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Background: Helicobacter pylori induces histologic inflammation of mucosa variably correlated to different macroscopic features. Recent studies highlight that the presence of Helicobacter pylori could be assessed on the basis of the macroscopic pattern only, in particular nodularity. The present prospective study has correlated this and other endoscopic features, defined by Sydney classification of gastritis, both to Helicobacter pylori presence and histological patterns. Results: Out of 532 patients, 364 were evaluable. The prevalence of Helicobacter pylori was 51.1% with a different distribution between the endoscopic features. Nodularity showed the highest positive predictive value in detecting the Helicobacter pylori presence (69.9%). The histological findings were: normal 26.9%, non atrophic gastritis 55.2%, atrophic gastritis 17.9%. There was a significant difference between abnormal endoscopic features in detecting the histologic gastritis, with endoscopic atrophy and nodularity showing the highest positive predictive value which reaches 96.7% and 91.8%, respectively. Helicobacter pylori infection and histologic gastritis were also present in 30.9% and 41.8%, respectively, of endoscopically normal subjects. Multivariate analysis has strictly correlated age with all abnormal endoscopic features, metaplasia with endoscopic atrophy, and chronic inflammation (gastritis) with nodularity. Conclusions: The single endoscopic features are poorly correlated with histologic changes and Helicobacter pylori status. Biopsies are mandatory in all cases. The causes of the different macroscopic findings are not yet fully understood.

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. Methods and Results: A total of 819 patients underwent a colonoscopy because of chronic watery diarrhea and among them we found 41 patients with LC and 23 with CC. These patients were later randomized and assigned to treatment with mesalazine or mesalazine + cholestyramine for 6 months. Fifty-four patients (84.37%) had resolved diarrhea in less than 2 weeks. After 6 months a colonoscopy with biopsies was repeated. Clinical and histological remission was achieved in 85.36% of patients with LC and in 91.3% with CC, with a better result in patients with CC treated with mesalazine + cholestyramine. During a mean period of 44.9 months, 13% of patients relapsed; four with LC and three with CC. They were retreated for another 6 months. At the end of this period one patient with CC was still symptomatic and persistence of CC was confirmed at histology. Conclusions: Treatment with mesalazine seems to be an effective therapeutic option for LC to date, while mesalazine + cholestyramine seems to be more useful in the treatment of CC.

To value whether omeprazole could induce the healing of DIS and regression of symptoms in patients with DGER.We enrolled 15 symptomatic patients with a pathological esophageal 24-h pH-metry and bilimetry. Patients underwent endoscopy and biopsies were taken from the distal esophagus. Specimens were analyzed at histology and transmission electron microscopy (TEM). Patients were treated with omeprazole 40 mg/d for 3 mo and then endoscopy with biopsies was repeated. Patients with persistent heartburn and/or with an incomplete recovery of DIS were treated for 3 more months and endoscopy with biopsies was performed.Nine patients had a non-erosive reflux disease at endoscopy (NERD) while 6 had erosive esophagitis (ERD). At histology, of the 6 patients with erosive esophagitis, 5 had mild esophagitis and 1 moderate esophagitis. No patients with NERD showed histological signs of esophagitis. After 3 mo of therapy, 13/15 patients (86.7%, P0.01) showed a complete recovery of DIS and disappearance of heartburn. Of the 2 patients treated for 3 more months, complete recovery of DIS and heartburn were achieved in one.Three or 6 mo of omeprazole therapy led to a complete regression of the ultrastructural esophageal damage in 86.7% and in 93% of patients with DGER, NERD and ERD respectively. The ultrastructural recovery of the epithelium was accompanied by regression of heartburn in all cases.

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.

Gastro-oesophageal reflux is an almost universal daily occurrence, but only a small percentage of the population develops gastro-oesophageal reflux disease (GORD) and, among them, a small number develop erosive oesophagitis (ERD) or one of its complications. It is well accepted that the pathophysiology of GORD is related to failure of antireflux mechanisms but several phenomena are not fully explained on the basis of this sequence. There is no apparent relation between damage and the amount and quality of refluxate. It is not known why the same amount of refluxate determines GORD in one patient and not in another.2 It is also unclear whether there is a relation between these unexplained questions and the possible influence of proliferative responses of epithelial proliferating cells to damage. Hence we evaluated cell proliferation of the oesophageal epithelium using Ki67 immunostaining in normal subjects and in patients with GORD, with or without erosions. Thirty five subjects were enrolled: nine were healthy voluntary controls with normal pH testing and normal endoscopic, histological, and ultrastructural patterns. Twenty six patients were affected by GORD, defined as frequent heartburn for at least a year, and abnormal 24 hour pH, histological, and ultrastructural parameters. Of these 26 patients, 13 had a normal appearing oesophageal mucosa at endoscopy (NERD) while 13 had ERD. All subjects underwent gastroscopy; six biopsies were obtained within the lower 5 cm of the oesophagus from areas of macroscopically intact oesophageal mucosa. The presence of oesophagitis was graded according to the Los Angeles classification. pH parameters were not statistically different between NERD and ERD. At transmission electron microscopy (TEM), all patients with GORD, with or without erosions, showed ultrastructural signs of damage, defined by the presence of dilation of intercellular spaces (>0.74 µm). No significant differences were observed between the two groups. For assessment of the proliferative activity of epithelial cells, we used the immunohistochemical approach based on the Ki67 marker of cell proliferation which provides an accurate estimate of the cell growth fraction. Ki67-labelling index (LI) ranged from 8.9% to 74.4% among all patients (mean (SD) 33.5 (19.7)%; median 27.8%). Mean Ki67-LI values for the three groups of patients (normal, NERD, and ERD) were 62.2%, 29.8%, and 17.2%, respectively, and the difference among the groups was significant (p

