUN) could in no instance be directly related to the substances on use.