Review article: Helicobacter pylori -negative duodenal ulcer disease (original) (raw)
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The American journal of gastroenterology, 2001
The proportion of Helicobacter pylori-negative duodenal ulcer disease appears to be increasing. Data on clinical outcome and prognosis in this subgroup are lacking. Two hundred seventy-six duodenal ulcer patients randomized, irrespective of H. pylori status, to either eradication therapy or maintenance omeprazole (double-blind, double-dummy design) for 1 yr were studied. Patients were followed up for a total of 2 yr, with visits performed every 2 months the first year and every 6 months the following year. Endoscopies for assessment of ulcer relapse were done at 6 and 12 months or in the event of symptomatic relapse. H. pylori status was assessed by culture, immunohistochemistry, and urea breath test at entry, at 6, 12, and 24 months or at failure. The primary endpoint was discontinuation, irrespective of reason. Patients were considered H. pylori negative if all three tests were negative. Patients were considered H. pylori-positive if any of the three diagnostic tests were positive...
Przeglad Gastroenterologiczny, 2015
Introduction: Helicobacter pylori (H. pylori) occurs throughout the world and causes gastroduodenal diseases. There is data indicating a change in the prevalence of H. pylori infection worldwide. The prevalence of H. pylori is 80% in Turkey, while it is higher in many developing countries, and the rate of infection varies throughout the world. In many developing countries, the prevalence of infection exceeds 90% by adulthood. Aim: To determine the change in the rate of H. pylori infection in gastric ulcers and duodenal ulcers for a 10-year period in a single centre. Material and methods: The study population included 550 patients (342 in 2004, 208 in 1994) with gastric and duodenal ulcers. Results: In 2004 there were 125 (36.5%) patients with gastric ulcer and 217 patients with duodenal ulcer (64.5%). CLO test positivity was 39.2% in patients with gastric ulcers and 60% in patients with duodenal ulcers. In 1994 there were 208 patients (159 duodenal ulcers, 49 gastric ulcers). Urease test was positive in 74.2% of patients with duodenal ulcer and in 65.2% of patients with gastric ulcer. The decrease in the rate of urease positivity in patients with gastric ulcer was statistically significant (p = 0.01) during this 10-year period. Conclusions: In the present study we found that the urease positivity decreased significantly in patients with gastric ulcer between 1994 and 2004.
Possible absence of Helicobacter pylori in the early stages of duodenal ulceration
QJM, 2002
Background: Helicobacter pylori is thought to be a cause of duodenal ulceration, but there is some evidence that it is found less often in early than in later disease. Aim: To assess the presence of H. pylori in patients undergoing endoscopy for dyspepsia, with respect to their duration of symptoms. Design: Retrospective case note review. Methods: Patients were categorized as having a history greater or less than 6 months, and as H. pylori-positive or-negative, using biopsy rapid urease, culture and PCR tests. Results: Thirty-two duodenal ulcer patients with a history)6 months were all H. pylori-positive according to the PCR test; the five with a shorter history were H. pylori-negative. No patient H. pylori-negative by PCR was positive by the other tests. Discussion: H. pylori was (at least) less commonly present before 6 months. It is possible that H. pylori, although nearly always present after 6 months, is not present at the onset of the disease. Confirmation of this finding would imply that infection with the organism is not the cause of duodenal ulceration, but a factor producing recurrence and chronicity.
Gut, 1995
The factors that determine which Helicobacter pylorn infected subjects develop duodenal ulcer (DU) are unclear. This study tested the hypothesis that infection density and urease activity are higher in DU than non-DU subjects. Fifty five DU and 55 age and sex matched non-DU subjects were studied. Quantitative methods were used for measuring infection density (viable organism count) and urease activity (Berthelot reaction). DU subjects had a greater antral infection density (geometric mean of colony forming units/mg biopsy protein; 10.5X1O0 v 1.3X105, p<0.001). They also had higher biopsy urease activity (geometric mean of NH3 nmollmin-l/mg protein-l; 103 v 25, p<0.001). Urease activity per organism, however, was similar in the two groups showing that high antral urease activity in DU was a reflection of organism density. DU was not present in subjects with an antral infection density less than 105 colony forming units/mg protein. A correlation was present between H pylori viable counts and the severity and activity of gastritis. Both severity and activity of gastritis were greater in the antrum of DU compared with non-DU subjects but there was no difference in the body between the two groups. It is concluded that antral H pyloni infection density is probably an important determinant of DU development, and that there is a baseline of infection density that is necessary for ulcer formation.
