Alessandra Areni

Reversibility of GERD ultrastructural alterations and relief of symptoms after omeprazole treatment.

BACKGROUND:Dilation of intercellular spaces (DIS) of human esophageal epithelium, evident at transmission electron microscopy (TEM), is an early marker of damage caused by gastroesophageal reflux, but its reversibility after therapy has not been investigated.AIM:To evaluate whether omeprazole can induce the healing of DIS.METHODS:Thirty-eight symptomatic patients, 22 with nonerosive reflux disease (NERD) and 16 with erosive esophagitis (EE), classified on the basis of 24-h pH monitoring, were enrolled. During upper gastrointestinal endoscopy, six biopsies from apparently normal mucosa were taken within the lower 5 cm of the esophagus for histological and TEM analysis. One hundred computer measurements were taken on TEM photomicrographs of the specimens in each patient. After 3 months of omeprazole 40 mg/die a further endoscopy with biopsies was performed. In patients with persistent heartburn and/or incomplete ultrastructural recovery of esophageal epithelium, a new endoscopy was performed after 3 more months of treatment.RESULTS:After 3 months of therapy, 35 patients (92.1%) showed a complete recovery of DIS and resolution of heartburn. Three patients required 3 more months of therapy because of an incomplete recovery of the epithelium correlated with sporadic heartburn. Healing of the mucosa was achieved in two patients, whereas one had an incomplete recovery of DIS with persistent heartburn.CONCLUSIONS:Three and six months of omeprazole therapy led to a complete recovery of DIS in 92.1% and 97.4% of cases, respectively. No significant differences of DIS between NERD and EE were noted. Complete recovery of DIS was accompanied by regression of heartburn in all cases.

Dilated intercellular spaces as a marker of oesophageal damage: comparative results in gastro-oesophageal reflux disease with or without bile reflux.

Background : The dilation of oesophageal intercellular spaces, clearly apparent in transmission electron microscopy images, is a marker of cellular damage induced by acid.

Mesalazine with or without cholestyramine in the treatment of microscopic colitis: Randomized controlled trial

Background:  Collagenous colitis (CC) and lymphocytic colitis (LC) are chronic inflammatory diseases of the colon with a benign and sometimes relapsing course. Frequency among patients with chronic diarrhea and normal looking colonoscopy is around 10–15%. To date, treatment of CC and LC is not well defined. Data about these conditions are mostly derived from retrospective studies. The aim of the present study was to evaluate the response to treatment and the clinical course of CC and LC in a large group of patients prospectively diagnosed.

Pantoprazole, azithromycin and tinidazole: short duration triple therapy for eradication of Helicobacter pylori infection

Azithromycin is an acid‐stable macrolide that achieves remarkably high concentrations in gastric tissue, persisting above the MIC90 for Helicobacter pylori over a period of 5‐days, after a single 500 mg oral dose.

Clinical course of microscopic colitis in a single-center cohort study.

BACKGROUND AND AIMS The long-term natural history of collagenous (CC) and lymphocytic colitis (LC) is not well known. The aims of this study were to evaluate the clinical course of microscopic colitis (MC) and to describe the morbidity evolution of the disease. MATERIAL AND METHODS This study is based on a cohort of 54 patients (35 LC/19 CC), previously included in a randomized trial treated with mesalazine with or without cholestyramine. Patients were followed-up closely during the subsequent 5 years, undergoing clinical, endoscopic and histologic evaluation at least yearly. After this period, they were encouraged to undergo periodical clinical evaluations. RESULTS In a mean follow-up time of 104.9 ± 14.1 months (range 81-138 months) at the end of the therapy, 12 patients (7 LC and 5 CC) relapsed. Of these patients, 4 reported a mild clinical relapse self-treated with antidiarrheal medication. In total 49 patients are clinically free from diarrhea, to date. At multivariate analysis the only predictive factor of relapse seems to be a slow response to treatment. CONCLUSIONS Only a minority of patients with MC had diarrhea more than once a week in a long-term follow-up and the symptom pattern was similar between CC and LC patients.

Familial adenomatous polyposis and inflammatory bowel disease associated in two kindreds.

SummaryWe describe two families in which some members are affected by familial polyposis syndrome: in one family a case of ulcerative colitis and in the other a case of Crohns disease were found. This is the first report about this family association, but in our opinion the fact that two cases have been found in one series suggests that this association could be more frequent than reported so far. The research for a genetic pattern of inflammatory bowel disease could be addressed towards chromosome 5.

CASE REPORT: Severe and Relapsing Upper Gastrointestinal Bleeding in a Patient with Glanzmann's Thrombasthenia

Glanzmann’s thrombasthenia (GT) is a rare familial thrombocytic disease inherited as autosomal recessive disorder that can induce hemorrhages. Rarely, these hemorrhages can be fatal. Glanzmann described it for the first time in 1918 (1). In 1974 Nurden and Caen (2) showed that the disease is due to a defect of platelet aggregation, resulting from the absence, or reduced concentration, of the membrane glycoproteic receptor binding the fibrinogen (integrin aIIbb3) (3‐ 5). The platelet numbers and morphology and tests of coagulation are normal, while the bleeding time is prolonged. Therefore, this disorder is to be suspected in all the patients with: purpura and/or hemorrhage, normal platelets count with absent macroscopic platelet aggregation, and prolonged bleeding time. The molecular aspects of the disease are now well known (6 ‐9), while its clinical features are not yet fully understood (10). We report a case of severe and relapsing upper digestive bleeding in a woman with GT and in which coexisting thrombocytopenia (from HCV-related liver cirrhosis) and H. pylori-positive duodenal ulcer.