An increasing dose of omeprazole combined with amoxycillin cures Helicobacter pylori infection more effectively.

BACKGROUND: The combination of omeprazole and amoxycillin has demonstrated effectiveness with very few side-effects in the treatment of H. pylori infection, however cure rates have varied widely. The present study addresses the question as to the extent to which the cure rate of H. pylori infection depends on the size of the daily omeprazole dose, and investigates other patient-related factors that influence treatment success. METHODS: In a randomized, controlled and investigator-blinded trial, 163 hospitalized patients with H. pylori-associated gastritis were treated with 20 mg omeprazole once daily in the morning, 20 mg omeprazole b.d., 40 mg omeprazole b.d. or 60 mg omeprazole b.d. for 14 days. In addition, all patients received 1000 mg amoxycillin b.d. on days 5-14. Endoscopic and histological examinations were performed prior to treatment, at the end of treatment and 4 weeks after completion of treatment. RESULTS: H. pylori infection was cured in 18 of 40 (45%, 95% CI: 29-62%), in 22 of 39 (56.4%, 95% CI: 40-72%), in 25 of 38 (65.8%, 95% CI: 49-80%), and in 33 of 40 (82.5%, 95% CI: 67-93%) patients, respectively, (P < 0.001). Side-effects leading to discontinuation of treatment occurred in only 1.2%. CONCLUSION: The daily dose of omeprazole is an important factor for the success of dual therapy comprising omeprazole and amoxycillin in curing H. pylori infection. Cure of H. pylori infection correlates positively and significantly with the size of the daily omeprazole dose. The combination of high-dose omeprazole and amoxycillin is an effective and well-tolerated regimen for the treatment of H. pylori-associated diseases.

Topographic association between active gastritis and Campylobacter pylori colonisation.

One thousand biopsy specimens obtained from 10 sites in the stomachs of 50 patients were examined for the presence of active chronic gastritis and Campylobacter pylori. All 32 patients with active chronic gastritis at 234 out of 320 sites were positive for C pylori: 227 showed colonisation with C pylori by the Warthin-Starry stain; and 222 were positive by culture. C pylori was not found in 18 patients with inactive chronic gastritis or histologically normal mucosa. The area of C pylori colonisation was larger than the area of active chronic gastritis in 289 positive specimens on culture and 261 on staining, respectively, suggesting that C pylori colonisation may precede the development of active chronic gastritis. It is concluded that patchy distribution of active chronic gastritis and C pylori colonisation must be considered, particularly in serology or breath test studies where the histological examination serves as a reference. Furthermore, it may have important implications for the follow up of patients after antibacterial treatment. The topographic and specific association of C pylori and active chronic gastritis provides further evidence for the pathogenic role of C pylori in active chronic gastritis.

Diagnostic sensitivity of fasting and postprandial serum bile acids determined by different methods.

The diagnostic sensitivities of serum bile acids determined by three different methods in the fasting and in the postprandial state were compared in 43 patients with cirrhosis of the liver. When a method with high analytical sensitivity (capillary gas-liquid chromatography, GLC, or radioimmunoassay, RIA) was used, the serum concentrations of bile acids exhibited similar diagnostic sensitivities in the fasting state (GLC, 98%; RIA, 93%) and in the postprandial state (GLC, 95%; RIA, 93%). By contrast, when an enzymatic method with limited analytical sensitivity was employed, the diagnostic sensitivity of fasting serum bile acids was lower (79%) than that of postprandial serum bile acids (93%). The measurement of individual serum bile acids by GLC did not add any further diagnostic information. The results of this study demonstrate that the diagnostic sensitivity of serum bile acids strongly depends on the analytical method used.

Helicobacter pylori reinfection is rare in peptic ulcer patients cured by antimicrobial therapy.

