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The aim of our work was to evaluate the morphological features of the mucous membrane of the stomach and duodenum in children with chronic diseases of the gastroduodenal zone on the background of food hypersensitivity. Morphological study was conducted for 50 adolescents aged 12 to 17 years who were in inpatient treatment in the gastroenterology department. In order to verify the diagnosis, all children were checked by fibroesophagogastroduodenoscopy of the upper digestive tract with biopsy of the mucous membrane of the stomach antrum and the descending part of the duodenum. Bioptates were stained by hematoxylin-eosin, Van Gieson and performed on light microscope. The results of the research of the mucous membrane of the stomach and duodenum show that adolescents with chronic gastroduodenitis and food hypersensitivity have 17 times higher risk of developing atrophy of duodenal mucous membrane, 11 times higher frequency of eosinophilic infiltration and 3 times higher incidence of mucous membrane fibrosis in the duodenum.

Background: The influence of Helicobacter pylori (HP) in inflammatory disorders of the digestive mucosa has been the subject of several studies since socioeconomic, personal and environmental factors were implicated in the bacteria transmission., Aim: To correlate the inflammatory endoscopic findings with HP infection and the onset of mucosal diseases mucous of the upper digestive tract., Method: Comparative observational study, in which were collected data from 2247 patients who underwent upper endoscopy and biopsies for HP with urease test. The patients were divided into two groups: HP+ and HP- (control) in which endoscopic findings were observed for the following changes: esophagitis, esophageal ulcer, gastritis, erosive gastritis, gastric ulcer, bulboduodenitis, bulbar ulcer and without disease., Results: As for esophagitis, there was little disparity in the distribution favorable to HP+ group (HP+ =67.11% and HP- =69.89%) and esophageal ulcer (HP+ =0% and HP- =0, 21%). Gastritis was favorable to HP- group (HP+ =78.34% and HP- =73.63%), as well as erosive gastritis (HP+ = 67,11% and HP- = 64,55%), in bulboduodenitis (HP+ =1,87% and HP- 1,23%), in gastric ulcer (HP+ =2,14% and HP- =2,03%) and in the absence of alterations in the HP+ group (4.81%) with the HP- control group (6,30%), in which there was little disproportion in favor of HP- group, but without statistical significance. As for the bulbar ulcer (HP +=10.16% and HP- =4.48%), there was statistically significant (p=0.00001)., Conclusion: There is no difference between HP+ and HP- groups in inflammatory changes in endoscopic gastroduodenal mucosa, except for the relationship between HP and bulbar ulcer., Competing Interests: none

Objective: To establish the diagnostic value of the determination of leukocyte composition of inflammatory infiltrate in chronic gastroduodenite in childhood., Patients and Methods: We examined 103 patients aged 8-17 with chronic gastroduodenitis associated with Helicobacter pylori. To detect Hp and Epstein-Barr viral infections we used esophagogastroduodenoscopy, quick urease test, bacterioscopy of gastrobiopsies. We performed the analysis of the cellular composition of the inflammatory infiltrate., Results: It was found that the number of lymphocytes and neutrophils located in the lamina and intraepithelial increases, which is associated with the degree of inflammation. Increased to the maximum was the number of intraepithelial lymphocytes, both in the body, and in the antrum. Intensity of leukocyte infiltration is directly correlated with the increased prevalence of inflammation. Persistence of Epstein-Barr virus (35.9% of patients) is followed by more severe intraepithelial lymphocytic infiltration in the stomach. In 4-6 months after treatment 18 patients with severe gastritis were repeatedly studied for the inflammatory infiltrate. A significant decrease in the number of intraepithelial neutrophils was found., Conclusion: Cellular composition of the infiltrate is an objective characteristic of chronic inflammation in the gastric mucosa. Persistence of Epstein-Barr virus is accompanied by an increase in the amount of intraepithelial lymphocytes and neutrophils.

Objective: Our aim was to reveale the features of histological mucosa with different composition of the microflora of stomach and duodenum in children with chronic gastroduodenitis., Methods: The study included 122 children with chronic gastroduodenitis from 5 to 17 years old. All patients underwent endoscopy with histology of biopsy specimens of gastric and duodenal mucosa in 94 patients and in 48 patients among them with morphometry of biological material. Identification of herpes simplex virus 1, 2 types, cytomegalovirus, human papilloma virus 16, 18 types, Helicobacterpylori was carried out using polymerase chain reaction in biopsies of gastroduodenal mucosa and gastric juice., Results: Children with chronic gastroduodenitis depending on the identified microorganisms were divided into groups: 1st (n = 51)--without detectable microorganisms, 2nd (n = 28)--with associations of H. pylori and viruses, 3rd (n = 15)--only with viruses, 4th (n = 28)--with H. pylori. Thus, in patients with H. pylori inflammation was noted mainly in the antral mucosa and dystrophic changes--in the duodenal mucosa. In the presence of viruses the inflammation was expressed more in the fundal stomach and duodenum. When viral-bacterial associations were observed most pronounced inflammatory-dystrophic process was localized throughout the gastroduodenal mucosa., Conclusion: In children with chronic gastroduodenitis in the presence of bacterial, viral and mixed microflora in the stomach and duodenum identified characteristic histological features of the mucosa, manifested in a different localization and severity of inflammatory and dystrophic changes.

