Active Duodenal Ulcer Disease Research Articles

High Eradication Rates of Helicobacter pylori Infection with First- and Second-Line Combination of Esomeprazole, Tetracycline, and Metronidazole in Patients Allergic to Penicillin

H. pylori eradication is a challenge in patients allergic to penicillin, both first-line and failures of prior therapy. We aimed to assess the eradication rate of H. pylori in patients allergic to penicillin, first-line and failures of prior therapy, the efficacy of healing of active duodenal ulcer disease (DUD) and erosive gastritis, and the safety and tolerability of the combination. Twenty patients with documented allergy to penicillin, DUD, and H. pylori infection, 17 (85%) for first-line treatment and 3 (15%) prior therapy failures, were given a 10-day regimen of esomeprazole, 40 mg qid, tetracycline, 500 mg qid, and metronidazole, 500 mg qid. Baseline and follow-up panendoscopy > or =30 days after end of treatment was performed for rapid urease test (Clotest), and four site biopsies for H. pylori, and to document endoscopic peptic ulcer disease. All adverse events during treatment were documented. Eradication rates by intention to treat (ITT) were 85% for first-line treatment and 100% for failures. Seventy percent of all cases had a normal endoscopy at follow-up, and 85 and 100% of patients had healed erosive gastritis and DUD, respectively, from baseline. There were histological improvements in most patients. A high eradication rate was obtained even in patients who had a shorter duration of treatment. The combination was well tolerated. A combination of esomeprazole, tetracycline, and metronidazole is effective for eradication of H. pylori in patients allergic to penicillin, for both first-line treatment and failures of prior treatment.

Density ofHelicobacter pylorimay affect the efficacy of eradication therapy and ulcer healing in patients with active duodenal ulcers

To evaluate the association of pre-treatment Helicobacter pylori (H. pylori) density with bacterial eradication and ulcer healing rates in patients with active duodenal ulcer. One hundred and four consecutive duodenal ulcer outpatients with H. pylori infection ascertained by gastric histopathology and (13)C-urea breath test (UBT) were enrolled in this study. H. pylori density was graded histologically according to the Sydney system (normal, mild, moderate, and marked). In each patient, lansoprazole (30 mg b.i.d.), clarithromycin (500 mg b.i.d.) and amoxicillin (1 g b.i.d.) were used for 1 week, then 30 mg lansoprazole once daily was continued for an additional 3 weeks. Follow-up endoscopy was performed at 4 weeks after completion of the therapy, and UBT was done at 4 and 8 weeks after completion of the therapy. The H. pylori eradication rates were 88.9 %/100.0 %, 94.3 %/100.0 %, and 69.7 %/85.2 %; and the ulcer healing rates were 88.9 %/100.0 %, 94.3 %/100.0 %, and 63.6 %/77.8 % (intention-to-treat/per protocol analysis) in the mild, moderate, and marked H. pylori density groups, respectively. The association of pretreatment H. pylori density with the eradication rate and ulcer healing rate was both statistically significant (P=0.013/0.006 and 0.002/<0.001, respectively; using results of intention-to-treat/per protocol analysis). Intragastric bacterial load may affect both the outcome of eradication treatment and ulcer healing in patients with active duodenal ulcer disease.

Rabeprazole is superior to ranitidine in the management of active duodenal ulcer disease: results of a double-blind, randomized North American study