BACKGROUND: Cure of H. pylori infection in peptic ulcer patients significantly reduces the risk of ulcer recurrence. Since data on the rate of H. pylori reinfection in patients undergoing successful anti-H. pylori therapy are sparse, this study was conducted with the aim of determining the H. pylori reinfection rate in peptic ulcer patients receiving antibacterial treatment to heal their ulcer and cure H. pylori infection. METHODS: A total of 217 patients with H. pylori-associated duodenal or gastric ulcer were followed up after treatment with various antibacterial regimens resulting in histologically documented cure of H. pylori infection. Endoscopic and histological examinations were performed 4 weeks after completion of treatment and after 1, 2 and 5 years, or whenever dyspeptic symptoms occurred. To assess the H. pylori status two antral and two corpus biopsies were obtained for histological examination. RESULTS: Out of 217 patients with initially cured H. pylori infection 175 were available for endoscopic follow-up. At the time of analysis, 44 patients were re-examined after 1 year, 113 patients after 2 years and 18 patients after 5 years, giving a total of 360 patient years of follow-up. The mean duration of follow-up was 24.7 months. H. pylori reinfection was confirmed histologically in eight patients, three of whom becoming H. pylori-positive again within the first year of follow-up. Six of the eight patients with H. pylori reinfection also suffered an ulcer relapse. Eight cases of reinfection in 360 patient years represents an overall reinfection rate of 2.2%. Within the first 2 years of follow-up the reinfection rate was 0.8% per year. CONCLUSION: Our data suggest that H. pylori reinfection is rare in peptic ulcer patients receiving successful anti-H. pylori therapy. H. pylori reinfection frequently coincides with ulcer recurrence. Cure of H. pylori infection results in cure of peptic ulcer disease, provided H. pylori reinfection does not occur.

Recurrence of duodenal ulcers during five years of follow-up after cure of Helicobacter pylori infection.

BACKGROUND: Chronic Helicobacter pylori-associated gastritis is now widely accepted as one of the most important pathogenic factors in duodenal ulcer disease. However, little is known about for how long patients remain free of duodenal ulcer relapses after H. pylori infection has been cured. In the present study, we investigated remission time during a 5-year follow-up period after anti-H. pylori treatment. METHODS: The patients were randomly allocated to treatment with either a combination of 3 x 600 mg bismuth subsalicylate and 2 x 1000 mg amoxycillin or 3 x 600 mg bismuth subsalicylate monotherapy. Endoscopy, including histological and microbiological examination of biopsies, was performed 4 weeks after termination of treatment and after 1 and 2 years. During the third, fourth and fifth years of the follow-up period, patients were monitored twice a year for symptoms compatible with ulcer relapse and for their use of anti-ulcer medication. Endoscopic and histological examinations were carried out whenever symptoms occurred. RESULTS: Of 56 evaluated patients, 47 showed healing of ulcers after bismuth subsalicylate plus amoxycillin compared with 44 of 57 after bismuth subsalicylate monotherapy. H. pylori infection was cured in 52% (29 of 56) of the patients after combined therapy and in 4% (2 of 57) after the monotherapy. The cumulative duodenal ulcer relapse rates after 5 years were 38% (18 of 47) after the combined therapy and 75% (33 of 44) after the monotherapy. In patients who were cured of H. pylori infection, the cumulative duodenal ulcer relapse rate after 5 years was 9.7% (3 of 31), compared with 81.7% (49 of 60) in those patients who remained H. pylori-positive after treatment (P < 0.001). In two of the three patients who suffered duodenal ulcer relapse after being cured of H. pylori infection, H. pylori was present again at the time of relapse. CONCLUSION: The data suggest that curing H. pylori infection results in long-term cure of duodenal ulcer disease and that duodenal ulcer relapses in successfully treated patients are most often associated with H. pylori reinfection.

Cure of gastric ulcer disease after cure of Helicobacter pylori infection--German Gastric Ulcer Study.