Unlabelled: The infection of Helicobacter pylori is the main reason of a duodenal and gastric ulcer disease. Among other virulence factors of Helicobacter pylori, there are outer membrane proteins (OMPs), such as babA2 and sabA., The Aim of the Study: An assessment of a relationship between the presence of genes babA2 and sabA and endoscopic and histopathologic changes during gastritis, duodenitis and an ulcer disease., Material and Methods: We included 119 patients aged from 3 to 17 (average 13.6) with gastritis and duodenitis and the infection of Helicobacter pylori. The endoscopy was conducted with taking samples of the mucosa for the histopathologic and genetic examination. The degree of endoscopic and histopatologic changes were determined according to Sydney's classification. The patients were devided in the extra groups with a small level (without erosion) and with a large level (with erosion) of endoscopic changes. To identify the infection of Helicobacter pylori, the PCR technique was used and then the presence of the babA2 and sabA genes of Helicobacter pylori was verified. The genetic confirmation of Helicobacter pylori infection was obtained in 88 patients and material was directed to the further examination., Results: Not statistically significant differences were determined between endoscopic and histopathologic pictures and either the presence or absence of the genes babA2 and sabA., Conclusion: The presence of the genes babA2 and sabA is not related with level of endoscopic and histopathologic changes in pediatrics patients.

Aim: To determine a population level and significance of Helicobacter pylori in normal microbiocenosis and dysbiosis of mucosal microflora in the esophagogastroduodenal zone., Material and Methods: Qualitative and quantitative composition of mucosal microflora was defined in biopsy specimens from different parts of the esophagus, stomach and duodenum and clinical and histological examinations were made in 50 healthy volunteers, 130 duodenal ulcer patients, 24 patients with gastric ulcer, 36 with chronic gastritis and 24 with chronic esophagitis., Results: H. pylori is a component of normal mucosal microbiota of the oesophagus, stomach and duodenum. These bacteria protect normal gastrointestinal microflora. Exacerbations of peptic ulcer, chronic gastritis and oesophagitis are accompanied with overgrowth of dysbiotic mucosal microflora and reduction of H. pylori content in most cases. Healing and scar formation occur both in the presence and absence of H. pylori., Conclusion: The presence of H. pylori in mucosal microbiocenosis in the oesophagogastroduodenal zone has no independent significance in exacerbation of ulcer disease, gastritis and oesophagitis and does not require eradication.

Number of children with chronic gastroduodenitis and duodenal ulcer, is increasing every year. A major role in the development of chronic inflammation of the mucous membrane of the gastroduodenal zone play cytoprotective properties of mucus produced blennogenic structures of these bodies. Therefore, the appointment of therapies to help improve the cytoprotective properties of gastric and duodenal ulcers, remains valid. Presents the results of the study lektingistohimicheskogo slizeobrazovaniya with chronic gastroduodenitis in adolescents.

Infection with H. pylori plays a role in the pathogenesis of gastritis, peptic ulcer, gastric carcinoma, and gastric lymphoma, but mechanisms leading to the various clinical manifestations remain obscure and are the primary focus of research in this field. Proliferation and apoptosis are essential in the maintenance of gastric tissue homeostasis, and changes seen in their balance may condition gastric mucosal changes during infection. Thus, excessive apoptosis or proliferation inhibition will result in cell mass loss, which is observed in gastric ulcers. On the other hand, accelerated epithelial cell turnover is characteristic of carcinogenic mucosas. There is also scientific evidence that demonstrates an association between H. pylori infection and exacerbated synthesis of free radicals, the latter being well known as a primary cause of cell death. A thorough review of the literature and the results of our experimental research lead to conclude that H. pylori-induced oxidative stress activates the intrinsic pathway of apoptosis. Structural and functional changes caused by this process on mitochondrial organelles lie at the origin of gastric mucosal toxicity, and lead to the development of the various manifestations associated with this infection. Based on these data we suggest that therapy with antioxidants should prove beneficial for the clinical management of patients with H. pylori infection.

Whether the regression of gastric metaplasia in the duodenum can be achieved after eradication of Helicobacter pylori is not clear. The aim of the present study was to investigate the relationship between H. pylori infection and gastric metaplasia in patients with endoscopic diffuse nodular duodenitis. Eighty-six patients with endoscopically confirmed nodular duodenitis and 40 control patients with normal duodenal appearance were investigated. The H. pylori-positive patients with duodenitis received anti-H. pylori triple therapy (20 mg omeprazole plus 250 mg clarithromycin and 400 mg metronidazole, all twice daily) for one week. A control endoscopy was performed 6 months after H. pylori treatment. The H. pylori-negative patients with duodenitis received 20 mg omeprazole once daily for 6 months and a control endoscopy was performed 2 weeks after treatment. The prevalence of H. pylori infection was 58.1%, and the prevalence of gastric metaplasia was 57.0%. Seventy-six patients underwent endoscopy again. No influence on the endoscopic appearance of nodular duodenitis was found after eradication of H. pylori or acid suppression therapy. However, gastric metaplasia significantly decreased and complete regression was achieved in 15/28 patients (53.6%) 6 months after eradication of H. pylori, accompanied by significant improvement of other histological alterations. Only mild chronic inflammation, but not gastric metaplasia, was found in the control group, none with H. pylori infection in the duodenal bulb. Therefore, H. pylori infection is related to the extent of gastric metaplasia in the duodenum, but not to the presence of diffuse nodular duodenitis.

The article analyzes the influence of course treatment with vegetomodulating preparations on morphofunctional changes in the gastric and duodenal mucosa. Thirty-eight patients with chronic gastroduodenitis dwelling in ecologically unfavorable territories were examined and treated. The study demonstrated positive changes in the histomorphological picture of the gastroduodenal mucosa in children who received conventional standard therapy in combination with the beta-adrenoblocker anaprilin and the M-cholinolytic atropine compared to controls who received only the basic therapy.

