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• W2047552597 abstract "“Helicobacter pylori is rarely found in gastric biopsy specimens from individuals with atrophic gastritis of the body mucosa” wrote Karnes et al in a 1991 article showing that no bacteria could be demonstrated in the gastric biopsies from two thirds of H. pylori-seropositive Finnish subjects with atrophic gastritis.1 Despite a lonely, largely speculative and mostly wrong 1993 statement (which, I am afraid, I wrote) suggesting that what really keeps H. pylori away is intestinal metaplasia (IM), not the mere reduction of gastric glands,2 the conventional wisdom has remained unchanged and unchallenged: H. pylori is difficult to find in an atrophic stomach. Why then would an editor devote valuable pages of a medical journal to a report that confirms what we have held true for 15 years? Yet, this is the message of the article by Yoo and his colleagues3 from the Seoul National University published in this issue of the Journal: in H. pylori-seropositive Korean subjects the detection of H. pylori by the CLO test or histopathologic examination becomes progressively more difficult as the grades of atrophy and IM increase. If this message is hardly revolutionary, its relevance is greater today than ever before. In part, this has to do with the expanded indications for eradication: 10 years ago treatment was recommended only for patients with peptic ulcer disease or mucosa-associated lymphoid tissue lymphoma. Irrefutable evidence has linked H. pylori infection to gastric adenocarcinoma; its eradication has been shown not only to resolve gastritis, but also, at least in some patients, to lead to a restitution of normal mucosal architecture with regression of atrophic gastritis. Thus, there is a widening consensus that H. pylori should be treated in most, if not all, infected adults.4–6 However, it remains unclear what categories of patients benefit the most from H. pylori eradication. The risk for gastric cancer is highest in patients with chronic atrophic metaplastic gastritis, a progressive condition caused by H. pylori infection. Therefore, one would assume that in these patients treatment could arrest the progression of the atrophic-metaplastic process, perhaps promote its regression, and ultimately reduce the risk for cancer. Yoo and his colleagues fully subscribe to this viewpoint when they state that “in atrophic gastritis, the detection of current H. pylori infection is becoming more important clinically, especially in young patients, because the eradication of the infection is likely to affect the natural course of the disease and modify the risk of gastric adenocarcinoma.” Although several recent controlled intervention trials for the prevention of gastric cancer by H. pylori eradication have yielded disappointing results and showed that cancer eradication may still appear in relatively high frequency after successful treatment of H. pylori,7–9 there is increasing evidence that H. pylori eradication may, to a certain extent, lead to the regression of atrophy and perhaps of IM, 2 lesions were typically considered as premalignant. Thus, one could reasonably expect that the widespread eradication of H. pylori will eventually result in a significant overall decrease in the incidence of atrophic gastritis with a concomitant decrease in the incidence of gastric cancer. What trials involving a few hundreds of subjects over periods of a few years cannot show will become evident as the infection is eliminated from millions of people and the observation period will be decades. The European Helicobacter Maastricht Study Group was driven in part by these considerations when, at its 2005 meeting10 “strongly recommended to treat H. pylori in subjects with atrophic gastritis, postgastric cancer resection, and those who are first-degree relatives of gastric cancer patients.” To treat H. pylori we need to find it. Yoo et al,3 as Karnes et al1 did before them have confirmed a reality well known to pathologists: H. pylori is very difficult, even impossible, to find precisely in those patients who may benefit the most from its eradication. Thus, from a practical viewpoint, what should a clinician do when the diagnosis from a gastric biopsy is “chronic atrophic metaplastic gastritis, no H. pylori organisms detected?” Clearly, it would be a mistake to tell the patient that no further treatment is needed because the infection that caused the atrophy is now gone. Helicobacters are not necessarily gone, but why are we unable to find them? Yoo et al3 have also shown that the CLO test was just as inaccurate as the histopathologic observation of Giemsa-stained gastric biopsies. This important piece of information (certain to be greeted with relief by pathologists frustrated by their inability to detect H. pylori—you see, it was not my fault!) indicates that these occult infections are sustained by such small numbers of organisms that not only escape visual detection, but also fail to produce enough urease to turn the CLO test pink. We do have some explanations for this phenomenon. First, biopsies from atrophic stomachs often consist mostly of metaplastic epithelium, where H. pylori do not usually dwell.11 Second, patients with atrophic gastritis may have dyspepsia, and even if the cause is not hyperacidity they may be receiving proton-pump inhibitors as an empirical treatment. Proton-pump inhibitors dramatically decrease the sensitivity of all direct detection methods for H. pylori.12–14 Finally, antibiotics liberally prescribed everywhere and in many countries readily available over the counter, can temporarily suppress H. pylori populations and make the infections undetectable. Some authors believe that in rapid urease test-negative patients (like the CLO-test negative subjects with atrophic gastritis described in the paper by Yoo et al) a positive serology could substitute for histology, and, implicitly, such patients should be treated.15 One would suspect that a better way to detect the infection would be the use of fecal antigen detection tests (HpSA). However, the only study that has specifically evaluated their use in a small group of patients with documented atrophic gastritis concluded that neither the urea breath test nor the HpSA add useful information regarding active H. pylori infection.16 Others advocate the use of several simultaneous serologic tests that can provide information about pepsinogens ratio, gastrin levels, and antibodies against H. pylori and its pathogenic factors (eg, Cag A).6,17 Although these combined tests yield interesting information, some clinicians remain reluctant to give an eradication course to a patient with “serologic atrophy” and circulating antibodies against H. pylori." @default.
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• W2047552597 title "Where have all the Helicobacters gone?" @default.
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