The Relationship between Primary Duodenogastric Reflux and Helicobacter pylori Gastritis in Children.

BACKGROUND: Most studies of the relationship between duodenogastric reflux (DGR) and Helicobacter pylori have reported that the presence of DGR decreases H. pylori colonization, while H. pylori infection increases the frequency of DGR by impairing antroduodenal motility. The present study aimed to investigate the relationship between primary DGR and the prevalence of H. pylori in children, as well as the degree of colonization and the presence and severity of gastritis. METHODS: Included in the study were 410 patients between the ages of 2 and 18 years, referred to the pediatric gastroenterology clinic with complaints of dyspepsia, abdominal pain, and nausea/vomiting, who underwent upper gastrointestinal system endoscopic examination and stomach biopsy. The study group included 60 patients with DGR, while 350 non-DGR patients formed the control group. RESULTS: The mean age of patients with DGR was 15.7 ± 2.1 years, while the mean age of the control group was 14.2 ± 3.8 years (p = 0.02). Of those with DGR, 50 (83.3%) were girls, while in the control group, 215 (61.4%) were girls (p = 0.001). Of patients with DGR, 16 were H. pylori (+) (26.7%), while in the control group, 168 were H. pylori (+) (48%) (p = 0.002). There was no significant difference between the 2 groups with respect to H. pylori degree of colonization (p = 0.08). Gastritis was present in 56 (93.3%) patients in the DGR group and 322 (92%) patients in the control group (p = 0.72). A significant difference was found between the 2 groups in terms of gastritis severity (p = 0.01). CONCLUSIONS: The mean age of patients with DGR was significantly higher than that of patients without DGR, and DGR was found to be more common in girls. In patients with DGR, H. pylori prevalence was significantly lower than in those without DGR; however, no significant difference was found between the 2 groups with respect to the colonization degree.

Development and characterization of a mouse model of duodenogastric reflux.

AIMS: Rat models of duodenogastric reflux have been used to study gastric stump cancer (GSC), but the underlying molecular mechanisms are poorly understood. Unlike rats, mice can be genetically modified, providing a superior model for studying the molecular mechanisms underlying GSC development, which is associated with duodenogastric reflux. This study aimed at developing a mouse model of duodenogastric reflux. MAIN METHOD: C57BL/6 mice were randomly assigned to the control (n = 6), sham operation (n = 9), or gastrojejunostomy group (n = 12). Mice were sacrificed at 1, 3, and 6 months after surgery. Stomach tissue was stained with hematoxylin and eosin. Lesions were classified as chronic inflammation, intestinal metaplasia, or atypical hyperplasia. KEY FINDINGS: Nine mice underwent gastrojejunostomy without mortality. The animals in the gastrojejunostomy group exhibited chronic inflammation at 1, 3, and 6 months after surgery, showing intestinal metaplasia (n = 2) and atypical hyperplasia (n = 1) at 3 months and intestinal metaplasia (n = 2) and atypical hyperplasia (n = 2) at 6 months. The mice in the control group did not exhibit chronic inflammation or intestinal metaplasia, whereas those in the sham operation group exhibited chronic inflammation at 1, 3, and 6 months after surgery, without intestinal metaplasia or atypical hyperplasia. Intestinal metaplasia or atypical hyperplasia were more common in the gastrojejunostomy group than in the sham operation group (p = 0.012). SIGNIFICANCE: A duodenogastric reflux mouse model can be created using gastrojejunostomy without gastrectomy.

The Effect of Primary Duodenogastric Bile Reflux on the Presence and Density of Helicobacter pylori and on Gastritis in Childhood.

