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.

Pantoprazole versus ranitidine in the treatment of duodenal ulcer: a multicenter study in Brazil.

OBJECTIVE: The aim of this study was to compare the effectiveness and tolerance of pantoprazole versus ranitidine in the treatment of duodenal ulcers in the Brazilian population. METHODS: A total of 222 patients with active duodenal ulcers (DU) were randomly allocated to a double dummy blind treatment, either with ranitidine (RAN) 300 mg (111, aged from 20-68 yr old, 56 female) or with pantoprazole (PANT) 40 mg (111 patients, 18-70 yr old, 45 female). After a 2-wk course of treatment, each patient was clinically and endoscopically assessed for ulcer healing. Failure to heal required a further 2-wk course of treatment and a new evaluation thereafter. RESULTS: In all, 77 of the 103 patients in the PANT group (74.8%) and 42 of the 94 patients in the RAN group (44.7%) who completed the study had ulcer healing after one 2-wk treatment course, and an additional 23 in the PANT group (22.3%) and 28 in the RAN group (29.8%) after the second 2-wk treatment course, totaling 100 (97.1%) and 70 (74.5%), respectively. Therapeutic gain in favor of pantoprazole was significant both at the end of the first and the second 2-wk treatment course (p<0.001). At 2 wk, symptoms remission was significantly higher in the PANT group (97.6%) than with the RAN group (77.5%) (p<0.001). The Intention-to-treat analysis showed results statistically similar to those observed in the per-protocol analysis. Minor adverse events were reported by four patients in the PANT group and three in the RAN group. No relevant laboratory abnormalities were seen. No patient withdrew from the study due to adverse events. CONCLUSIONS: Our results show that pantoprazole is more effective than ranitidine in the treatment of duodenal ulcer providing faster ulcer healing in most patients (97.1%), in 4 wk. Adverse events were rare and were similar in both groups, and had no influence on the therapeutic outcome.

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.

The screening sensitivity of endoscopy, acid perfusion test and 24-hour pH-monitoring to evaluate esophagitis in patients with heartburn and histological esophagitis.

The sensitivity of endoscopic examinations, acid perfusion test and 24-hour esophageal pH-monitoring, were studied in patients with heartburn. Thirty six adult patients with histological esophagitis were included in this prospective study. Endoscopy showed esophageal lesion in 18/36 (sensitivity of 50%): esophagitis grade I in 10 (55.6%) and, grade II in eight (44.4%). Acid perfusion test was positive in 10/25 (sensitivity of 40%) of the patients submitted to the test. Twenty-four-hour pH-monitoring was positive in 17/29 patients (sensitivity of 58.6%): eight (61.5%) did not have esophageal lesion at endoscopy, two (25%) had esophagitis grade I and seven (87.5%) had esophagitis grade II. In the patients submitted to 24-hour pH-monitoring, a greater number or reflux episodes in orthostatic position than in supine position (P < 0.0001) was observed. The total number of reflux episodes, the most prolonged reflux and the total pH time < 4 were statistically higher in post-prandial period than during meals (P = 0.005).

[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.

Very-low dose antacid in treatment of duodenal ulcer. Comparison with cimetidine.

Antacid (AA) in a very low dose (88 mmol/day) was compared to the standard 800-mg dose of cimetidine in healing duodenal ulcers. The influence of sex, age, symptom duration at entry, night pain, smoking, coffee consumption, and alcohol on ulcer healing was studied. The antacid was given in two different schedules: group I--20 ml 1 hr after breakfast and at bedtime; group II--10 ml 1 hr after breakfast and lunch and 20 ml at bedtime. Cimetidine (group III) was given in two divided doses: 400 mg 1 hr after breakfast and 400 mg at bedtime. Endoscopic control was performed after four weeks and, if necessary, after eight weeks of treatment. The healing rate after four weeks of treatment was, respectively, for groups I, II, and III, 45.5%, 55.8%, and 69.4% (group I = group II, and group III different from groups I and II). After eight weeks of treatment the healing rate was 61.5%, 80.8%, and 88.0% for groups I, II, and III, respectively (group II = group III, and group I different from groups II and III). Except for group I, smoking did not influence healing rate. Age, sex, symptoms at entry, night pain, and coffee consumption did not influence the treatment results. The authors concluded that the very low dose of magaldrate (88 mmol/day), when administered in three divided doses (10 ml after breakfast and lunch and 20 ml at bedtime) for eight weeks was as effective as 800 mg of cimetidine (400 mg twice a day) in healing duodenal ulcer.

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.

[Splenic vein thrombosis as cause of digestive hemorrhage: ruptured esophageal varices or hemorrhagic gastritis secondary to portal hypertension?]. / Trombose da veia esplênica como causa de hemorragia digestiva: varizes gástricas rotas ou gastrite hemorrágica secundária à hipertensão portal?

The clinical evolution and treatment of two patients with alcoholic chronic pancreatitis complicated with digestive hemorrhage localized in the gastric corpus and fundus are discussed. The clinical picture and the endoscopic features suggested that the hemorrhage was due to hemorrhagic gastritis and not to rupture of varicose veins. Hemorrhagic gastritis as a consequence of segmentary portal hypertension may be responsible for the difficulty in establishing the etiology of digestive hemorrhage in such cases.

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.