BACKGROUND: Helicobacter pylori infection is associated with gastric ulcer disease in about 75% of cases. OBJECTIVE: The aim of this study was to determine whether H. pylori eradication reduces gastric ulcer relapse rates. DESIGN: The study was randomized, controlled, multicentric and investigator blinded, and was conducted at three university hospitals, two teaching hospitals, and by six practising gastroenterologists. METHODS: During a period of 1 year 152 patients with gastric ulcers were randomly assigned to one of two treatment regimens: omeprazole 20 mg daily in the morning for 8 weeks (74 patients), or bismuth subsalicylate 600 mg three times daily for 8 weeks combined with 500 mg amoxicillin twice daily and 1000 mg tinidazole twice daily for the first 10 days (triple therapy) (78 patients). Follow-up examinations were performed 6, 12 and 18 months after treatment and whenever ulcer symptoms occurred. RESULTS: Of the 152 randomized patients five were excluded because of gastric cancer, 10 missed follow-up examinations and seven receiving triple therapy terminated treatment because of side effects. Of the remaining 130 patients, five of 69 (7.2%) in the omeprazole and six of 61 (9.8%) in the triple group were H. pylori negative. After 8 weeks' therapy, the gastric ulcer was healed in 85.9% (omeprazole) and in 81.8% triple) in H. pylori-positive patients, and in 80% (omeprazole) and 16.7% (triple) in H. pylori-negatives. H. pylori was eradicated in 8.1% of the patients who received omeprazole monotherapy and in 78.2% receiving triple therapy, and in 8.1% and 69.4% in an intention-to-treat analysis. The subsequent relapse rates during a follow-up period of 12 months were 50% in the omeprazole group and 4% in the triple group. Gastric ulcer relapse was observed in 49% of patients who were H. pylori positive and in 2% who were H. pylori negative after treatment. CONCLUSION: The data show that the presence of H. pylori is an important predictor of gastric ulcer relapse and that eradication of H. pylori may heal gastric ulcer disease.

Long-term follow-up after eradication of Helicobacter pylori with a combination of omeprazole and amoxycillin.

Early studies have suggested that omeprazole may facilitate the eradication of Helicobacter pylori. Sixty patients with duodenal ulcer and H. pylori colonization were randomly assigned to receive either omeprazole monotherapy (n = 30) or combination therapy with omeprazole and amoxycillin (n = 30) for a total duration of 6 weeks. Four patients receiving monotherapy and three receiving combination therapy had to be withdrawn from the study. All (100%) duodenal ulcers healed in patients receiving combination therapy, and 25 out of 26 (96%) healed in the group receiving monotherapy. H. pylori was eradicated in 22 out of 27 (82%) patients receiving combination therapy; only two ulcer relapses (9%) occurred within 18 months in these 22 patients. Of the five patients who remained H. pylori-positive after combination therapy, two relapsed during the 18-month follow-up. In the monotherapy group, all patients remained H. pylori-positive after treatment, and duodenal ulcer relapsed in 16 out of 25 (64%) patients within the median follow-up of 18 months. Adverse events were not reported in the group treated with combination therapy; one patient receiving monotherapy reported severe headache. These results lend further support to existing data that H. pylori eradication prevents duodenal ulcer relapse and show that combination therapy with omeprazole and amoxycillin is effective and well tolerated.

[Helicobacter pylori eradication therapy with omeprazole and amoxicillin: current status]. / Helicobacter pylori-Eradikationstherapie mit Omeprazol und Amoxicillin: Heutiger Stand.

Combined therapy with the proton pump inhibitor omeprazole and amoxicillin has become an important alternative in the treatment of ulcer disease associated with Helicobacter pylori infection. Due to the high efficacy in eradicating H.pylori, missing resistance of H.pylori against amoxicillin and high tolerability and digestibility this regimen may be recommended for widespread routine use. In a randomized, double-blind multicenter trial an H.pylori eradication rate of over 90% has been achieved for the first time by dual therapy using a daily omeprazole dose of 120 mg (3x40 mg) in combination with 3 x 750 mg amoxicillin for 14 days, which is comparable with classical triple therapy containing bismuth and two antibiotics. On the basis of an "intention-to-treat-analysis" dual therapy of omeprazole 3x40 mg + 3x750 mg amoxicillin is considered at present to be the most effective regimen for the treatment of H.pylori-associated diseases.

Increased serum bile acids in cirrhosis with normal transaminases.

