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Treatment of Helicobacter pylori Infection

CLINICOPATHOLOGICAL APPROACH TO GASTRITIS | Biopsy Protocol | TOOLS TO DIAGNOSE AND CLASSIFY GASTRIC CONDITIONS | Clinical Manifestations | Disease-Specific” Virulence Factors | Invasive Tests | Clinical Manifestations | Endoscopic Appearance | Macroscopic and Endoscopic Appearance | Clinical Manifestations and Pathogenesis |


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At present, the only universally agreed on indications for treatment are H.pylori–related duodenal and gastric ulcers and low-grade, primary B-cell MALT lymphoma. H.pylori should be eradicated in patients with documented ulcer disease, whether or not the ulcers are currently active, to reduce the likelihood of relapse. Most clinical trials do not provide convincing data in support of the benefits of eradication of infection in patients with nonulcer dyspepsia, and there are no controlled studies showing that eradicating H.pylori from a population will reduce the incidence of gastric cancer. For various logistical and ethical reasons, it is unlikely that such trials will be ever carried out to the satisfaction of those who demand unequivocal evidence. The most pressing question then is whether we should hold back and wait for more data or act now based on current information. Today, there is ample epidemiologic and biologic evidence that whereas H.pylori gastritis may not be the only cause of the development of atrophy and intestinal metaplasia, it almost always provides the necessary background on which these lesions arise. By treating H.pylori gastritis, we can prevent the development of atrophy and metaplasia, and most likely we would also arrest the progress of these lesions in infected persons who have already developed them. As a result, we should be able to prevent millions of gastric cancers. The incidence of non–NSAID-induced peptic ulcers would also be greatly reduced, and primary gastric lymphomas would all but disappear. Thus, we ought to put aside the teleological questions on the ultimate significance of our immemorial amphibiotic relationship with H.pylori and its intriguing evolutionary and metaphysical implications and proceed to cure infected patients.

In vitro, H.pylori is susceptible to a wide range of antibiotics, but monotherapy has been disappointing in vivo, probably because of inadequate antibiotic delivery to the sites of colonization. Thus, several multidrug regimens have been developed, the most successful of which are triple and quadruple combinations that achieve H.pylori eradication rates of more than 90% in many trials and more than 75% in clinical practice. The most commonly used 7- and 14-day drug regimens consisting of a proton pump inhibitor and two or three antimicrobial agents. The major determinants of therapeutic failures are inadequate patient compliance and drug resistance, particularly to metronidazole and clarithromycin.

There are no established guidelines for posttreatment testing. When eradication therapy is given for gastric ulceration or MALT lymphoma, there is an opportunity to retest for H.pylori at repeat endoscopy, which is performed to evaluate healing or regression. For duodenal ulceration, a urea breath test, a stool antigen test, or an endoscopy with gastric biopsy should be performed 4 to 6 weeks after treatment. When therapy is administered to treat asymptomatic infections, posttreatment testing is generally not deemed necessary.


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Noninvasive Tests| Evolution and Associations of Helicobacter pylori Gastritis

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