The authors analysed clinical picture and morphological (macroscopic and histopathologic) changes in gastric and duodenal mucosa in 150 children diagnosed with Helicobacter pylori infection chosen randomly among the hospitalized in 1998-2000 years.

Background/aims: Duodenal gastric metaplasia seems to be linked to infection by Helicobacter pylori, to the extent of acid secretion and to bulbitis. An investigation was made of the relationship between bulbitis and duodenal gastric metaplasia, or whether bulbitis can arise along with duodenal gastric metaplasia after Helicobacter pylori eradication in an average of six years., Methodology: We compared 22 patients with duodenal ulcers [male/female 16/6; (mean age+/-SD) 55+/-12 years] Helicobacter pylori-negative after eradication, with 23 Helicobacter pylori-positive patients free from active duodenal ulcers [male/female 17/6; (mean age+/-SD) 59+/-12 years]., Results: The bulbitis score was found to be lower in the Helicobacter pylori-negative than in the Helicobacter pylori-positive group (p=0.02). The duodenal gastric metaplasia score in the Helicobacter pylori-negative was higher than in the Helicobacter pylori-positive group (p=0.001). We failed to find any relationship between the presence of bulbitis and duodenal gastric metaplasia. We found a non-significant inverse correlation between the presence of duodenal gastric metaplasia and chronic body gastritis (p=0.07)., Conclusions: Bulbitis and duodenal gastric metaplasia may depend on different causal factors not related to Helicobacter pylori infection. The extension of duodenal gastric metaplasia with time following recovery from peptic ulcer disease may represent a mucosal protection factor against acid.

Unlabelled: The aim of the study was to demonstrate morphological traits of Candida-induced upper alimentary tract mucosa inflammation. The material for the study comprised 18 children aged 4 to 18 years treated at the I Department of Paediatrics and Gastroenterology, Institute Polish Mother Health Centre. In these children positive mycologic cultures were obtained from alimentary tract inflammed mucosa sections. Upper alimentary tract endoscopy was performed and macroscopic and microscopic evaluation was made. Children with excluded H. pylori infection, reflux disease, lambliosis and allergy were included into the investigated group. Savara-Muller's classification was used for oesophageal mucosa inflammation evaluation, whereas gastric and duodenal mucosa inflammation were assessed according to Tytgat., Results: the most frequent macro lesions concerned simultaneously gastric and duodenal mucosa (44.46%). 27.77% of patients demonstrated oesophagitis, gastritis and duodenitis. In histopathological examination inflammatory lesions in oesophageal mucosa were observed in 38.88% (most frequently I degree). Chronic gastritis was found in all children, non-active in 11 and active in 7. Duodenal mucosa demonstrated traits of chronic active inflammation in 8 children and chronic in 5 of them., Conclusions: Candida fungi may be an etiopathogenetic factor of oesophageal, gastric and duodenal mucosa inflammation, Candida-induced mucosa inflammation is most frequently of chronic nature.

Background: Chronic inflammation and gastric metaplasia are often observed in biopsy specimens from the duodenal bulb of Heliobacter pylori positive patients with duodenal ulcer disease (DU)., Aims: We set out to investigate the prevalence of these lesions and their associations with other gastric and duodenal histopathological lesions., Patients: A total of 1255 consecutive patients who underwent upper gastrointestinal endoscopy were recruited into the present study., Methods: Two biopsy specimens were obtained from each of the following sites: duodenal bulb, gastric antrum, gastric body, and distal to the superior duodenal angle. These specimens were stained with hematoxylin-eosin, alcian blue periodic acid Schiff (pH 2.5) and modified Giemsa (Heliobacter pylori infection was determined only by histology)., Results: The mean age of the study population was 57 years, and male:female ratio 1:1.6. Overall, 235 (19%) had gastric metaplasia and/or chronic inflammation in the duodenal bulb mucosa, and H. pylori organisms could be found in 17 (1%). In univariate analyses, gastric metaplasia and/or chronic duodenal bulb inflammation positively associated with male sex (p = 0.046), Heliobacter pylori-positive chronic gastritis (p = 0.033), villous atrophy of distal duodenal mucosa, i.e., coeliac disease (p < 0.001), duodenal ulcer (p < 0.001), and duodenal bulb deformity and scarring in endoscopy (p < 0.001), but not with age (p = 0.7) nor use of nonsteroidal anti-inflammatory drugs (p = 0.055). Multivariate analysis revealed that independent risk factors for gastric metaplasia and chronic inflammation in duodenal bulb were duodenal Heliobacter pylori infection (odds ratio 1.6, 95% confidence interval CI 1.1-2.1), and villous atrophy of the distal duodenal mucosa (odds ratio 12.7, 95% CI 4.4-36.5), while chronic atrophic gastritis was protective against them (odds ratio 0.5, 95% CI 0.3-0.8)., Conclusions: In addition to Heliobacter pylori infection, duodenal bulb gastric metaplasia and chronic inflammation may result from predisposition to toxic dietary components in gluten-sensitive subjects.

Examining the gastroduodenal mucosa (GDM) in 61 patients with chronic obstructive pulmonary diseases (COPD) showed changes in the areas studied in all cases. GDM atrophy increased with the severity of COPD. Helicobacter pylori are essential in developing gastric pathology in patients with mild bronchopulmonary disease. The severity of atrophic gastritis increases with the longer duration of COPD and with more severity of hypoxia and bronchial obstruction.