OBJECTIVE: The primary purpose of this study was to compare the efficacy and tolerability of rabeprazole versus ranitidine in the treatment of patients with active duodenal ulcer disease. METHODS: This multicenter, double-blind, randomized, parallel-group study enrolled 376 patients. Patients were randomly assigned to receive rabeprazole 20 mg administered once daily in the morning ( q.a.m.) with matching ranitidine placebo twice daily ( b.i.d.) (n = 188), or ranitidine 150 mg b.i.d. with matching rabeprazole placebo q.a.m. (n = 188). Three visits were scheduled: wk 0 (baseline; days −3 to −1), wk 2 (day 15 ± 3 days), and wk 4 (day 29 ± 3 days). The primary efficacy response variable was defined as complete regeneration of the mucosa at the site of all ulcers identified during the study. Secondary efficacy variables included patients’ ratings of frequency and severity of ulcer pain, frequency of antacid use, and improvement of overall physical well-being. Tolerability was evaluated with analyses of adverse events, laboratory evaluations, fasting serum gastrin levels, vital signs, body weight, and electrocardiograms. RESULTS: Up to 4 wk of treatment with rabeprazole 20 mg q.a.m. produced significantly greater healing rates, compared to treatment with ranitidine150 mg b.i.d. (83% vs 73%; p = 0.017). Significant differences between treatment groups were also observed for secondary efficacy indices. At wk 2, rabeprazole was more likely than ranitidine to produce complete resolution of duodenal ulcer pain (39% vs 25%; p = 0.006), improvement in duodenal ulcer nighttime pain severity (76% vs 65%; p = 0.044), and improvement in overall well-being (55% vs 41%; p = 0.009). At wk 4, the proportion of patients with normalization of overall well-being was significantly higher in the rabeprazole group than in the ranitidine group (45% vs 29%; p = 0.003). Rabeprazole was safe and well tolerated in this study. CONCLUSIONS: In patients with active duodenal ulcer disease, rabeprazole 20 mg q.a.m. is superior to ranitidine 150 mg b.i.d. in healing, resolving ulcer pain frequency, improving nighttime pain severity, and improving overall well-being. Rabeprazole is an effective and well-tolerated alternative treatment for patients with active duodenal ulcer disease.

Rabeprazole is superior to ranitidine in the management of active duodenal ulcer disease: results of a double-blind, randomized North American study

The primary purpose of this study was to compare the efficacy and tolerability of rabeprazole versus ranitidine in the treatment of patients with active duodenal ulcer disease. This multicenter, double-blind, randomized, parallel-group study enrolled 376 patients. Patients were randomly assigned to receive rabeprazole 20 mg administered once daily in the morning (q.a.m.) with matching ranitidine placebo twice daily (b.i.d.) (n = 188), or ranitidine 150 mg b.i.d. with matching rabeprazole placebo q.a.m. (n = 188). Three visits were scheduled: wk 0 (baseline; days -3 to -1), wk 2 (day 15+/-3 days), and wk 4 (day 29+/-3 days). The primary efficacy response variable was defined as complete regeneration of the mucosa at the site of all ulcers identified during the study. Secondary efficacy variables included patients' ratings of frequency and severity of ulcer pain, frequency of antacid use, and improvement of overall physical well-being. Tolerability was evaluated with analyses of adverse events, laboratory evaluations, fasting serum gastrin levels, vital signs, body weight, and electrocardiograms. Up to 4 wk of treatment with rabeprazole 20 mg q.a.m. produced significantly greater healing rates, compared to treatment with ranitidine 150 mg b.i.d. (83% vs 73%; p = 0.017). Significant differences between treatment groups were also observed for secondary efficacy indices. At wk 2, rabeprazole was more likely than ranitidine to produce complete resolution of duodenal ulcer pain (39% vs 25%; p = 0.006), improvement in duodenal ulcer nighttime pain severity (76% vs 65%; p = 0.044), and improvement in overall well-being (55% vs 41%; p = 0.009). At wk 4, the proportion of patients with normalization of overall well-being was significantly higher in the rabeprazole group than in the ranitidine group (45% vs 29%; p = 0.003). Rabeprazole was safe and well tolerated in this study. In patients with active duodenal ulcer disease, rabeprazole 20 mg q.a.m. is superior to ranitidine 150 mg b.i.d. in healing, resolving ulcer pain frequency, improving nighttime pain severity, and improving overall well-being. Rabeprazole is an effective and well-tolerated alternative treatment for patients with active duodenal ulcer disease.

