The aim of the study was to ascertain the existence of intestinal metaplasia in gastric mucosa of patients with gastric carcinoma coupled with H. pylori positive chronic atrophic gastritis and possible connection of IM with the development of gastric carcinoma. The paper presents prospective study that included 50 patients with gastric carcinoma and 50 patients with chronic atrophic H. pylori positive gastritis. All the patients were subjected to gastroscopy as well as biopsy targeted at antrum, lesser curvature and corpus and at the area 1-2 cm removed from tumor lesion. Biopsy samples were sliced by microtome and stained. We analyzed presence, frequency and severity of inflammatory-regenerative, metaplastic and dysplastic changes in the mucosa and evaluated their prognostic value. We typed IM immunohistochemically. This study confirmed responsibility of H. pylori for inflammatory events in gastric mucosa in patients with gastric carcinoma. According to our findings incomplete IM of types IIa and IIb as precancerous lesion is responsible for the development of gastric carcinoma and is associated with chronic atrophic gastritis grade I and II (92% of subjects, p=0.0097, h=1, p=0.01). Thus, the finding of incomplete intestinal metaplasia may be used as an indicator for early gastric carcinoma detection. Patients with patho-histologically verified incomplete intestinal metaplasia associated with active chronic atrophic gastritis of levels I and II represent risk group for the development of gastric carcinoma of intestinal type.

The aim of the study was to ascertain presence of Helicobacter pylori in gastric carcinoma as a responsible promoter of inflammatory-regenerative changes, which lead to pathological differentiation and transformation of normal epithelial cells into intestinal type and, in progression, cause epithelial dysplasia that develops into early gastric carcinoma. The paper presents prospective study that includes clinical, pathohistological and microbiological aspects of carcinogenesis initiation in gastric mucosa. The subjects are patients treated at Gastroenterohepatology Clinic divided into two groups. One group included 50 patients with gastric carcinoma while the control group included 50 patients with chronic atrophic H. pylori positive gastritis. All the patients were subjected to endoscopy as well as biopsy targeted at antrum, lesser curvature and corpus and at the region 1-2 cm removed from tumor lesion. We used HUT test to verify H. pylori presence in biopsy samples. We analyzed the samples for presence, frequency and severity of inflammatory-regenerative, metaplastic and dysplastic changes in gastric mucosa and evaluated their meaning for the prognosis. Our study confirmed Helicobaster pylori responsibility for inflammatory events in gastric mucosa in patients with gastric carcinoma. Slight and mild epithelial dysplasia with chronic atrophic gastritis grade I and II coupled with intestinal metaplasia may be considered an indicator for early detection of carcinoma. Such patients represent risk group for gastric carcinoma development.

The aim of the study was to ascertain presence of Helicobacter pylori in gastric carcinoma as a responsible promoter of inflammatory-regenerative changes, which lead to pathological differen- tiation and transformation of normal epithelial cells into intestinal type and, in progression, cause epithelial dysplasia that develops into early gastric carcinoma. The paper presents prospective study that includes clinical, pathohistological and microbiological aspects of carcinogenesis initiation in gastric mucosa. The subjects are patients treated at Gastroenterohepatology Clinic divided into two groups. One group included  patients with gastric carcinoma while the control group included  patients with chronic atrophic H. pylori positive gastritis. All the patients were subjected to en- doscopy as well as biopsy targeted at antrum, lesser curvature and corpus and at the region - cm removed from tumor lesion. We used HUT test to verify H. pylori presence in biopsy samples. We analyzed the samples for presence, frequency and severity of inflammatory-regenerative, metaplas- tic and dysplastic changes in gastric mucosa and evaluated their meaning for the prognosis. Our study confirmed Helicobaster pylori responsibility for inflammatory events in gastric mucosa in patients with gastric carcinoma. Slight and mild epithelial dysplasia with chronic atrophic gastritis grade I and II coupled with intestinal metaplasia may be considered an indicator for early detection of carcinoma. Such patients represent risk group for gastric carcinoma development.

Th e aim of the study was to ascertain the existence of intestinal metaplasia in gastric mucosa of patients with gastric carcinoma coupled with H. pylori positive chronic atrophic gastritis and possible connection of IM with the development of gastric carcinoma. Th e paper pres- ents prospective study that included  patients with gastric carcinoma and  patients with chronic atrophic H. pylori positive gastritis. All the patients were subjected to gastroscopy as well as biopsy targeted at antrum, lesser curvature and corpus and at the area - cm removed from tumor lesion. Biopsy samples were sliced by microtome and stained. We analyzed pres- ence, frequency and severity of infl ammatory-regenerative, metaplastic and dysplastic chang- es in the mucosa and evaluated their prognostic value. We typed IM immunohistochemically. Th is study confi rmed responsibility of H. pylori for infl ammatory events in gastric mucosa in patients with gastric carcinoma. According to our fi ndings incomplete IM of types IIa and IIb as precancerous lesion is responsible for the development of gastric carcinoma and is as- sociated with chronic atrophic gastritis grade I and II ( of subjects, p=,, h=, p=,). Th us, the fi nding of incomplete intestinal metaplasia may be used as an indicator for early gastric carcinoma detection. Patients with patho-histologicaly verifi ed incomplete intestinal metaplasia associated with active chronic atrophic gastritis of levels I and II represent risk group for the development of gastric carcinoma of intestinal type.