Alcohol consumed in small quantities is not dangerous for health but if it is drunk in big amounts it has a negative effect on somatic and psychical health. A number of studies have been published on the harmful effect of ethanol on the nervous system, circulation, endocrine and immune systems. Ethyl alcohol can directly damage the mucosa of the alimentary tract. The studies conducted and published so far have estimated acute ethanol damage of gastric mucosa in experimental animals. The views found in literature on the effect of continuous consumption of ethanol on the stomach are differentiated. The purpose of the paper was to provide a morphological and functional analysis of stomach and duodendum in patients who continuously abuse alcohol. Besides, at attempt was made to find the answer to the question whether the changes observed in gastric mucosa point to any connection with the period of alcohol abuse. The study referred to 79 persons: 61 male aged 17-65 who had been chronically drinking alcohol for the period of 5-37 years and 18 persons aged 17-59 (9 male and 9 female) who had never drunk alcohol or who had drunk it only rarely and in small were divided into three groups differing with the period of addiction (I--5-10 years; II--10-20 years; III--over 20 years). Hydrochloric acid secretion in gastric juice was marked and gastroscopy was performed in all the examined patients. Gastroscopy estimated the appearance of the gastric and duodenal mucosa, while biopsy specimens were taken for histological examination from the pyloric area, the body of the stomach and the duodendal bulb. Hydrochloric acid secretion was determined using the Kay's aspiration method. Pentagastrin was used to stimulate gastric secretion. Within the group of 79 patients, gastric mucosa inflammation was observed in all patients chronically drinking alcohol and in 72% patients who were the control. Both groups differed considerably with the degree of progression of the inflammatory process, which was estimated with histological examination. Atrophic gastritis was observed only in patients addicted to alcohol. The appearance of atrophic changes pointed to a close relation with the period of addiction. 13 out of 14 people with this type of inflammation had been drinking alcohol for at least 10 years. The studies did not show any relation existing between the percentage of cases with atrophic inflammation and the kind of drinks or the content of ethanol in them. Examinations concerning the secretory function of the stomach showed lower values of hydrochloric acid secretion, both in basic conditions and after pentagastrin stimulation, in patients addicted to alcohol as compared to the control. The results prove that continuous abuse of alcohol predisposes to atrophic inflammation of the gastric mucosa, and the appearance of this type of inflammatory changes is related to the duration of addiction. The longer the addiction, the lower the secretion of hydrochloric acid is.

Background/aims: Limited efforts have been made to determine changes in the upper gastrointestinal tract in ulcerative colitis. The aim of this study was to analyze gastroduodenal lesions in patients with ulcerative colitis., Methodology: The endoscopical appearance of lesions in the duodenum and stomach was first examined. Biopsy specimens taken from 25 patients with ulcerative colitis, as well as 21 with Crohn's disease and 16 with nonspecific gastroduodenitis who had no Helicobacter pylori infection, were then evaluated by histology and immunohistochemistry for CD8, CD68 and HLA-DR. In ulcerative colitis patients, the HLA-phenotype was also analyzed by the standard NIH complement-dependent microlymphocyte toxicity assay., Results: Endoscopically evident alteration of nodularity in the descending part of duodenum was prominent in ulcerative colitis and Crohn's disease, but not gastroduodenitis. Histological inflammatory change of the duodenal bulb in ulcerative colitis and Crohn's disease was mild as compared to gastroduodenitis cases. Endoscopic and histological change (redness and deformity of villi) in the duodenum were more prominent in ulcerative colitis patients with pancolitis than those with left-sided/proctitis. CD8+ cells infiltrating both the duodenum and stomach were increased in ulcerative colitis and Crohn's disease as compared to gastroduodenitis whereas focal perifoveolar accumulation of CD68+ cells and enhanced epithelial expression of HLA-DR were characteristic of Crohn's disease. Histopathological alteration in the duodenum was particularly prevalent in ulcerative colitis patients with HLA-DR4 and Cw1., Conclusions: Nodular, histologically mild duodenitis involving CD8+ cell infiltration, the severity of which positively correlates with the extent of colitis, is characteristic of ulcerative colitis.

Background and Aims: The purpose of this study was to investigate the relationship between gastric metaplasia and Helicobacter pylori in patients with endoscopic duodenitis., Methods: The subjects were 57 patients with endoscopic duodentitis with or without H. pylori-associated gastritis. Biopsy specimens were obtained from the stomach and duodenal bulb to assess the histological findings and H. pylori infection. Gastric metaplasia was divided into three types: complete, intermediate and incomplete, according to the amount of mucus in the metaplastic cells. In 10 H. pylori-positive patients, endoscopic and histological findings of duodenitis were compared before and after eradication of the bacteria., Results: There was no significant difference in the extent of gastric metaplasia or the appearance and severity of endoscopic duodenitis between H. pylori-positive and -negative groups. The complete type of gastric metaplasia was frequently detected in the H. pylori-negative group, whereas the incomplete type was frequently observed in the H. pylori-positive group. After eradication of H. pylori, the incomplete type changed to the complete type with a decrease of histological inflammation., Conclusions: The complete type of gastric metaplasia occurred frequently without H. pylori infection, whereas the incomplete type was frequently associated with H. pylori infection.

Gastric metaplasia is one of the factors in duodenal ulcer appearance. The aim of this study was to investigate the frequency of gastric metaplasia and its connection with age, sex, cigarette smoking and H. pylori infection. In the study 216 patients were included. There were 98 patients with duodenal ulcer, 60 with duodenitis, and 58 healthy control subjects. There was no statistically significant difference in gastric metaplasia frequency according to age and sex. Gastric metaplasia was statistically more significant in patients with duodenal ulcer (p < 0.01). In all the subjects cigarette smoking did not significantly influence gastric metaplasia. In smokers with duodenal ulcer, and those who besides duodenal ulcer and smoking had H. pylori infection gastric metaplasia was more frequent (p < 0.01). However, in patients with duodenal ulcer, there was no statistically significant difference of gastric metaplasia related to H. pylori presence. It may be suggested that H. pylori infection is not of indispensable significance for gastric metaplasia appearance.

