The link between duodenal ulcer and Helicobacter pylori has revolutionised A causal association between H pylori and chronic gastritis was. The majority of patients with duodenal ulcer (DU) are infected withHelicobacter pylori(H. pylori). However, in multicenter trials,H. pyloriwas. Persons with H. pylori positivity had an odds ratio of (95% confidence interval (CI): , ) for gastric ulcer and (95% CI: , ) for duodenal ulcer.
A nested case-control study was done, based on a cohort of 5, Japanese-American men examined on the Hawaiian island of Oahu from to A total of men with gastric ulcer, 65 with duodenal ulcer, and 14 with both diseases were identified.
The authors matched the cases with population controls and tested their serum for immunoglobulin G antibodies to H. For CagA positivity, the odds ratios were 1. Subjects who were seropositive for both H. CI, confidence intervalIgG, immunoglobulin G Helicobacter pylori is commonly present in the human stomach, and investigations over the past 15 years have focused on its relation to disease 1 —3. The treatment of peptic ulcer disease patients with antimicrobial regimens can eliminate H.
A prospective study of Japanese-American men in Hawaii has shown that the presence of H. However, most persons carrying H.
Helicobacter pylori and peptic ulcer disease--a causal link.
One gene, cagA, was the first discovered gene on the island and is a marker for its presence 13 This different ascertainment of the significance of CagA positivity may reflect differences in the populations studied as well as the cross-sectional, rather than prospective, nature of the previous investigations.
In this report, we return to the prospective cohort of Japanese-American men we have previously examined to assess relations between H. By examining men who developed such disease and their matched controls in a nested case-control study with 21 years of follow-up, we are able to address that question.
Briefly, 8, Japanese-American men were examined on the Hawaiian island of Oahu from to Serum cholesterol values were determined by the Auto Analyzer NA method, and serum glucose values were determined by the Auto Analyzer N-2B method 1 hour after a g glucose load was given A total of 7, A total of patients with previous gastrectomy or a previous diagnosis of peptic ulcer disease were excluded, leaving 5, men in the study. During the year surveillance period from tomen were hospitalized and diagnosed with peptic ulcer disease.
Sufficient serum frozen from the examination of the men in — was available from of these patients. In total, there were men with gastric ulcer, 65 with duodenal ulcer, and 14 with both types of ulcer. Each of these patients was matched with one control from the study cohort on the basis of age at examination, date of serum collection, availability of sufficient amount of sera, and being alive at the time of hospitalization of the matched case, so that death was not a competing factor.
The presence of H. However, in our study, no such association was found. When the prevalence of H.
The number of Asian patients analyzed in our study was very small only two patientsprecluding any conclusion regarding H. A strong correlation between the presence of H.
In the present study, H. On the other hand, our data suggest that ingestion of NSAID is associated with gastritis and erosive gastritis development, as well is the smoking habit with gastritis. Interestingly, an inverse correlation was found between alcohol beverages ingestion and gastritis development. This effect was only seen in men but this could be because a higher proportion of men ingested this type of beverage.
As discussed before, we did not find a correlation between ingestion of beverages and H. However, we can not rule out an antagonist effect of alcohol ingestion on H. This antagonistic action could reduce the number of bacterial cells colonizing this organ reducing the inflammatory process. The present study indicates a strong correlation between H. The ingestion of alcohol beverages increased the risk for peptic ulcer in men as indicated by the logistic regression analysis.
We speculated that this effect is a consequence of the liberation of more acid secretions by the parietal cells, stimulated by alcohol ingestion , worsening the tissue damage caused by H. Thus, although alcohol beverages ingestion has a beneficial action on gastritis, an inverted effect is seen since more severe tissue damages leading to peptic ulcerations could develop.
Therefore, we did not find a protective effect of alcohol ingestion on PUD development. Published data is contradictory regarding the association between H. Several authors  have shown that the H. However, other studies [33,34] demonstrated that the eradication of H. In the present work, a greater proportion of patients with gastroesophageal reflux was observed within the group that was not colonized by H. Thus, our study supports that H. In certain circumstances, chronic inflammation induced by H.
People with intestinal metaplasia in their stomach exhibit a significant increase in the risk of developing gastric cancer [reviewed by 35]. The presence of intestinal metaplasic cells is described in the literature as being strongly associated with colonization by H.
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Helicobacter pylori and peptic ulcer disease--a causal link.
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