How do practicing clinicians manage Helicobacter pylori-related gastrointestinal diseases in Germany? A survey of gastroenterologists and family practitioners.
Breuer T. Sudhop T. Goodman KJ. Graham DY. Malfertheiner P.
Department of Medicine, Baylor College of Medicine, VA Medical Center, Houston, TX, USA.
BACKGROUND: Since the bacterium H. pylori was identified in 1982, overwhelming evidence has implicated it as the causal factor in the occurrence and relapse of peptic ulcer disease. The major objective of this study was to examine the extent to which physicians recognize H. pylori as a causal agent in peptic ulcer disease or as potential cofactor in other gastrointestinal diseases, and the extent to which this knowledge has influenced diagnostic and therapeutic practices. MATERIALS AND METHODS: Using a national mail survey in Germany in September 1995, 1197 family practitioners and 1197 gastroenterologists were selected for the study. RESULTS: Of the surveyed physicians, 756 (32%) responded. Family practitioners treated almost 50% of their patients with initial presentation of suspected ulcer disease without ordering further diagnostic tests. More than 25% of the family practitioners and 14% of the gastroenterologists reported that they do not treat diagnosed H. pylori infection in the first presentation of duodenal ulcer. At the time we conducted the study, 22% of responding family practitioners and 5% of responding gastroenterologists treated the first presentation of H. pylori-positive ulcer disease with regimens determined to be ineffective according to the available literature. CONCLUSIONS: Gastroenterologists preferred to treat H. pylori infection when the associated disease was one for which a causal relationship had been more clearly established, while family practitioners showed less discrimination. In order to provide optimal therapy aimed at minimizing the course and consequences of H. pylori-related diseases, researchers in the field must ensure continuous dissemination of current knowledge.
Serologic detection of CagA positive Helicobacter pylori infection in a northern Italian population: its association with peptic ulcer disease.
Orsini B. Ciancio G. Surrenti E. Macri G. Biagini MR. Milani S. Surrenti C.
Department of Clinical Pathophysiology, University of Florence, Italy.
BACKGROUND: About 60-70% of Helicobacter pylori strains possess cagA (cytotoxin associated gene A) gene and express its product CagA, a highly immunogenic 128-140 kD protein. Patients infected with CagA positive strains develop serum IgG anti-CagA. A serologic response to CagA has been detected in Helicobacter pylori infected patients with peptic ulcer more frequently than in those with gastritis alone. It is nuclear whether this finding is consistent in different geographical populations. We investigated the relationship between anti-CagA seropositivity and peptic ulcer disease in a Northern Italian population. MATERIALS AND METHODS: We studied 135 H. pylori infected patients: 65 with duodenal ulcer (DU), 28 with gastric ulcer (GU) and 42 with non ulcer dyspepsia (NUD). Sera from these patients were assayed by EIA (enzyme immunoassay) for anti-CagA IgG. RESULTS: A high prevalence of anti-CagA was found associated with DU (86.1%) and GU (96.4%), while NUD patients showed anti-CagA seropositivity of 52.4% (Odd ratio, 5.66; 95% confidence interval, 2.23 to 14.32; p < .001, DU vs. NUD; Odd ratio, 24.5; 95% confidence interval, 3.05 to 197.6; p = .003, GU vs. NUD). DU patients showed anti-CagA seropositivity titer (1.15 (0.61 OD, mean (SD) higher than that of NUD patients (0.78 (0.60 OD, mean (SD) (p < .05). CONCLUSIONS: These data demonstrate in a Northern Italian population that anti-CagA seropositivity is strongly associated with peptic ulcer disease and suggest that CagA might play an important role in ulcer pathogenesis.
Follow-up of Helicobacter pylori positive gastritis and argyrophil cells pattern during the natural course of gastric ulcer.
Maaroos HI. Havu N. Sipponen P.
Faculty of Medicine, University of Tartu, Estonia.
BACKGROUND: A follow-up of argyrophil cell hyperplasia in Helicobacter pylori-positive corpus gastritis in gastric ulcer patients during the natural course of ulcer disease. METHODS: Endoscopic biopsies (4 specimens) were obtained step-wise from the posterior wall of the corpus mucosa in 55 gastric ulcer (GU) patients. The natural course of GU was followed up in 38 patients during more than 10 years (maximum 19 years), and altogether 115 endoscopic examinations were made: 20 patients were re-examined once, 14 twice, and 4 three times. A total of 364 biopsies from 307 biopsy sites were stained by Grimelius' silver, hematoxylin-eosin, and Giemsa method for the analysis of the argyrophil endocrine cells, chronic gastritis, and H. pylori colonization, respectively, according to the Sydney System. RESULTS: Of 307 biopsy sites, 153 (50%) showed some grade of ACH. Focal (linear/micronodular) hyperplasia was found in 118 (77%) of biopsy sites; it was detected in 78 (66%) cases of atrophic corpus mucosa, but was present in only 14 (12%) cases of gastritis without atrophy or in the normal mucosa. In the follow-up patients, ACH evolved in 17 and progressed in 6 cases, and a simultaneous development of atrophic corpus gastritis was found in 20 cases. CONCLUSION: This study demonstrates that ACH evolves during the natural course of GU, alongside the development of chronic atrophic gastritis.
Assessment of a new triple agent regimen for the eradication of Helicobacter pylori and the nature of H. pylori resistance to this therapy in Japan.
Suzuki J. Mine T. Kobayasi I. Fujita T.
Department of Internal Medicine IV, University of Tokyo School of Medicine, Japan.