Aim: Morphological study of gastric and duodenal mucosa in patients with vibration disease., Materials and Methods: 64 patients with vibration disease stage I and II were examined endoscopically, histologically, bacterioscopically and morphometrically irrespective of the presence or absence of gastrointestinal complaints., Results: Erosive gastroduodenitis, non-erosive gastroduodenitis and gastritis, polyps in the stomach and gastric ulcer were diagnosed in 19(29.7%), 40(62.5%), 2(3.2%) and 1(1.6%) patients, respectively. Small intestinal metaplasia occurred in 22% of patients. Helicobacter pylori occurred most frequently in the antral part of the stomach (90.24%). Advanced dissemination often combined with metaplasia of the small bowel. Morphometrically, there were slight differences from relevant values in patients with chronic gastroduodenitis who were not exposed to occupational hazards. Vibration disease patients exhibited impairment of duodenal vessels (large endothelial nuclei, thick arteriolar walls) 2 times more frequently than controls., Conclusion: In vibration disease, gastric and duodenal mucosa, as a rule, shows signs of chronic gastroduodenitis.

Background: Duodenal gastric metaplasia (DGM) is commonly found in association with Helicobacter pylori (Hp)-associated gastritis in adults. DGM is also considered a risk factor for duodenal ulcer development. The prevalence of DGM in children and its association with gastritis, duodenitis, or the presence of Hp organisms is not clear. We investigated the prevalence of DGM in children and explore its association with several possible risk factors, including age, gender, gastritis, duodenitis, or Hp presence in the gastric antrum., Methods: A retrospective analysis of 173 upper endoscopy procedures performed between 1993 and 1995 at Cabell Huntington Hospital, Huntington, WV, was done. Gastric and duodenal biopsies were stained with Giemsa for Hp detection, periodic acid-Schiff for DGM, and hematoxylin and eosin for histologic assessment. Gastric mucosal inflammation was graded according to Sydney criteria., Results: Duodenal gastric metaplasia was identified in 23 of 173 (13%) patients. Duodenitis but not age, gender, gastritis, or the presence of Hp in the gastric antrum was associated with DGM development. In 4 of 23 DGM foci, Hp was identified., Conclusions: In children, DGM is not the consequence of Hp infection.

62 Chernobyl wreckers with erosive gastroduodenitis (50 cases) and ulcer (12 cases) were admitted to hospital where they received standard drugs and local He-Ne laser treatment of erosions and ulcer located in the antral stomach and duodenal bulb. Histological, bacterioscopic, morphometric and immunohistochemical examinations have identified chronic inflammation and disturbance of local immunity. After treatment epithelialization of erosions was not accompanied by normalization of morphometric and immunohistochemical parameters. This suggests a high risk of recurrences.

The course of gastric type epithelium during the healing process and beyond the scarring stage of duodenal ulcer was studied in patients with and without Helicobacter pylori (H. pylori) eradication. Materials were consist of 110 patients with active H. pylori ulcers, 27 patients with H. pylori positive ulcer scars and 6 patients with active H. pylori positive duodenitis. The results obtained were as follows. 1) In the non-eradication group, the degree of gastric type epithelium increased as the ulcers healed, but gastric type epithelium remained immature compared with the eradication group. 2) In the non-eradication group, the degree of gastric type epithelium decreased subsequently with or without recurrence of the duodenal ulcer. Under H. pylori positive condition, the degree of gastric type epithelium appeared to be reduced because of invasion by H. pylori. When this condition continued, ulcers probably recurred because of diminished defences against acid in damaged areas of gastric type epithelium. 3) In the successful eradication group, gastric type epithelium became well developed and mature state (grade 4), and remained in this condition for long period because it was not invaded by H. pylori. The appearance of mature state of gastric type epithelium appears to play a role in the prevention of ulcer recurrences by maintaining an adequate defence mechanisms against acid. 4) In the unsuccessful eradication group, the degree of gastric type epithelium remained lower mature state than that of successful eradication group. 5) In cases of H. pylori positive ulcer scar, the degree of gastric type epithelium reached also well developed and mature state when H. pylori was successfully eradicated, and maintained in this condition for a prolonged period. Ulcer recurrence was not observed. 6) In case of H. pylori positive duodenitis, the degree of gastric type epithelium reached mature state after successful eradication, and endoscopic findings of inflammation was improved.

They examined 114 young health volunteers to establish a frequency of inflammation of gastric mucous membrane and(or) duodenal bulbous, a frequency of Helicobacter pylori infection and interdependence between infection and inflammation, smoking and nourishment. They evaluated a frequency and intensity of inflammation in antrum, fundus and duodenal bulbus and present of Helicobacter pylori using an urease test and microscopic examination. They noted in young inhabitants of Warsaw, appearance of asymptomatic gastritis in more than 53% cases, an inflammation of duodenal bulbus in 34% and H.pylori infection in 50% cases.