Fasting and postprandial serum concentrations of total conjugated primary bile acids determined by radioimmunoassay have been compared with conventional liver function tests in patients with cirrhosis of the liver and normal transaminases. While gamma-glutamyl-transferase had the highest sensitivity (69%) among the conventional liver function tests, it was much less sensitive for the detection of cirrhosis with normal transaminases than fasting (93% sensitivity) or postprandial (93% sensitivity) bile acid concentrations in serum. When a combination of fasting and postprandial bile acid concentrations was used, the sensitivity increased to 97%.

Increased risk of 'high-risk' colorectal adenomas in overweight men.

BACKGROUND: Epidemiologic studies have suggested that the incidence of colorectal carcinoma may be related to overnutrition, but retrospective analysis of its relation to the body mass index (BMI: kg/m2) has produced conflicting data. METHODS: To avoid as many sources of statistical bias as possible, the relation between BMI and the presence of colorectal adenomas was investigated in a cross-sectional study. RESULTS: Two thousand twelve consecutive colonoscoped patients were investigated (532 patients with malignancies or other conditions associated with weight loss were excluded). The relation between BMI and observed colorectal adenomas was evaluated by a logistic model controlling for other prognostic factors such as age, sex, and serum cholesterol level. The subgroup of "high-risk" adenomas with an increased risk of malignant transformation was positively associated with the BMI in men of the age group 50.5-68.1 years (quintiles III and IV: odds ratio for the top quintile vs. the lowest quintile, 3.21; 95% confidence interval, 1.15-8.98). CONCLUSIONS: It was concluded that the risk of developing high-risk adenomas tends to be increased in men who are overweight and that this association is independent of the positive association with the serum cholesterol level recently described.

Predictive value of serum procollagen-III-peptide for the survival of patients with cirrhosis.

The value of the aminoterminal procollagen-III-peptide (P-III-P) in predicting death or survival was evaluated in a group of 43 patients with proven postnecrotic or alcoholic cirrhosis. Patients were followed-up prospectively for 2 years. The prognostic value of P-III-P was compared with the Child classification, fasting and postprandial serum bile acids, and standard laboratory tests such as bilirubin, prothrombin index, pseudocholinesterase, albumin, GOT, GPT, gamma-GT, and clinical findings such as ascites, encephalopathy (assessed with the number connection test = NCT), and nutritional status. Between patients who died and those who survived the following 2 years, there were significant differences in the following parameters at the time of inclusion in the study: encephalopathy judged by NCT (p = 0.001), serum albumin (p = 0.0012), postprandial serum bile acids (p = 0.0024), fasting serum bile acids (p = 0.0025), pseudocholinesterase (p = 0.0044), GOT (p = 0.015), bilirubin (p = 0.016), and prothrombin index (p = 0.01). None of the other parameters investigated, including SP-III-P (p = 0.46), revealed any statistically significant differences between patients who died and survivors. The prognostic significance of laboratory tests and recorded clinical findings was evaluated, either alone or in combination with life-table analysis using the Cox model. SP-III-P, alone or in combination with other parameters, failed to improve prediction of mortality in patients with cirrhosis. In comparison to the Child classification (p = 0.0004) the combination of NCT and postprandial serum bile acids showed a similar ability (p = 0.0003) to predict patient survival.

Unconjugated secondary bile acids in the serum of patients with colorectal adenomas.

A positive association between deoxcholic acid (DCA) in the serum and colorectal adenomas, the precursors of colorectal cancer has recently been found, which supported the hypothesis of a pathogenic role of DCA in colonic carcinogenesis. This approach was based on the hypothesis that DCA formed in the colon is absorbed into the portal venous blood and exhibits a constant spillover to the systemic circulation. To further substantiate this hypothesis this study investigated whether in the serum of adenoma patients DCA was higher in the unconjugated fraction, which originates directly from the colon. DCA was found to be 2.8-fold higher in the unconjugated fraction of patients with colorectal adenomas than in controls (0.89 v 0.32 mumol/l, p < 0.0025), 1.9-fold in the total DCA fraction (1.89 v 0.95 mumol/l, p < 0.0001), and 1.4-fold in the conjugated fraction (0.67 v 0.47 mumol/l, p < 0.05). It was further found that the bacterial isomerisation product 3 beta-DCA was twofold higher in the unconjugated fraction of adenoma patients than in controls (0.08 v 0.04 mumol/l, p = 0.27), 1.8-fold in the total iso-DCA fraction (0.11 v 0.06 mumol/l, p < 0.05), and 1.5-fold in the conjugated iso-DCA fraction (0.03 v 0.02 mumol/l, p = 0.68). The data suggest that the positive association between the serum DCA concentration and colorectal adenoma as described previously results from the DCA fraction that is absorbed from the colon. This further supports a pathogenic role of DCA in the carcinogenesis of colorectal cancer.