DOES THE ERADICATION OF HELICOBACTER PYLORI CURE DUODENAL ULCER DISEASE IN COMMUNITIES WITH A HIGH PREVALENCE RATE? COMPARISON WITH LONG‐TERM ACID SUPPRESSION

SUMMARYThe long‐term effect of Helicobacter pylori eradication on the natural history of duodenal ulcer has been investigated and compared with long‐term acid suppression treatment in an endemic community for infection. Seventy‐three patients with endoscopically verified H. pylori positive active duodenal ulcer disease were included in this prospective study. Patients were divided into two groups. Group A patients (n=39) were given an omeprazole‐based triple eradication regimen, while group B patients (n=34) were given omeprazole alone followed by long‐term famotidine 20 mg daily as maintenance treatment. A control endoscopy was performed at the third month of treatment. The bacterium was eradicated in 32 (82%) of group A patients. All patients were followed up for two years and an endoscopy performed at the end of each year. H. pylori recurred in 13 patients and the reinfection rate was 44.8% over two years. Duodenal ulcer recurred in seven of these patients at two years (24.1%). There was a close association between H. pylori reinfection and ulcer relapse. Group B patients remained H. pylori positive during the study and the ulcer recurred in five of these patients (16.6%) despite continuous famotidine treatment. There was no statistically significant difference in ulcer relapse rate between the groups. These results suggested that H. pylori eradication is not an absolute solution for duodenal ulcer disease in high endemic regions and continuous maintenance treatment with H2‐receptor antagonists is still an alternative approach in some chronic recurrent cases.

Dyspepsia on withdrawal of ranitidine in previously asymptomatic volunteers

OBJECTIVE: H 2 receptor antagonist therapy has been shown to produce rebound acid hypersecretion. The clinical significance of this phenomenon is not known. We performed this study to determine whether withdrawal of H 2 receptor antagonist therapy results in dyspepsia in previously asymptomatic volunteers. METHODS: Thirty-five Helicobacter pylori-positive asymptomatic volunteers were randomized in double-blind fashion to receive 2 months’ treatment with either ranitidine 300 mg nocte or placebo. Dyspeptic symptoms were measured before starting treatment and over the course of 10 days after stopping treatment by means of a validated questionnaire. RESULTS: Thirty-one subjects completed the study; 17 were randomized to ranitidine. The pretreatment median aggregate dyspepsia score of the placebo group was 0 (0–4), as was that of the ranitidine group (0–8) (N.S.). During the 10 days after completion of ranitidine, the median aggregate dyspepsia score was 1.4 (0–30), compared with 0 (0–6.3) after placebo ( p < 0.01). Of those given ranitidine, 59% experienced dyspepsia after treatment, compared with only 14% who took placebo. In the subgroup that developed dyspepsia after active therapy, the median duration of symptoms was 2 days, symptom severity being maximal on the second day after completion of the tablets. On the days when dyspepsia was experienced, the median daily dyspepsia score was 5 (range, 2–10), which was similar to that of a control group with active duodenal ulcer disease (5; range, 0–11). CONCLUSIONS: Withdrawal of a 2-month course of ranitidine 300 mg nocte results in the development of dyspeptic symptoms in a proportion of previously asymptomatic subjects. Patients receiving ranitidine should be warned about this rebound dyspepsia and advised not to immediately resume treatment, as rebound symptoms are likely to improve within a few days.