Investigations designed to study gastric mucosa (GM) in patients with chronic primary gastroduodenitis with the aid of electron microscopy showed the abnormal changes in the cellular, subcellular membranes and capillaries to be of the same type as they are in peptic ulcer (PU) though poorly manifest. Changes in GM under chronic atrophic gastroduodenitis (ChGD) suggested involutive changes while in chronic secondary gastroduodenitis (ChSGD) it was generally not different from the mucosa ultrastructure in healthy subjects except for changes in surface epithelium. Based on the histoenzymologic studies it has been ascertained that in ChPGD there occurs a rise in lysosomal enzymes similar to that encountered in PU, reflecting the intensity of catabolic processes, decrease in the activity of enzymes of the capillary wall and mitochondria respiratory chain against the background of compensatory enhancement of the activity of the glycolytic enzyme lactate dehydrogenase. In ChAGD the activity of all the enzymes was low, while in ChSGD it did not differ significantly from that in healthy subjects.

Background & Aims: The pathogenesis of gastric metaplasia (GM) in the duodenum is unclear. The aim of this investigation was to study the effect on the extent of GM of ulcer healing, Helicobacter pylori eradication, and acid suppression singly and in combination. The relationship between GM and gastroduodenal inflammation and H. pylori infection density was also studied., Methods: Duodenal and gastric antral biopsy specimens were obtained from H. pylori-positive patients with duodenal ulcer and from H. pylori-positive nonulcer subjects. Biopsy procedures from patients with duodenal ulcer were repeated after 6 months of treatment. Nonulcer subjects were treated symptomatically and did not undergo re-endoscopy., Results: Ulcer healing alone produced no change in GM or in gastroduodenal inflammation. H. pylori eradication produced a 42% reduction in GM and improvement in inflammation. Acid suppression produced a 43% reduction in GM but without a significant change in inflammation. A combination of H. pylori eradication and acid suppression produced an additive effect with a 66% reduction in GM. A positive relationship was detected between the extent of GM and antral H. pylori density, duodenitis score, and antral gastritis score., Conclusions: This study shows that the extent of duodenal GM is unrelated to the presence or absence of ulceration but is partly due to H. pylori and partly due to acid.

Biopsies of stomach and duodenum different regions mucosa obtained from patients with gastroduodenitis (liquidators of consequences of accident in Chernobyl nuclear station--LCA CNS-- and control patients) were studied cultured in vitro. The following are the differences found. Mononuclear cells, differentiating into macrophages were exposed from control biopsies. Mononuclear cells exposed from LCA CNS biopsies formed rosette-like accumulations after mitotic dividing on a distance from the explant. Part of cells within the rosettes acquired processes and formed syncytial structure.

Biopsy specimens from antral and duodenal mucosa were obtained from 64 patients with active duodenal ulcer and from 78 with nonulcer dyspepsia. Gastric metaplasia in the duodenal bulb was more frequent in patients with duodenal ulcer (82.5%) than in patients with dyspepsia and duodenitis (53.1%) or in patients with dyspepsia without duodenitis (34.5%). Helicobacter pylori infection in the duodenal bulb was found more often in patients with moderate to severe gastric metaplasia (62.3%) than in patients with mild gastric metaplasia (20%). Therefore, patients from a developing country, China, showed the same relationship between duodenitis, gastric metaplasia, duodenal colonization with H. pylori, and duodenal ulcer previously demonstrated in developed countries.

Morphological electron-microscopic evaluation of gastroduodenal mucosa in subjects who worked in the zone of radionuclide contamination after the Chernobyl accident in 1986-1987 and therefore exposed to low-dose ionizing radiation (18, 62 sGy on the average) discovered deficiency of tissue immunocompetent cells, dystrophic changes in the epithelium and stroma. In epithelial cells there were structural shifts in microvillae, organoids and nuclei. Epithelium, stroma and endothelium of blood vessels contained dark cells with thick hyaloplasm.

Helicobacter pylori infection causes chronic-active gastritis and is associated with peptic ulceration. However, the link between gastric H pylori colonization and duodenal ulcers is not well understood. Therefore, a retrospective, case-controlled study was conducted to determine whether H pylori infection is associated with gastric metaplasia and mucosal inflammation in the duodenum. Biopsy specimens from the duodenal bulb were obtained from 31 of 47 children with H pylori-induced gastritis. Two control groups, matched for age and sex, consisted of 33 children with normal antral histologic evaluation and 33 with H pylori-negative gastritis. Coded duodenal sections were stained with periodic acid-Schiff, hematoxylin-eosin, and silver to examine for gastric metaplasia, mucosal inflammation, and Helicobacter-like organisms, respectively. Thirteen of 31 (42%) H pylori-infected children had gastric metaplasia, in contrast to 1 of 33 with normal histologic characteristics (P < .0001) and 2 of 33 with H pylori-negative gastritis (P < .001). H pylori was detected overlying ectopic gastric mucosa in only 2 of 13 cases. Duodenal ulcers were identified endoscopically in 10 of 13 children with gastric metaplasia and 9 of 18 H pylori-infected subjects without metaplasia (P = NS). Twenty-four of 31 (77%) children with H pylori gastritis had duodenitis compared with 4 of 33 (12%) with H pylori-negative gastritis (P < .001) and 2 of 33 (6%) with a normal antrum (P < .001). Duodenitis was present in 14 of 19 children with H pylori infection and duodenal ulcers and 10 of 12 infected patients without mucosal ulceration (P not significant). These findings demonstrate a higher frequency of both gastric metaplasia and mucosal inflammation in the proximal small intestine of H pylori-infected children. However, there was a lack of correlation between the presence of duodenal ulceration and both gastric metaplasia and duodenitis.