BACKGROUND: Multiple regimens for the eradication of Helicobacter pylori have been tested, but the best therapy has not been determined yet. To determine the efficacy of a new triple agent regimen using a combination of lansoprazole, amoxicillin, and clarithromycin against Helicobacter pylori (H. pylori), and to examine H. pylori resistance to this therapy in ineffective cases. METHODS: We studied a total of 71 patients infected with H. pylori who had gastric ulcer (n = 37) or duodenal ulcer (n = 34) as confirmed by endoscopy. Patients received 1500 mg amoxicillin, 400 mg clarithromycin and 30 mg lansoprazole for 2 weeks followed by 30 mg lansoprazole for 6 weeks in patients with gastric ulcer or for 4 weeks in those with duodenal ulcer. Endoscopic examination was performed before treatment and at 1 month, 2 months, and 5 months after initiating treatment to check the status of ulceration and H. pylori infection. RESULTS: The eradication rate of H. pylori was 92% (CI, 83-100%) in the gastric ulcer group and 94% (CI, 86-100%) in the duodenal ulcer group at 5 months, as determined by per-protocol analysis. Resistance to clarithromycin was present in 1 of 71 (1%) patients before treatment and in 2 of 5 (40%) patients after treatment. No resistance to amoxicillin and lansoprazole was found in patients before or after treatment. The resistance to clarithromycin changed during the observation period. CONCLUSIONS: The new triple agent regimen was effective against H. pylori. Resistance to clarithromycin may not be permanent and it might be one of the risk factors which affect the efficacy of a clarithromycin-based therapy.
Helicobacter pylori colonization density and gastric acid output in non-ulcer dyspepsia and duodenal ulcer disease.
Mullins PD. Steer HW.
Department of Medicine, Southampton University Hospitals, U.K.
BACKGROUND: 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. METHODS: 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. RESULTS: 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). CONCLUSIONS: 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.
Helicobacter pylori and peptic ulcer disease therapies: a survey of gastroenterologists in Israel.
Fireman Z. Segal A. Moshkowitz M. Kopelman Y. Sternberg A.
Gastroenterology Department, Hillel Yaffe Medical Center, Hadera, Israel. firstname.lastname@example.org
BACKGROUND: Eradication of Helicobacter pylori has become a therapeutic option in the treatment of patients with peptic ulcer disease. The aim of this study was to evaluate the current management strategies of Israeli gastroenterologists in the diagnosis and treatment of H. pylori-related peptic ulcer disease, 14 years after the discovery of H. pylori. MATERIALS AND METHODS: A questionnaire was mailed to all specialists in gastroenterology, members of the Israel Gastroenterological Association (IGA). Replies were received from 60% of Israel Board-certified gastroenterology specialists. RESULTS: Over 89% of the gastroenterologists (89.1%) noted that they recommend anti-H. pylori treatment. 94.5% said that they treat duodenal ulcer in the first presentation with anti-H. pylori medication and 75% said that they do so in cases of recurrent duodenal ulcer. According to the replies received, there is a strong consensus towards triple treatment as the favored anti-H. pylori treatment; no one noted the use of dual treatment. Seven-day triple treatment was prescribed by 83.6% of the gastroenterologists who responded. Of these, the great majority, 89.1%, stated that they use proton pump inhibitors (PPI) in combination with any two of the following antibiotics: metronidazole (47.3%), tinidazole (29.1%), clarithromycin (61.8%), and amoxicillin (40%). CONCLUSION: At the time of the survey, most Israel Board-certified gastroenterology specialists prescribed triple anti-H. pylori treatment of one-week's duration.
An alternative non-macrolide, non-imidazole treatment regimen for curing Helicobacter pylori and duodenal ulcers: ranitidine bismuth citrate plus amoxicillin. The RBC H. pylori Study Group.
Graham DY. Breiter JR. Ciociola AA. Sykes DL. McSorley DJ.
Veterans Administration Medical Center, Houston, TX 77030, USA.
BACKGROUND: Because patients who fail to be cured of H. pylori infection following macrolide or imidazole therapy are difficult to treat, there is a clear need for a reasonably effective and simple second-line treatment regimen. The purpose of these two studies was to evaluate the efficacy of ranitidine bismuth citrate (RBC) plus amoxicillin for the cure of H. pylori infection and for healing duodenal ulcers and preventing ulcer relapse. MATERIALS AND METHODS: Two identically designed randomized, double-blind, double-dummy studies were conducted in patients with an H. pylori-associated duodenal ulcer. Patients were treated with either RBC 400 mg bid for 4 weeks plus amoxicillin 500 mg qid for 2 weeks, RBC 400 mg bid for 4 weeks and placebo qid for 2 weeks, placebo bid for 4 weeks and amoxicillin 500 mg qid for 2 weeks, or placebo bid for 4 weeks and placebo qid for 2 weeks. Patients with healed ulcers after 4 weeks of treatment were eligible for entry into a 24-week observation phase for the assessment of H. pylori status (culture, histology, and CLOtest) and ulcer relapse. RESULTS: A total of 229 patients with confirmed H. pylori infection at baseline were evaluated. Of these, 132 whose ulcers had healed entered the 24-week posttreatment observation phase. The combination of RBC plus amoxicillin resulted in higher H. pylori cure rates (55%) and higher duodenal ulcer healing (74%) than did either treatment alone. All treatment were well tolerated. CONCLUSIONS: The combination of ranitidine bismuth citrate plus amoxicillin cures H. pylori infection in more than half of the patients treated. This treatment regimen shows promise as the basis for future non-macrolide, non-imidazole triple therapy regimens for curing H. pylori infection. Such regimens may be appropriate second-line treatment for patients who are resistant to or who are unable to tolerate macrolide- or imidazole-containing therapies.