The aim of this paper is to establish by immunohistochemistry the expression of keratin 7 in inflammatory-regenerative flat bowel mucosa and in different grades of epithelial dysplasia regarding the sub-units expressed in normal and carcinomatous colonic mucosa. Biopsy specimens from 270 patients were examined: 74 were classified as inflammatory-regenerative changes and 196 as dysplastic lesions. There were 108 cases of mild dysplasia, 58 cases of moderate and 30 cases of severe dysplasia, respectively). Demonstration of location and intensity of cytokeratin 7 staining was performed by immunohistochemistry using monoclonal antibody (anti-cytokeratin 7). Findings of cytokeratin 7 in dysplastic lesions were compared with those in normal mucosa, inflammatory -regenerative mucosa and adenocarcinoma. Cytokeratin 7 is not found in normal colonic mucosa. In inflammatory-regenerative mucosa it was found in solitary cells in small number of cases. It is found in all cases of epithelial dysplasia and its expression showed no difference regarding moderate and severe dysplasia. In few cases of adenocarcinoma, cytokeratin 7 is found in traces and showed minimal staining intensity. Having in mind that cytokeratine 7 is primarily found in dysplastic lesions of the flat colonic mucosa it can be a valuable diagnostic tool in the histological interpretation of epithelial dysplasia.

UNLABELLED The aim of this research is to establish by immunohistochemistry if there is a change in the expression of collagen type IV, as a substitute of basement membrane, in development of epithelial dysplasia in chronically inflamed colon mucosa. METHODS Biopsy specimens from 270 patients were examined: 74 were classified as inflammatory-regenerative and 196 as dysplastic lesions. There were 108 cases of mild dysplasia, 58 cases of moderate and 30 cases severe dysplasia, respectively. Visualisation of collagen IV and its way of expression within basement membrane of glandular crypts was performed by immunohistochemistry and then compared with findings in normal colon mucosa and colon adenocarcinoma tissue. RESULTS Changes in the expression of collagen IV comprised of its focal irregularities, diffuse thinning and/or thickening, focal interruptions or its complete absence. Significant changes in the expression of collagen IV in relation to normal mucosa already occur in inflammatory-regenerative mucosa. In mild dysplasia, these changes are more intensive in relation to those in inflammatory altered mucosa as well as at severe dysplasia in relation to moderate dysplasia. Changes in the expression of collagen IV in severe dysplasia are significantly more serious than in moderate dysplasia but are identical to those in colon adenocarcinoma tissue. CONCLUSION These findings suggest that change in the expression of collagen IV is in correlation to a degree of epithelial dysplasia that developed in flat chronically inflamed colon mucosa.

Stomach cancer is one of the most common tumors in human pathology. More than 95% of all gastric malignancy are adenocarcinomas developed from epithelial cells of gastric mucosa. Still, this is highly lethal disease with five-year surveillance of 20%. This review explains most frequently used classifications of gastric cancers, molecular and cellular abnormalities in gastric cancer, chromosomal abnormalities, tumor suppressor genes, oncogenes and growth factors involved in gastric carcinogenesis.

The gastroesophageal reflux disease (GORD) is frequent and causes by retrograde flow of the gastric content through incompetent gastroesophageal junction. Epidemiological studies have proved that GORD is associated with hearburn in high prevalence. In western countries several studies reported that 20-40% of adult population experience heartburn symptoms at least once in the year, approximately 10% have symptoms weekly and 5% daily. Esophagitis was objectively defined as a mucosal damage and it was endoscopically verificated in 25% of patients. Indeed, GORD symptoms and esophagitis are in poor correlation and less than half of patients with heartburn symptoms had esophagitis on endoscopy. From 1989, Savary Monniér and Metaplasia-Ulcer-Stricture-Erosion (MUSE) endoscopically classification is in use. From 1994, LA (Los Angeles) classification of reflux disease is also in use by endoscopists. During its life cycle, gastric mucosa is exposed to different harmful agents and its response is restitution "ad integrum" on the beginning and at the end of process. First line defence is mucuse barrier which prevent contact between epithelial cell and possible irritant. Important role in mucuse layer plays prostaglandins. After several classification systems previously used, in 1991 Price introduced Sydney system gradation and gastritis classification. Pointing out importance of topographical differences in gastritis distribution, system has introduced 5 histological variations in its Morphological section: chronic inflammation, neutrophylic activity, glandular atrophy, intestinal metaplasy and H. pylori colonisation, with 4 points grading.