Relation between the frequency of colorectal adenoma and the serum cholesterol level.

Several investigators have reported an association between low serum cholesterol levels and an increased frequency of colorectal cancer. Because low cholesterol levels may be a result of an established cancer, we have investigated the relation between serum cholesterol levels and the frequency of colorectal adenomas, which are thought to be precursors of colon cancer. We prospectively studied 1083 consecutive patients who underwent colonoscopy (241 of whom were excluded because of malignant disease, chronic inflammatory bowel disease, familial polyposis, or partial colectomy). In the remaining 842 patients, analysis of covariance was performed to evaluate the contribution of serum cholesterol to the risk of colorectal adenoma. Serum cholesterol levels were significantly and positively associated with the frequency of colorectal adenoma in subjects of both sexes. After adjustment for age and body-mass index, this positive association remained significant between the top quintile and the lowest quintile for serum cholesterol, with regard to the total study group (odds ratio, 2.0; 95 percent confidence limits, 1.1 and 3.6) and men only (odds ratio, 2.2; 95 percent confidence limits, 1.0 and 4.8). We conclude that there is not an inverse correlation between serum cholesterol levels and the risk of colorectal adenomas; on the contrary, there appears to be a small positive association.

Prognostic significance of serum bile acids in cirrhosis.

The value of serum bile acid concentrations for predicting prognosis in cirrhotics was compared with the prognostic significance of clinical and laboratory findings in a prospective 1-year study of 76 patients with cirrhosis. A commercial radioimmunoassay for total serum-conjugated primary bile acids was used. Of 76 patients, 16 died within the follow-up period. The concentration of bile acids in serum more closely correlated with mortality in cirrhosis than the commonly used clinical and laboratory parameters such as the Number Connection Test, ascites, albumin, pseudocholinesterase, bilirubin, prothrombin time and nutritional state. Serum bile acids alone yielded a prediction of mortality comparable to the Child classification. When logistic regression analysis was performed, optimal prediction of prognosis was achieved with the combination of serum bile acids and the Number Connection Test. Serum bile acid levels alone or in combination with the Number Connection Test may be a clinically useful prognostic index in cirrhosis.

Variation of serum bile acids in patients with colorectal adenomas during a one-year follow-up.

We were recently able to show that patients with colorectal adenomas have an increased serum level of the secondary bile acid deoxycholic acid [Bayerdörffer et al.: Gastroenterology 1993; 104:145-151]. The course of individual serum bile acids was followed for 1 year in a random subgroup of these patients. The individual serum bile acids of 39 patients, 10 men with adenoma, 12 men without adenoma, 8 women with adenoma, and 9 women without adenoma, were determined at 6-month intervals by gas liquid chromatography (GC). The mean individual differences in serum bile acids between baseline and 6-month follow-up and baseline and 12-month follow-up ranged from +19 to -15 nmol/l in men with adenoma, and from +66 to -64 nmol/l in men without adenoma. In women, the ranges were +73 to -74 nmol/l in those with adenoma and +33 to -81 nmol/l in those without adenoma. The variations of the relative percentages of the individual bile acids in the three investigations were lower than those of the absolute values. The differences between the baseline, the 6-month, and the 12-month follow-up were not significant for the major bile acids deoxycholic acid, chenodeoxycholic acid and cholic acid. The main finding, namely an increase in the serum levels and the relative proportion of deoxycholic acid in men with colorectal adenomas remained unchanged throughout the follow-up. The data indicate that measurement of the bile acid pattern by GC is a useful and reproducible parameter in investigating the role of secondary bile acids in the pathogenesis of colorectal cancer.