Helicobacter pylori Colonization Density and Gastric Acid Output in Non‐ulcer Dyspepsia and Duodenal Ulcer Disease

The pattern of intragastric Helicobacter pylori colonization and its density may be determined by parietal cell function. H. pylori bacterial products can inhibit gastric acid secretion from the parietal cell. The aim of this investigation was to study the relationship between acid output and intragastric H. pylori distribution and colonization density in duodenal ulcer (DU) and non-ulcer subjects. The study included 14 patients with active DU, 10 with inactive DU and 10 non-ulcer dyspeptics. Acid output studies in response to fasting and maximal pentagastrin stimulation, basal (BAO) and peak (PAO) acid outputs were calculated. A quantitative assessment of H. pylori colonization density in biopsies from five sites of the gastroduodenum in the active ulcer group, and from the antrum in inactive duodenal ulcer and non-ulcer groups. There were negative correlations between total gastroduodenal bacterial colonization density and, PAO (r - 0.87, p = 0.0025) and BAO (r - 0.635, p < 0.02) in the active ulcer group. There were negative correlations between antral H. pylori colonization density and PAO in the active duodenal ulcer (r - 0.7449, p < 0.01) and non-ulcer (r - 0.5837, p < 0.1) groups but not in the inactive duodenal ulcer group (r - 0.1869, p > 0.2). An equilibrium is reached between gastroduodenal H. pylori colonization density and gastric acid secretory capacity in active duodenal ulcer disease. It is hypothesized that thresholds of bacterial load and acid secretory capacity, in combination, are required for active ulceration in DU disease.

Triple Versus Dual Therapy for Eradicating Helicobacter pylori and Preventing Ulcer Recurrence: A Randomized, Double-Blind, Multicenter Study of Lansoprazole, Clarithromycin, and/or Amoxicillin in Different Dosing Regimens

Objective: The efficacy and safety of dual and triple therapies with a proton pump inhibitor and antibiotic(s) for therapy of Helicobacter pylori-associated duodenal ulcer disease have been compared using results from independent studies using different methods and regimens, making interpretation difficult. In a large, double-blind, multicenter study conducted in the United States, we compared a triple therapy regimen with four dual therapy and one monotherapy regimens in the eradication of H. pylori and the prevention of ulcer recurrence. Methods: Patients with active duodenal ulcer disease or history of duodenal ulcer disease within the past year and H. pylori infection were randomized to receive one of six 14-day treatment regimens: lansoprazole 30 mg, clarithromycin 500 mg, and amoxicillin 1 gm b.i.d.; lansoprazole 30 mg b.i.d. and either clarithromycin 500 mg b.i.d. or t.i.d.; lansoprazole 30 mg b.i.d. or t.i.d. with amoxicillin 1 gm t.i.d.; or lansoprazole 30 mg t.i.d. alone. No additional acid suppression therapy followed eradication therapy. Primary efficacy endpoints were eradication of H. pylori and ulcer recurrence. Results: Of 396 patients enrolled in the study, 352 met the entry criteria for duodenal ulcer status and H. pylori positivity. At 4–6 wk after the end of therapy, H. pylori was eradicated from 94% (44 of 47) of patients receiving lansoprazole, clarithromycin, and amoxicillin triple therapy, 77% (39 of 51) of those receiving lansoprazole t.i.d./amoxicillin t.i.d., 75% (36 of 48) of those receiving lansoprazole b.i.d./clarithromycin t.i.d., 57% (28 of 49) of those receiving lansoprazole b.i.d./clarithromycin b.i.d., 53% (26 of 49) of those receiving lansoprazole b.i.d./amoxicillin t.i.d., and 2% (1 of 53) of those receiving lansoprazole monotherapy ( p ≤ 0.05, triple therapy vs each dual therapy and each dual therapy vs monotherapy). Of those patients who were documented as free of ulcer at 4–6 wk after treatment, ulcers recurred within 6 months in 7% of patients receiving triple therapy, as compared with 13–23% of patients receiving dual therapy, and 69% of patients receiving lansoprazole monotherapy. Patients who were H. pylori negative at 4–6 wk after treatment were less likely to have an ulcer recurrence than were patients who were H. pylori positive (11% [10 of 95] vs 47% [20 of 43], respectively, across treatment groups). For triple therapy and dual therapy, a similar proportion of patients reported a drug-related adverse event (23% vs 17–33%, respectively). Conclusions: In patients with active or a recent history of duodenal ulcer, a 14-day course of lansoprazole-based triple therapy without additional acid suppression therapy is highly effective in the eradication of H. pylori and in preventing ulcer recurrence. Among the dual therapies, higher eradication rates occurred when lansoprazole (with amoxicillin) or clarithromycin (with lansoprazole) was administered t.i.d. vs b.i.d., but the rates were still significantly lower than with lansoprazole triple therapy with all three drugs administered b.i.d.