Background: The dilation of oesophageal intercellular spaces, clearly apparent in transmission electron microscopy images, is a marker of cellular damage induced by acid. Aim: To analyse the presence of dilated intercellular spaces and to quantify the scores in controls and in patients with gastro-oesophageal reflux disease or duodenal gastro-oesophageal reflux accompanied by erosive or non-erosive reflux disease. Methods: Thirty-eight symptomatic patients with gastro-oesophageal reflux disease or duodenal gastro-oesophageal reflux and 12 asymptomatic controls, classified on the basis of pH-metry and bilimetry, underwent endoscopy. Six tissue biopsies were taken from the normal mucosa for light microscopy and transmission electron microscopy evaluation. Dilated intercellular spaces were measured on photomicrographs of the specimens (at least 100 transects were measured for each patient). Results: Twenty-two patients with gastro-oesophageal reflux disease had normal macroscopic mucosa but, at histology, five patients with erosive gastro-oesophageal reflux disease had mild oesophagitis and one had moderate oesophagitis. Seven patients with duodenal gastro-oesophageal reflux had normal mucosa, whilst three with erosive duodenal gastro-oesophageal reflux had mild oesophagitis at histology. At transmission electron microscopy, all controls had dilated intercellular spaces of less than 1.69 μm. Each symptomatic patient had a mean dilated intercellular space value and a mean value of the maximum dilated intercellular space at least three or more times greater than that in controls (P < 0.001). No statistical differences were observed between erosive and non-erosive oesophagitis. Conclusions: The dilated intercellular space is an extremely sensitive marker of damage in gastro-oesophageal reflux disease, duodenal gastro-oesophageal reflux and non-erosive reflux disease, and serves as the most appropriate marker of damage evaluation in non-erosive reflux disease reported to date. A mean dilated intercellular space of 0.74 μm provides a cut-off score for damage. No quantitative or qualitative differences in dilated intercellular space scores were found between pure and mixed acid reflux.

Carlo Calabrese, MD, PhD, Anna Fabbri, MD, Marco Benni, MD, Alessandra Areni, MD, Carlo Scialpi, MD, Mario Miglioli, MD, Giulio Di Febo, MD Lichen planus (LP) is a chronic disease of skin and other squamous epithelium of unknown etiology. The estimated prevalence ranges from 0.02% to 2%. 1"3 An association has been suggested with acute alopecia and chronic hepatitis, especially hepatitus C virus-induced, and autoimmune disorders. 4-6 Although LP of the skin affects both genders with equal frequency and can appear at any age, mucosal LP is mainly a disease of middle-aged women.7, 8 It can involve the oral cavity, pharynx, esophagus, geni- talia, and anus. 3 Coexistent skin lesions are present in approximately 30% to 50% of patients.9,10 Skin lesions are tiny, flat-topped, violaceus papulae, ofter~ with a network of delicate white lines on the surface. Mucosal IJP has a different pattern: it is more com- monly found within the oral cavity and it appears in at least 6 forms that can occur separately or simulta- neously: reticular, papular, plaque-like, atrophic, ero- sive, and bullous. 11 Esophageal involvement in LP is rare, but its prevalence is probably underestimated. 12 Only 35 cases have been reported in French and English language publications to date. 1-3,7,8-10,12-33 At endoscopy, the most common features include peeling mucosae and plaque-like lesions and/or benign stric- tures in the proximal and middle thirds of the esoph- agus. It can involve the entire length of the esopha- gus, but the gastroesophageal junction is always spared. Histopathol0gic features are nonspecific and resemble those of chronic mucosal inflammation. In particular, the band-like infiltrate with a predomi- nance of mature T-cells and basal layer degeneration, including characteristic Civatte bodies, typical of skin involvement may not be present.7,19, 22 Mucosal LP has a recognized risk of malignant transformation to squamous cell carcinoma (SCC) of approximately 0.5% to 1%. 34-36 However, no case of malignant evolu- tion of esophageal LP has been described to date. CASE REPORT A 49-year-old white woman was referred to our endo- scopic unit because of recurrent epigastric pain, regurgita

Glanzmann's thrombasthenia (GT) is a rare familial thrombocytic disease inherited as an autosomal recessive disorder that can induce hemorrhages due to a defect of platelet aggregation, resulting from the absence or reduced concentration of the membrane glycoproteic receptor binding the fibrinogen (integrin α(IIb)β3). The gastrointestinal tract is the site of bleeding in only about 10% of cases but the related mortality is high (12.8%) (Table 2). Among the deaths due to hemorrhage, digestive bleeding causes 57.1%. According to reported data, the source of bleeding may be from preexisting gastroduodenal chronic and acute lesions. We report a case of severe and relapsing upper digestive bleeding in a woman with GT and coexisting thrombocytopenia (from HCV-related liver cirrhosis) and H. pylori-positive duodenal ulcer.