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- W2035373670 abstract "At a recent national conference the speaker-a pathologist-suggested that the intense inflammation and extensive gastric mucosal damage seen in biopsy specimens from patients with Helicobacter pylori are sufficient reasons for treating the infection, even if the patient is asymptomatic. So, you recommend that we treat biopsies, not patients, sneered a member of the expert panel, and a roar of laughter rose from the audience. While the expert's remark made an amusing sound bite, the distracted clinicians seemed to forget for a moment that a histopathological diagnosis is often the sole basis for the decision to perform major surgery, to embark on long treatment courses, or to place a patient in a surveillance program. Adenocarcinoma in a colonic biopsy specimen will prompt a colectomy; active inflammation in the absence of cirrhosis will make a patient with hepatitis C eligible for interferon treatment; and a focus of dysplasia in Barrett's mucosa will require the patient to face a lifetime of innumerable endoscopic procedures. We do not treat biopsies, we manage patients based on a constellation of findings. In some cases, the histopathological finding is the one that determines the treatment course. Tursi and Gasbarrini, in a thoughtful review in this issue of the Journal, call our attention on a relatively new and still unresolved issue: what to do when prominent lymphoid follicles are detected in a gastric biopsy.1 One aspect of this question has an easy answer: if H. pylori is present, treat the infection and the lymphoid follicles. Whether the infiltration is typical or atypical, it will go away.2-4 This approach seems to be effective even when a lymphoma has already developed. Eradication of H. pylori results in the regression and possible cure of approximately 70% of low-grade B cell primary gastric lymphomas.5,6 However, a small portion of gastric mucosa associated lymphoid tissue (MALT) lymphomas (between 10% and 37%) appear to be surrounded by virtually normal gastric mucosa with no evidence of H. pylori gastritis.7-9 One must presume that these lymphomas have originated from lymphoid follicles induced by stimuli other that chronic H. pylori infection. Although H. pylori is by far the most common promoter of gastric MALT, the presence of lymphoid follicles has been documented in the gastric mucosa of H. pylori-negative patients with celiac disease and with certain autoimmune diseases, such as Sjögren's syndrome and Hashimoto's thyroiditis.10-13 Whereas gastric MALT in H. pylori gastritis can be interpreted intuitively as a local response to a chronic antigenic stimulus, the acquisition of gastric MALT during the course of celiac disease and other systemic autoimmune disorders is less obvious. Even less obvious is the therapeutic approach that should be taken in these circumstances. As a result of a study performed several years ago, we offered a set of practical suggestions to pathologists who encounter lymphoid aggregates in a gastric biopsy specimen.14 Here, we re-propose those suggestions, slightly modified in light of the new information emerged in the last five years: A) if the aggregate is small, there is no germinal center. If the remainder of the mucosa is normal, it should be interpreted as one of the aggregates of lymphocytes found in the normal gastric mucosa; B) if the aggregate is large, without germinal center, and lymphoepithelial lesions are present, the possibility of lymphoma should be considered and Isaacson's criteria should be applied15; C) if a germinal center is present and the remainder of the mucosa shows chronic active gastritis, a thorough search for H. pylori is warranted. If no organisms are detected, use one of the special stains in the slides stained with hematoxylin and eosin; D) if a germinal center is present and the surrounding mucosa appears normal, a thorough search for H. pylori is still warranted, because both chronic and active inflammation may be patchy in some patients, and the gastric body may look deceptively normal even with heavy H. pylori infection. Failure to detect H. pylori in such a situation would suggest recently (less than 1 year) treated infection or one of the less common conditions in which lymphoid follicles have been described, such as autoimmune gastritis, celiac disease, or one of the systemic autoimmune diseases. As for the therapeutic strategy, eradicating H. pylori from infected patients will almost certainly result in the eventual disappearance of lymphoid follicles. When patients are referred with evidence of gastric MALT without demonstrable H. pylori infection, it would be advisable to rule out other gastric or extra-gastric diseases known to be associated with gastric MALT development. Robert M. Genta, M.D. Francesco Franceschi, M.D." @default.
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- W2035373670 date "1999-09-01" @default.
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- W2035373670 title "Treating Biopsies to Cure Patients" @default.
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- W2035373670 doi "https://doi.org/10.1097/00004836-199909000-00003" @default.
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