Helicobacter pylori eradication in the African setting, with special reference to reinfection and duodenal ulcer recurrence.

The aim of this study was to determine the effect of Helicobacter pylori eradication on the natural history of duodenal ulcer disease, and to determine the incidence of reinfection in adult patients where H pylori had been eradicated in a community with a high prevalence of the infection. An investigator blinded study, with 24 month endoscopic follow up, in subjects where H pylori had been eradicated, and similarly treated subjects where it had not been eradicated was conducted at a tertiary referral hospital. The patients consisted of a volunteer sample of 48 patients with endoscopically proved active duodenal ulcer disease. Duodenal ulcers were healed with omeprazole, 20 mg/day. After endoscopically confirmed healing, patients were treated with either one (17 patients) or two weeks (31 patients) of 'triple therapy'. H pylori status (urease reaction, histological tests, and culture of antral biopsy specimens) was determined at entry, four weeks after the finish of triple therapy and six, 12, and 24 months after this, or whenever an endoscopically proved recurrent duodenal ulcer was found. The main outcome measures were the recurrence of duodenal ulceration, over 24 months in the eradicated and non-eradicated groups and the incidence of reinfection by H pylori in the eradicated group during this follow up period. Five patients in the eradicated group experienced a duodenal ulcer relapse, of which only three were unexplained (1 = reinfected, 1 = gastrinoma). Fifteen of 21 patients in the non-eradicated group relapsed over the same period (p < 0.001). Only two of 27 patients in the eradicated group were reinfected during the 24 month follow up period. It is concluded that H pylori eradication is an effective treatment strategy for the longterm treatment of duodenal ulcer disease, even in the high prevalence, African setting. Reinfection is uncommon.

High-Dose Omeprazole plus Amoxicillin or Clarithromycin Cures &lt;i&gt;Helicobacter pylori &lt;/i&gt;Infection in Duodenal Ulcer Disease

Treatment with omeprazole plus amoxicillin or clarithromycin resulted in encouraging Helicobacter pylori cure rates in pilot and controlled studies. The present prospective, randomized study was designed to compared the efficacy and safety of amoxicillin and clarithromycin as constituents of omeprazole-enhanced antibiotic therapy of H. pylori infection. Fifty patients with active duodenal ulcer disease and histologically and/or culturally confirmed H. pylori colonization of the gastric mucosa were treated with omeprazole (day 1-14: 40 mg twice daily, day 15-42: 20 mg once in the morning). The patients were randomly assigned to receive either amoxicillin (1 g twice daily; group I: n = 25) or clarithromycin (500 mg twice daily; group II: n = 25) during the first 2 weeks of treatment. The patients of group I and II had comparable demographic and clinical characteristics. One patient of group I was lost to follow-up. H. pylori infection was cured in 87.5% of group I and 84.0% of group II (p = 1.00). All ulcers had healed after 6 weeks of omeprazole treatment. Pain relief occurred within the first day of treatment in the majority of patients of both groups (p = 0.89). Minor side effects were recorded in 6 patients of group I and in 4 patients of group II (25 vs. 16%; p = 0.50). In 1 female patient amoxicillin had to be withdrawn after 3 days because of nausea and emesis. In conclusion, 2 weeks of treatment with omeprazole plus amoxicillin or clarithromycin are highly and equally effective regimens to cure H. pylori infection in patients with duodenal ulcer disease.