Background and Objectives: Although there are many studies that investigate the relationship between duodenogastric reflux (DGR) and Helicobacter pylori in adult patients, the reported data are contradictory. In addition, there are very few studies in the literature investigating the relationship between DGR and H.pylori in the pediatric age group. In the present study, we investigated the effect of primary DGR on H.pylori and gastritis. Materials and Methods: A total of 361 patients who were referred to the clinic of our hospital with dyspeptic complaints who had an upper gastrointestinal system endoscopy and a gastric biopsy were included in the study. Results: DGR was detected in 45 cases, and 316 cases that did not have DGR were considered as the control group. Comparisons were made between the DGR cases and the control group in terms of risk factors (age, gender), the presence and density of H.pylori, and the presence and severity of gastritis. The average age of the patients who were included in the study was 11.6 ± 4.6 years. A total of 128 (36%) of the cases were male and 233 (64%) were female. DGR was present in 45 (13%) of the cases. The average age of the patients with DGR was 13.9 ± 3.1 years, the average age of the control group was 11.3 ± 4.7, and there were statistically significant differences (p < 0.001). No significant differences were detected in terms of gender between DGR and the control group (p > 0.05). H.pylori (+) was detected in 29 (64%) of patients with DGR, and in 202 (64%) of the control group. No significant differences were detected between H.pylori prevalence (p = 0.947). Gastritis was detected in 37 (82%) of the patients with DGR, and in 245 (77%) of the control group (p = 0.476). No significant differences were detected between the presence and density of H.pylori, gastritis presence, severity and DGR (p > 0.05). Conclusions: The ages of patients with DGR were significantly higher than in the control group, and advanced age was shown to be a risk factor for primary DGR. It was found that the presence of DGR has no effect on the presence and severity of H.pylori. Given this situation, we consider it is important to eradicate H.pylori infection, especially in the case where H.pylori is present together with DGR.

Hyperinsulinemia Promotes Esophageal Cancer Development in a Surgically-Induced Duodeno-Esophageal Reflux Murine Model.

Hyperinsulinemia could have a role in the growing incidence of esophageal adenocarcinoma (EAC) and its pre-cancerous lesion, Barrett's Esophagus, a possible consequence of Gastro-Esophageal Reflux Disease. Obesity is known to mediate esophageal carcinogenesis through different mechanisms including insulin-resistance leading to hyperinsulinemia, which may mediate cancer progression via the insulin/insulin-like growth factor axis. We used the hyperinsulinemic non-obese FVB/N (Friend leukemia virus B strain) MKR (muscle (M)-IGF1R-lysine (K)-arginine (R) mouse model to evaluate the exclusive role of hyperinsulinemia in the pathogenesis of EAC related to duodeno-esophageal reflux. FVB/N wild-type (WT) and MKR mice underwent jejunum-esophageal anastomosis side-to end with the exclusion of the stomach. Thirty weeks after surgery, the esophagus was processed for histological, immunological and insulin/Insulin-like growth factor 1 (IGF1) signal transduction analyses. Most of the WT mice (63.1%) developed dysplasia, whereas most of the MKR mice (74.3%) developed squamous cell and adenosquamous carcinomas, both expressing Human Epidermal growth factor receptor 2 (HER2). Hyperinsulinemia significantly increased esophageal cancer incidence in the presence of duodenal-reflux. Insulin receptor (IR) and IGF1 receptor (IGF1R) were overexpressed in the hyperinsulinemic condition. IGF1R, through ERK1/2 mitogenic pattern activation, seems to be involved in cancer onset. Hyperinsulinemia-induced IGF1R and HER2 up-regulation could also increase the possibility of forming of IGF1R/HER2 heterodimers to support cell growth/proliferation/progression in esophageal carcinogenesis.

Gastroesophageal Mucosal Injury after Cholecystectomy: An Indication for Surveillance?