Antibiotic prophylaxis of infectious complications with endoscopic retrograde cholangiopancreatography. A randomized controlled study.

Biliary sepsis represents a major percentage of fatal complications after endoscopic retrograde cholangiopancreatography. We performed a randomized controlled study to investigate the value of antibiotic prophylaxis, and to assess the frequency and source of infectious complications associated with ERCP. Ninety-six patients who underwent 100 endoscopic retrograde cholangiopancreatographies were included in the study. Half of the patients received antibiotic prophylaxis (Cefotaxime 2 g i.v. 15 min before the procedure). Bacteremia was detected in 2% of the patients receiving antibiotic prophylaxis, as compared with 16% (p less than 0.02) in the control group. In order to determine the source of bacteremia, bile samples and irrigation fluid from the suction channel of the endo-scope were obtained for bacteriological evaluation. Several lines of evidence suggested that bacteremia associated with ERCP was essentially caused by mucosal lesions of the oropharynx. Bacteremia was asymptomatic, with the exception of two patients who subsequently developed fever, but recovered rapidly under antibiotic therapy. The frequency of cholangitis following ERCP was not significantly reduced by antibiotic prophylaxis (4% vs. 2%). Recommendations for antibiotic prophylaxis are discussed.

Decreased high-density lipoprotein cholesterol and increased low-density cholesterol levels in patients with colorectal adenomas.

OBJECTIVE: To study the relation between serum lipoprotein levels and the frequency of colorectal adenomas, the benign precursors of colorectal cancer. DESIGN: Cross-sectional. SETTING: University hospital in Germany. PATIENTS: The study included 822 of 1124 consecutive patients who underwent colonoscopy at our institution (302 patients were excluded because of malignant disease, chronic inflammatory bowel disease, familial polyposis, partial colectomy, or other chronic diseases). Of the 822 study patients, 194 had colorectal adenoma. MEASUREMENTS: Serum cholesterol fractions (high-density lipoprotein [HDL], low-density lipoprotein [LDL], and very low-density lipoprotein [VLDL]) and presence or absence of adenomas; univariate and logistic regression analyses were carried out to evaluate the association between serum HDL, LDL, and VLDL cholesterol levels and the frequency of colorectal adenoma. RESULTS: Univariate analysis of the total patient group showed that the HDL cholesterol level was inversely related to the frequency of colorectal adenoma (odds ratio, 0.36; 95% Cl, 0.21 to 0.62) and that LDL and VLDL cholesterol levels were positively associated with adenoma frequency (odds ratio, 2.31 [Cl, 1.36 to 3.92] and 1.72 [Cl, 1.03 to 2.86], respectively). Univariate analysis of the subgroup of 89 patients with high-risk adenomas showed an inverse association between such adenomas and HDL cholesterol (odds ratio, 0.37; Cl, 0.18 to 0.76). A logistic regression analysis that included age and body mass index showed an association between lipoprotein levels and the presence of adenomas. The relative strength (in descending order) of these associations was as follows: HDL, LDL, VLDL, and total serum cholesterol. A logistic regression analysis of patients with high-risk adenoma showed a significant association between such adenomas and the HDL cholesterol level. CONCLUSIONS: Patients with colorectal adenomas have lower HDL cholesterol levels and higher LDL and VLDL cholesterol levels; these lipoproteins may have prognostic significance for the development of colorectal adenomas.

Increased serum deoxycholic acid levels in men with colorectal adenomas.