Improved duodenal ulcer healing with pantoprazole compared with ranitidine

Objective: To compare the efficacy and tolerability of pantoprazole 40 mg (once daily in the morning) with ranitidine 300 mg (once daily at bedtime) in duodenal ulcer healing. Design: Prospective multicentre, randomized, double-blind, parallel-group comparison. Patients: The study included 199 outpatients aged from 18 to 75 years, with endoscopically confirmed active duodenal ulcer disease. Methods: Endoscopy and standard laboratory assessments, including serum gastrin levels, were carried out at the beginning of the study, after 2 and, where applicable, after 4 weeks. Results: Of the patients, 182 (98 on pantoprazole, 84 on ranitidine), median age 39 years, completed the study

Short report: high‐dose omeprazole and amoxycillin in the treatment of Helicobacter pylori‐associated duodenal ulcer

Thirteen consecutive patients with active duodenal ulcer disease were assigned to a treatment schedule with high-dose omeprazole and amoxycillin. Duodenal ulcer was diagnosed endoscopically in all patients, at which time antral biopsies were taken for culture and histology. All were positive for Helicobacter pylori and histological gastritis. Treatment was for 2 weeks: 80 mg omeprazole daily plus 500 mg amoxycillin syrup t.d.s. in the first week, followed by 40 mg omeprazole daily in the second week. Repeat gastroscopy was performed 4 weeks after completion of treatment in all patients. Duodenal ulcer healing occurred in 4/13 patients. H. pylori eradication was achieved in 2/4 patients with healed ulcers and in 3/9 patients with persistent ulceration. This study suggests that a short period of treatment with high-dose omeprazole and amoxycillin achieves low rates of ulcer healing and H. pylori eradication.

Spontaneous Nonfistulous Barium Reflux Into the Biliary Tract

Reflux of barium into the bile duct system during a barium study of the upper gastrointestinal tract is rare in the absence of spontaneous or postoperative fistula. We report four patients, three men and one woman, who had such reflux, associated with active duodenal ulcer disease, shown at radiologic and endoscopic investigation. Reflux of gastrointestinal contents into the biliary tract can result from peptic ulcer disease with duodenal involvement. The finding does not necessarily imply fistulous communication, ulcer perforation, or surgical emergency.

Suppression of Helicobacter pylori reduces gastrin releasing peptide stimulated gastrin release in duodenal ulcer patients.

Helicobacter pylori increases gastrin release in duodenal ulcer patients. This may be through disruption or changes in the mucus layer affecting the access of luminal stimulants to gastrin releasing cells. The effect of suppressing H pylori on gastrin release stimulated by a non-luminal stimulus, gastrin releasing peptide (GRP), was examined. Eleven patients with active duodenal ulcer disease and colonised with H pylori received an intravenous infusion of GRP (2.9 pmol/kg/minute for 30 minutes) and the plasma gastrin response was measured. Basal and peak pentagastrin stimulated acid output were also determined. Patients were treated with tripotassium dicitratobismuthate (De-Nol) and metronidazole to suppress H pylori and the tests were repeated. Suppression of H pylori decreased plasma gastrin concentrations during GRP infusion, but acid output was not affected. Chromatographic analysis of the forms of gastrin in plasma showed a significant fall in gastrin 17, the predominant form found in the gastric antrum. Gastrin 34 did not fall significantly. This study shows that suppression of H pylori decreases the hypergastrinaemia caused by the nonluminal stimulant, GRP, mainly via decreasing gastrin 17.