A prospective double-blind randomized placebo-controlled study was conducted to compare the injurious effects of aspirin and naproxen on the gastroduodenal mucosa. Patients with rheumatoid arthritis attending the immunology clinic of a tertiary care center were included in the study. Ninety consecutive patients were randomized to receive aspirin, naproxen, or placebo. Clinical evaluation was done every 2 wk. Upper gastrointestinal endoscopy, biopsies from the gastric antrum and duodenum for histological examination, and Helicobacter pylori studies were done at entry and after 2 months. The number of patients with dyspeptic symptoms was similar in the aspirin (12) and naproxen (9) groups. In both cases, however, it was higher (p less than 0.01) than in the placebo group (none). Naproxen was associated with a higher score of endoscopic abnormalities in the gastric body (0.6 +/- 1.3) than aspirin (0.2 +/- 0.6) or placebo (0.03 +/- 0.18). H. pylori was present in a similar proportion of patients in the three groups (33-43%). A greater fall in hemoglobin was observed with aspirin (0.35 +/- 0.48 g%) and naproxen (0.44 +/- 0.53 g%) than with placebo (0.09 +/- 0.4 g%). The present study suggests that aspirin and naproxen produce a similar degree of injury to the gastroduodenal mucosa.

The evidence obtained on 280 ulcer patients, 107 of whom have preulcer erosive gastritis, duodenitis or gastroduodenitis, suggest the conclusion on ulcerogenesis dependence on the type and site of erosions, response of blood germs, characteristics of protein, carbohydrate and electrolyte metabolism. Erosive processes in the gastroduodenal mucosa seem a facultative preulcer state.

Biopsy specimens were taken from the duodenal bulb and the distal duodenum in 45 duodenal ulcer patients before and after treatment with histamine-2 antagonists, prostaglandin analogues or antacids. After four weeks of treatment, the ulcer had healed in 31 patients. The treatment did not lead to a reduced frequency of helicobacter-associated duodenitis or gastric metaplasia of the duodenal epithelium. We found gastric metaplasia in 52.3% of all biopsy specimens from the duodenal bulb, chronic active duodenitis in 71.9% and helicobacter-like structures in 15.9%. The helicobacter organisms were found only in areas of gastric metaplasia, and an accompanying chronic active duodenitis was found in 94.1%. In the distal duodenum, we observed chronic active duodenitis in 15.0% of the specimens. Here the inflammation was not associated with gastric metaplasia or helicobacter-like structures. These observations support the hypothesis that Helicobacter pylori colonizes the duodenal mucosa only in areas of gastric metaplasia, and that such colonization may lead to an active duodenitis.

In bioptic specimens of the gastric mucosa of 57 patients with dyspeptic complaints and/or a duodenal ulcer Helicobacter pylori was detected under the microscope in 82,4% of chronic active gastritis and in 28,6% and 61,5% resp. of chronic gastritis grade I and II. The finding of helicobacteria depended on the number of collected specimens. They were never found at sites with intestinal metaplasia and their numbers did not correspond to the intensity and character of the inflammatory changes. As compared with the antrum, in the corpus of the stomach helicobacteria were found more frequently not only in mild forms of the inflammation but also in the normal mucosa. In the duodenum the finding was negative and the inflammatory changes were only mild. In all patients with a duodenal ulcer and a scar after ulceration in the antrum chronic active or inactive gastritis grade II was found with helicobacteria in 84,6% of the observations. Cultivation was consistent with microscopic evidence in 50 patients (87,7%).

A total of 53 patients with dermatomyositis aged 4-14 with the disease duration of three months to eight years were under observation. Twenty seven patients complained of stomach-ache, II felt pain during palpation, 30 lost appetite. Electrogastrography revealed disorders in bioelectric activity of the stomach muscles in 99.9% of the patients. Endoscopic studies revealed lesions in the stomach and duodenum in all the patients, in 39 of them gastroduodenitis in the stage of exacerbation was diagnosed, in 7 erosion, in 3 peptic and duodenal ulcer. In 81.3% of the children during clinico-laboratory remission of dermatomyositis gastroduodenitis persisted at the stage of exacerbation. The vessels lying in the mucosa of the antral area of the stomach and duodenum underwent peculiar changes: arterial walls looked thickened, nuclei of the endothelial cells were enlarged, rounded up. One could observe infiltrates around the vessels consisting mainly of lymphocytes. Morphometric indices of the mucosa were also different in the antral area of the stomach and duodenum. Apparently, changes revealed in the gastric and duodenal mucosa of children with dermatomyositis occur due to vascular processes developing as a result of the main disease. This should be taken into consideration in the treatment of such children.

Biopsies were obtained from non-ulcerated sites of the duodenum from 100 dyspeptic patients. Helicobacter (Campylobacter) pylori was cultivated from 19 of these biopsies. Active chronic duodenitis (ACD) was found in 17 biopsies and more than 5% gastric metaplasia in 20 biopsies. H. pylori as well as ACD occurred with a significantly increased frequency when more than 5% gastric metaplasia was found in the duodenal biopsies. H. pylori on metaplastic tissue without ACD was, however, seen in two cases. H. pylori was cultivated from 9% and ACD was found in 5% of the biopsies with less than 5% gastric metaplasia. Gastric metaplasia in the duodenum was found significantly more frequently in patients with endoscopic duodenitis or duodenal ulceration than in patients with normal endoscopy. No association between gastric metaplasia in the duodenum and gastric pH or serum antibodies against H. pylori was seen. This study indicates that there is an established, but not exclusive, connection between gastric metaplasia and the colonization of the duodenum by H. pylori, the most important role being played by the antral gastric mucosa rather than the duodenum.