BACKGROUND: Epidemiological and animal studies have suggested that the secondary bile acid deoxycholic acid is cocarcinogenic in colorectal cancer, but this hypothesis was not confirmed by case-control studies investigating fecal bile acids. METHODS: Individual serum bile acid concentrations were investigated in 25 men and 25 women with colorectal adenomas and in an equal number of age- and sex-matched controls by gas-liquid chromatography. RESULTS: Deoxycholic acid levels were significantly higher in the sera of men with colorectal adenomas (1.70 +/- 0.59 vs. 1.16 +/- 0.39 mumol/L, P < 0.0005) and in a combined analysis of both sexes (1.47 +/- 0.78 vs. 1.08 +/- 0.39 mumol/L, P < 0.0025). Six- and 12-month follow-up measurements of deoxycholic acid concentrations in a subgroup of 22 men and 17 women showed higher serum levels in men with adenomas, indicating that measurement of deoxycholic acid concentration may be a reliable parameter to investigate its pathogenetic role in colonic neoplasia. CONCLUSIONS: The data of this study support the hypothesis that deoxycholic acid may play a role in the pathogenesis of colorectal cancer.

Difference in expression of Helicobacter pylori gastritis in antrum and body.

Seven hundred seventy biopsy specimens obtained from 10 different sites in stomachs of 77 patients were examined for the presence of active chronic gastritis (ACG) and Helicobacter pylori to investigate the characteristics of gastritis in the antrum and body. Forty-eight patients with ACG at one or more sites were all H. pylori positive. H. pylori was not found in 20 patients who had chronic gastritis with no activity or in 9 patients who had histologically normal mucosa. In patients with ACG in at least one biopsy site, a strong positive topographic association between H. pylori colonization and ACG was seen in the Warthin-Starry stain. The frequency of H. pylori colonization was similar in the antrum and body. However, the incidence of ACG declined significantly proximal to the borderline between the antrum and body (P less than 0.001). The average grade of gastritis at the individual biopsy sites was distributed evenly throughout the antrum but decreased markedly in the body (P less than 0.0001). In the same manner, the average grade of H. pylori colonization decreased in the body (P less than 0.0027). The grade of H. pylori colonization in the individual biopsy specimens was closely related to the grade of gastritis (r = 0.51); also, the grade of neutrophil infiltration was related to the grade of gastritis (r = 0.79). A good correlation existed between the grade of H. pylori colonization and the grade of neutrophil infiltration (r = 0.70). The results of this study show a different expression of H. pylori gastritis in the antrum and body, which is the main subtype of chronic type B gastritis. The close topographic and graded association between the presence of H. pylori and the activity and grade of gastritis lend further support to the major pathogenic role of H. pylori in active chronic gastritis. The different expression of gastritis in antrum and body is suggested to be increased reactivity of the antral mucosa to the infection, possibly on the basis of an enhanced immunologic response to H. pylori in this region.

Double-blind trial of omeprazole and amoxicillin to cure Helicobacter pylori infection in patients with duodenal ulcers.

BACKGROUND/AIMS: Anti-Helicobacter pylori treatment with combinations of omeprazole and amoxicillin is a promising treatment option. The aim of this study was to investigate whether a daily omeprazole dose of 120 mg combined with amoxicillin would cure H. pylori infection at a rate comparable with that achieved with "triple therapy." METHODS: In a double-blind, randomized, controlled, and multicenter trial in Germany, 270 patients with an H. pylori-associated duodenal ulcer were treated with 40 mg omeprazole three times a day and 750 mg amoxicillin three times a day for the first 14 days (n = 139) followed by 20 mg omeprazole once daily until day 42 or with omeprazole plus 750 mg amoxicillin placebo three times a day for the same time period (n = 131). RESULTS: Cure rates of H. pylori infection were 91% in the omeprazole plus amoxicillin group, 0% in the omeprazole plus placebo group, and 89% and 0%, respectively, performing an intention-to-treat analysis. Cure of H. pylori infection in patients pretreated with omeprazole was only 58% compared with 95% in patients who were not. The cumulative 12-month relapse rates were 11.3% and 44% in the treatment groups and 1.6% in H. pylori-negative and 49% in H. pylori-positive patients. CONCLUSIONS: The combination of 120 mg omeprazole daily and 2.25 g amoxicillin daily with its H. pylori cure rate of around 90% is one of the best tolerated and most effective treatment regimens.