Effect of Misoprostol and Antacids on Gastric and Duodenal Mucosal Enzyme Activities in Duodenal Ulcer Patients

The activities of 11 marker enzymes from the gastric and duodenal mucosa were determined in 15 patients with active duodenal ulcer disease before therapy, after 4 weeks of therapy with the prostaglandin E1 analogue misoprostol, 400 micrograms twice daily, and after another 4 weeks without any therapy. Another 15 patients were given a high-dose liquid antacid regimen. The activities were measured in homogenized material obtained with forceps through an endoscope. The healing rates of the two groups at 4 weeks were 53% and 80%, respectively. No changes in mucosal inflammation were noted during therapy. During treatment with misoprostol the activities in the descending duodenum of the membrane enzymes alkaline phosphatase, leucyl-beta-naphthylamidase, gamma-glutamyltransferase, and 5'-nucleotidase increased towards the values seen in normal controls. Despite a higher healing rate, no changes in the enzyme activities occurred in the group given high-dose antacid therapy. Four weeks after cessation of therapy the enzyme activities in the misoprostol group were not significantly different from the pretreatment values. In the biopsy specimens from the duodenal bulb the activities of monoamine oxidase fell during treatment with misoprostol and were restored to the pretreatment activity when therapy was stopped. In the stomach mucosa the enzyme activities were largely unchanged during treatment with both misoprostol and antacids. These results indicate that misoprostol and antacids have different mechanisms of action but may also suggest that the demonstrated enzymic changes are unrelated to the healing process.

Helicobacter pyloriand Duodenal Ulcer. A Study of Duodenal Ulcer Patients and Their First-Degree Relatives

Out of 59 duodenal ulcer (DU) probands and their 199 first-degree relatives Giemsa-staining for the determination of Helicobacter pylori (HP) was performed in 51 probands and 155 relatives. Controls were matched by age and sex from a family sample representing the same geographical area. In all, 155 controls were found for the probands and relatives. The occurrence and score of HP density showed an excellent correlation with morphology of the mucosa, signs of acute inflammation and presence of gastric metaplasia in the duodenal bulb. The prevalence of HP was 94% in DU probands and significantly higher than in their relatives and controls. In sibs of DU probands the prevalence of HP (64%) was also significantly higher than in controls (51%) obviously due to the presence of a subgroup of sibs with signs of active or past duodenal ulcer disease, which show higher than expected prevalence of HP, and of acid hypersecretion and high levels of serum pepsinogen I (PG I). Peak acid output (PAO), serum pepsinogen I and II and fasting serum gastrin levels were in relatives without atrophy higher in HP positive than negative cases but significant differences were present only with regard to the pepsinogens. The occurrence of HP positivity as well as of high PAO and pepsinogen levels might be considered risk factors of DU disease in close relatives of DU probands. On the other hand, the significance of HP positivity as cause of abdominal complaints is doubtful, in view of the complete lack of correlation between HP and morphology and complaints in the present study.

Effect of Ranitidine on Gastric and Duodenal Mucosal Enzyme Activities in Duodenal Ulcer Patients

The activities of 11 marker enzymes from the gastric and duodenal mucosa were determined in 19 patients with active duodenal ulcer disease (DU) before therapy, after 4 weeks of therapy with ranitidine, 300 mg/day, and after another 4 weeks without treatment. The activities were measured in homogenized material obtained with forceps through an endoscope. The healing rate at 4 weeks was 68%. In the descending duodenum the activities of the membrane enzymes increased during the treatment period compared with pre-treatment activities. Although not as extensive as in the descending duodenum, an increase of membrane enzyme activities was also noted in the duodenal bulb during treatment. In the gastric mucosa only minor enzymic activity changes were seen. The altered enzyme activities in duodenum and stomach during treatment were independent of ulcer healing, smoking, antacids, and mucosal inflammation. Previously, significant differences in mucosal enzyme activities have been demonstrated between DU patients and controls. During ranitidine treatment the enzyme activities in the duodenal mucosa of the same DU patients tended to normalize, whereas they were mostly unchanged in the gastric mucosa. Four weeks after treatment the mucosal enzyme activities in the duodenum were as before treatment started, without occurrence of ulcer relapse. The altered enzymic activities of the duodenal mucosa in DU patients therefore seem to be largely independent of the presence of active ulcer.

Chronic gastritis and gastroduodenal ulcer: a case control study on risk of coexisting duodenal or gastric ulcer in patients with gastritis.

