Cure of H. pylori infection is associated with reversal of iron dependence and recovery from iron deficiency anemia.

A screening for celiac disease should be carried out in adult patients with iron deficiency anemia. Recovery from anemia occurs between 6 and 12 months on a gluten-free diet alone as a consequence of normalization of histological alterations of the intestinal mucosa.

The aim of the present study was to evaluate the correspondence of the classification of non‐antral endocrine cell growths proposed by Solcia and co‐workers with clinical features and non‐endocrine mucosal changes. For this purpose, 94 cases of newly diagnosed atrophic body gastritis were investigated using endoscopic biopsies and compared with 18 control subjects. The patients were subdivided into the following four groups according to the most severe pattern of endocrine cell proliferation found in the body mucosa, as shown by chromogranin A immunostaining: group 1, normal pattern (7 cases, 7·5 per cent); group 2, simple hyperplasia (6 cases, 6·5 per cent); group 3, linear hyperplasia (24 cases, 25·8 per cent); group 4; micronodular hyperplasia (56 cases, 60·2 per cent). Adenomatoid hyperplasia was found in only one case, thus precluding further analysis. Patients in groups 1 and 2 had lower acid secretion, higher gastrin level, and higher mean scores in all histopathological variables of chronic gastritis considered by the Sydney system when compared with controls, but did not differ among them in any parameter investigated. When compared with groups 1 and 2, patients of groups 3 and 4 showed higher values of circulating gastrin, higher scores of glandular atrophy, and lower values of acid secretion and of mononuclear and neutrophil inflammatory cell infiltration. Moreover, group 4 patients differed significantly from those of group 3 in their higher gastrin levels and atrophy scores, and lower scores of neutrophil cell infiltration. On the basis of these results, it is proposed that for practical purposes the normal and the simple hyperplasia patterns may be incorporated into a single group. It is concluded that this classification in its simplified form, based on a qualitative histological approach, shows clinical relevance without the need to perform expensive, time‐consuming morphometric evaluations. © 1997 John Wiley & Sons, Ltd.

Severe gastrointestinal hemorrhage is an uncommon complication of Crohn's disease. Most bleeding episodes originate from colonic ulcers or ulcerated areas. The management of severe gastrointestinal bleeding in Crohn's disease is a therapeutic challenge. Several approaches including surgical resection, specific medical therapy of Crohn's disease, endoscopic treatment, or angiographic intervention have been attempted, but recurrence of bleeding is high. Monoclonal anti TNFalpha antibodies (infliximab) can induce relatively rapid mucosal healing. We report two cases of severe recurrent Crohn's disease presenting with massive lower gastrointestinal bleeding in which infliximab induced rapid mucosal healing and prevented recurrent bleeding.

Aneurysms and dissections affecting thoracic aorta are associated with smooth muscle cell (SMC) dysfunction. NO/cGMP signaling pathway in smooth muscle cells has been shown to be affected in sporadic thoracic aortic aneurysms. We analyzed the mRNA levels of PDE5, a cGMP-hydrolyzing enzyme highly expressed in aortic SMCs, that regulates arterious vascular tone by lowering cGMP levels. We found that aortic tissue obtained from Marfan, tricuspid and bicuspid thoracic aneurysms expressed lower levels of PDE5 mRNA compared to control aortas. In particular, we found that affected aortas showed lower levels of all the PDE5A isoforms, compared to control aortas. Transfection of vascular SMCs (VSMCs) with NOTCH3 activated domain (NICD3) induced the expression of PDE5A1 and A3 protein isoforms, but not that of the corresponding mRNAs. VSMC stimulation with GSNO, a nitric oxide analogue or with 8-br-cGMP, but not with 8-br-cAMP, up-regulated PDE5 and NOTCH-3 protein levels, indicating a negative feedback loop to protect the arterial wall from excessive relaxation. Finally, we found that PDE5 is expressed early during human aorta development, suggesting that if loss of function mutations of PDE5 occur, they might potentially affect aortic wall development.