Helicobacter pylori and Early Duodenal Ulcer Status Post-Treatment: a Review
Helicobacter, 2001
Background. Data submitted to the FDA were reviewed to analyze the relationship between Helicobacter pylori infection and the incidence of early duodenal ulcers, within 6 weeks, following treatment. Materials and Methods. Retrospective analyzes were performed on data from three H. pylori development programs submitted to the FDA: ranitidine-bismuth-citrate (RBC), lansoprazole (L) and omeprazole (O). Efficacy assessments for the RBC, L and O programs were made at end of a 4-week treatment period, 4-6 weeks following the end of a 14-day treatment period, and 4 weeks following the end of a 4-week treatment period, respectively. Results. Overall, there was a 15%, 21% and 23% decrease in the number of patients in the RBC, L and O programs, respectively, with ulcers among H. pylori cleared/eradicated patients post-treatment compared with patients with persistent infection. Among patients who did not have cleared/eradicated H. pylori in the RBC and O programs, where antisecretory agents were continued beyond the antimicrobial treatment period, the number of ulcers was lower in the antisecretory plus antimicrobial subgroups compared with the antimicrobial alone subgroups (37% vs. 46% for RBC and 33% vs. 42% for O). Among patients with cleared/eradicated H. pylori , the number of patients with ulcers in the antimicrobial alone subgroups and antisecretory plus antimicrobial subgroups were similar within each program. Antimicrobials alone had significantly lower rates of ulcers among patients with cleared/ eradicated H. pylori as compared with patients without clearance/eradication. Conclusions. The early incidence of duodenal ulcers is significantly decreased in patients with H. pylori clearance/eradication.
Digestion, 2003
Background: Although Helicobacter pylori is a significant etiologic factor of peptic ulcer disease, it remains unknown why ulcers develop only in the minority of infected individuals. Aim: The aim of this cross-sectional study was to evaluate the association between the presence of duodenal ulcer in H. pylori-infected patients and different risk factors. Methods: A total of 122 H. pyloriinfected patients were enrolled; 79 had duodenal ulcer and 43 gastritis. Univariate analysis was conducted using either Fisher's exact test or exact Cochrane-Armitage trend test. In multivariate analysis the logistic model was used. Results: Univariate analysis indicated six factors (male sex, smoking, antral H. pylori density, cagA presence in antrum, and vacA s1a presence in antrum and corpus). Four factors (sex, smoking-alcohol index, H. pylori density index, and cagA index) were found to be significant in multivariate analysis. The best model predicting duodenal ulcer included male sex, smoking, presence of H. pylori on histopathology in antrum and cagA presence in corpus. Conclusion: Although several risk factors were significantly associated with duodenal ulcer, we failed in the identification of either a single risk factor or a set of factors that can unequivocally differentiate patients with ulcer from those with gastritis.
Helicobacter pylori (H. pylori) has a role in the multifactorial etiology of peptic ulcer disease. A link between H. pylori infection and duodenal ulcer disease is now established. Other contributing factors and their interaction with the organism may initiate the ulcerative process. The fact that eradication of H. pylori infection leads to a long-term cure in the majority of duodenal ulcer patients and the fact that the prevalence of infection is higher in ulcer patients than in the normal population are cogent arguments in favor of it being the primary cause of the ulceration. Against this concept there are issues that need explanation such as the reason why only a minority of infected persons develop duodenal ulceration when infection with H. pylori is widespread. There is evidence that H. pylori infection has been prevalent for several centuries, yet duodenal ulceration became common at the beginning of the twentieth century. The prevalence of duodenal ulceration is not higher in countries with a high prevalence of H. pylori infection. This paper debate puts forth the point of view of two groups of workers in this field whether H. pylori infection is the primary cause of duodenal ulcer disease or a secondary factor.