Chronic (atrophic) gastritis (AG) is common in active duodenal (DU) and gastric ulcer (GU) disease. In this case control study in consecutive prospective outpatients (571 cases and 1074 controls) who had undergone diagnostic upper gastrointestinal endoscopy and routine biopsies from both antral and body mucosa, we calculated the risk of coexisting active DU and/or GU in different gastritis of the antrum or body and according to grade (superficial gastritis, mild, moderate or severe atrophic gastritis). The risk of coexisting active gastroduodenal ulcer (ulcer in duodenum and/or stomach), as well as the risk of DU or GU, was dependent upon the presence and grade of gastritis in antrum and body mucosa. The risk of coexisting ulcer, as expressed as an age adjusted relative risk (RR) and calculated as odds ratio of gastritis in cases and controls, was significantly increased in the presence of superficial antral and body gastritis (RR = 8.5 (7.0-20.0) in men; RR = 5.8 (3.3-10.2) in women), as compared with the risk of ulcer in subjects with histologically normal mucosa (RR = 1). The risk of ulcer, and the risk of GU in particular, increased further with increasing severity of antral gastritis. In such patients with moderate or severe atrophic antral gastritis the RR of coexisting ulcer even exceeded 20 in men and 10 in women (RR = 25.6 (9.0-72.7) in men; RR = 11.7 (5.9-23.0) in women). On the other hand, the RR of ulcer, and the RR of DU in particular, was below 1 in the presence of atrophic gastritis in the gastric body, irrespective of the grade of gastritis in the antrum. We conclude that the type and grade of gastritis strongly predicts the risk of coexisting peptic ulcer, and that the risk of coexisting DU or GU increases with an increase in grade of AG of the antrum but decreases with an increase in grade of AG of the gastric body.

Rioprostil, a New Prostaglandin E1Analogue, in the Once-Daily Treatment of Acute Duodenal Ulcer: A Comparison with Ranitidine

The efficacy of Rioprostil (a new prostaglandin E1 analogue) is compared with ranitidine in the once-a-day treatment in the evening for 4 or 6 weeks of active uncomplicated duodenal ulcer disease. A total of 255 patients are entered in this study; of these 243 have been statistically evaluated. One hundred and twenty (120) patients receive rioprostil 600 micrograms/daily, and 123 patients receive ranitidine 300 mg/daily. After 4 weeks 63.3% of the patients on rioprostil are endoscopically healed, as compared with 69.1% on ranitidine. After 6 weeks the cumulative cure rates are 87.3% and 89.9%, respectively, the difference not being statistically significant. Pain relief is similar for both drugs. Diarrhoea with rioprostil occurs in about 2% of the treatment days and is generally self-limiting.

A Multicenter, Randomized, Double-Blind Study Comparing Famotidine with Cimetidine in the Treatment of Active Duodenal Ulcer Disease

The efficacy and safety of famotidine (40 mg at night), a new potent H2-receptor antagonist, has been studied in 119 patients by four investigators in four Spanish hospitals in a randomized double-blind comparative study with cimetidine (800 mg at night). Antacid tablets were allowed as additional treatment, if needed for pain relief. There were no significant differences between the groups in baseline characteristics, including duodenal ulcer size. Efficacy parameters included daytime and nocturnal symptom relief and duodenal ulcer healing, documented by endoscopy, and defined as complete reepithelization of the ulcer crater. Endoscopy was performed at baseline and after 4 and 6 weeks of treatment. One hundred and five patients fulfilled the evaluation criteria (51 patients in the famotidine group and 54 in the cimetidine group). After 4 weeks, in 91.6% of the patients receiving famotidine and 82.3% of the patients receiving cimetidine ulcers were healed. After 6 weeks, healing rates were 96% (famotidine) and 85.1% (cimetidine) (p = 0.056). Pain relief was rapid in both treatment groups, with a tendency to better response during the day in the famotidine group. The intake of antacids, as well as the clinical and laboratory safety profile were similar for both groups.