Histological, morphometric, and immunohistochemical studies of biopsy specimens from the mucosa of the body and antral portion of the stomach, the bulb and descending portion of the duodenum were performed in 27 children with systemic lupus erythematosis (SLE) and in 12 with chronic gastroduodenitis. The inflammatory infiltrate from SLE patients was found to contain higher levels of young and mature fibroblasts than that from patients with chronic gastroduodenitis, mature fibroblasts being prevalent. The inflammatory changes in the gastric and duodenal mucosa were ascertained to be associated with the progression of SLE. In exacerbation of SLE, the walls of vessels (arterioles) exhibited immune complexes classified mainly as IgG and, to a lesser degree, as IgM. In remission, the luminescence of the vessels decreased. The serum level of immunoglobins did not correlate with their regional production in the gastric and duodenal mucosa.

This study aimed to determine the prevalence of endoscopic and histological gastroduodenitis as well as helicobacter-like organisms in patients with end stage renal failure undergoing maintenance dialysis treatment. A total of 322 out of 422 patients in our dialysis programme underwent endoscopy and gastroduodenal biopsy specimens were taken from 260. Endoscopic gastroduodenitis occurred in 158 (49%). Histological gastritis occurred in the gastric body or antrum in 134 patients (52%) and duodenitis in 52 (21%). There was no correlation between endoscopic and histological gastritis in contrast to a significant correlation for duodenitis. Helicobacter-like organisms occurred in the body or antrum in 81 (31%). Their presence was associated with gastritis--in particular acute and acute on chronic gastritis rather than chronic gastritis. Patients with gastritis were significantly older than those without (p less than 0.001) and had lower basal and peak acid outputs.

Endoscopic biopsies from 310 patients were studied for the presence of Campylobacter pylori (Cp). In the first group of 150 patients duodenal and antral biopsies were obtained and in the second (160 patients) biopsies were taken from various sites in the stomach including the antrum, incisura, body and fundus. In the duodenum there was a strong association with active inflammation and the presence of gastric metaplasia. Cp were never seen in the normal duodenum. In the stomach Cp presence was associated with gastritis irrespective of severity and site, but was absent in areas showing intestinal metaplasia. Cp were seen in histologically normal biopsies from all areas of the stomach but were significantly more common in normal fundal than normal antral mucosa.

A specified endoscopic picture, consisting of standing prepyloric mucosal folds, injection, and erosions, is denoted erosive prepyloric changes (EPC) and is divided into three grades. In a prospective study in 1001 patients referred for routine upper endoscopy, active EPC (grades 2 and 3) was found in 25.8%, rising to 32.2% in dyspeptic patients with non-ulcer conditions. EPC was significantly more frequent in those below than those above 50 years of age, the male to female ratio being 1.1. In 34.5% of the EPC patients, EPC was an isolated finding. Maximal acid output was, on an average, significantly lower in patients with EPC than in duodenal ulcer patients and similar to that of healthy subjects. Non-ulcer conditions were significantly more frequent, and ulcer in general significantly less frequent, in the EPC group than in a randomly selected control group without EPC. In 34 asymptomatic volunteers the frequency of EPC was 17.6%, significantly lower than in patients of comparable age with non-ulcer conditions. The findings indicate that EPC is related to non-ulcer dyspepsia. The recognition of this condition may lead to a more accurate definition of a patient group with ulcer-like symptoms, without ulcer, and thus, in turn, result in more efficient treatment procedures.

Biopsy specimens were collected during endoscopy from pre-established sites in the corpus (n = 60), antrum (n = 53), and the duodenal bulb (n = 54) from the same patient before and 2-3 years after parietal cell vagotomy (PVC) or after a similar period of treatment with cimetidine. There was a significant increase in scores of chronic body gastritis after PCV (p less than 0.001) even in comparison with the cimetidine group (p less than 0.01), for which the scores of chronic body gastritis remained essentially unchanged. The scores of chronic antral gastritis and the incidence of intestinal metaplasia of the antrum increased significantly (p less than 0.05) in both the PCV and the cimetidine groups when the two treatment groups were analyzed together. The degree of polymorphonuclear infiltration in the body and antral mucosa, the incidence and severity of duodenitis, and the incidence of gastric metaplasia in the duodenal cap were unaffected by the treatment. In contrast to maintenance treatment with cimetidine PCV seems to accelerate the development of chronic body gastritis. The kappa statistics, as indicator of the reproducibility of histopathologic scoring, were acceptable.

The presence of gastric epithelium or mucosa at any level of the gastrointestinal tract is a well-known phenomenon. In duodenal mucosa, congenital heterotopic gastric mucosa or acquired metaplastic gastric surface epithelium (MGE) may be found. In the present study 325 duodenal biopsies (260 upper gastrointestinal endoscopy and 65 abdominal surgery biopsies) from 297 patients were retrospectively reviewed. Normal duodenal mucosa was present in 119 specimens, duodenitis in 155 and duodenal ulcer in 51. Heterotopic gastric mucosa was present in only one patient with duodenal ulcer, and MGE in 31% of the biopsies with a normal mucosa, in 21.7% with duodenitis and in 82% with duodenal ulcer (P less than 0.01). MGE was present in 120 biopsies of 109 patients--68 men and 41 women, 91% Jews, and 9% Arabs. The hospitalized population of our region comprised 82% Jews and 18% Arabs. Duodenal ulcer was more frequently found in Arab (69%) than in Jewish patients (41%). We conclude that MGE is a common finding, even in the presence of normal duodenal mucosa (30%) and occurs in most (80%) duodenal ulcer cases. The fact that MGE is more frequent in the Jewish population suggests that a genetic factor may be involved.