BACKGROUND: Cholecystectomy alters bile release dynamics from pulsatile meal-stimulated to continuous, and results in retrograde duodeno-gastric bile reflux (DGR). Bile is implicated in mucosal injury after gastric surgery, but whether cholecystectomy causes esophagogastric mucosal inflammation, therefore increasing the risk of metaplasia, is unclear. STUDY DESIGN: This study examined whether cholecystectomy-induced DGR promotes chronic inflammatory mucosal changes of the stomach and/or the esophagogastric junction (EGJ). Four groups of patients were studied and compared with controls. A group of patients was studied before and 1 year after cholecystectomy; 2 further groups were studied long-term post-cholecystectomy (LTPC) at 5 to 10 years and 10 to 20 years. All underwent abdominal ultrasound and upper gastrointestinal endoscopy with gastric antral and EGJ biopsies, noting the presence of gastric bile pooling. Biopsy specimens were stained for Ki67 and p53 overexpression, and the bile reflux index (BRI) was calculated. RESULTS: At endoscopy, bile pooling was observed in 9 of 26 (34.6%) controls, in 8 of 25 (32%) patients pre-cholecystectomy, in 15 of 25 (60%) 1 year post-cholecystectomy patients (p = 0.047), and 23 of 29 (79.3%) LTPC patients (p = 0.001). Bile reflux index positivity at the EGJ increased from 19% of controls through 41% of LTPC patients (p = 0.032). Ki67 was overexpressed at the EGJ in 19% of controls, but in 62% of LTPC patients (p = 0.044); p53 was overexpressed at the EGJ in 19% of controls compared with 66% of LTPC patients (p = 0.001). CONCLUSIONS: Duodeno-gastric bile reflux was more common in patients with gallstones than in controls, and its incidence doubled after cholecystectomy. This was associated with inflammatory changes in the gastric antrum and the EGJ, evident in most LTPC patients. Ki67 and p53 overexpression at the EGJ suggests cellular damage attributable to chronic bile exposure post-cholecystectomy, increasing the likelihood of dysplasia. Further studies are required to determine whether DGR-mediated esophageal mucosal injury is reversible or avoidable, and whether surveillance endoscopy is indicated after cholecystectomy.

miR-21, miR-155, miR-192, and miR-375 Deregulations Related to NF-kappaB Activation in Gastroduodenal Fluid-Induced Early Preneoplastic Lesions of Laryngeal Mucosa In Vivo.

UNLABELLED: Gastroduodenal refluxate found in the upper aerodigestive tract is not clinically uncommon. We recently demonstrated the neoplastic potential of gastroduodenal fluids (GDF) on hypopharyngeal mucosa, via NF-κB, using in vitro and in vivo models. Here we will explore the in vivo effect of GDF on laryngeal mucosa (LM) to induce early preneoplastic lesions related to NF-κB activation, along with deregulation of specific microRNA (miRNA) markers previously linked to laryngeal cancer. We used histological, immunohistochemical, automated quantitative analysis and quantitative polymerase chain reaction to examine LM from 35 C57Bl/6J mice previously treated with topical GDF against corresponding controls (4 experimental and 3 control groups; 5 mice/group). Our analysis showed that GDF produced early preneoplastic lesions in treated LM related to NF-κB activation. LM treated by acid and bile combination demonstrated significantly higher expression of the analyzed cell proliferation markers (Ki67, CK14, ∆Np63), oncogenic p-STAT3, and changes of cell adhesion molecules (E-cadherin, ϐ-catenin) versus untreated LM or LM exposed to acid alone (P < .0005). Furthermore, acidic bile but not neutral bile appeared to accelerate the expression of "oncomirs" miR-21, miR-155, and miR-192 (acidic bile versus neutral bile, P < .0001), while reducing tumor suppressor miR-375 (acidic bile versus neutral bile, P = .0137), previously linked to NF-κB and laryngeal cancer. Finally, acidic bile induced reduction of miR-34a, miR-375, and miR-451a, exhibiting an inverse correlation with NF-κB activation. SIGNIFICANCE: Bile in combination with acid has a selective tumorigenic effect on LM, inducing deregulation of "oncomirs" and tumor suppressor miRNAs, produced by NF-κB activation with molecular and early histopathological alterations linked to neoplastic transformation. Systematic acid suppression may in part convey a protective role.

[DISSEMINATION BY H. PYLORI IN PATIENTS, SUFFERING VARIOUS FORMS OF CHOLECYSTITIS].

Comparative analysis of dissemination by H. pylori of the bile portions in patients of a control group, suffering an acute calculous cholecystitis (ACCH), was performed. Dissemination of H. pylori in a control group was significantly less, than in a bile portions of patients, suffering ACCH. While analyzing the rate and degree of dissemination by H. pylori of the gastic and gallbladder mucosa biopsies of patients, suffering chronic non-calculous cholecystitis, associated with duodenogastric reflux and gastroduodenitis, bacteria were revealed trustworthy more often and in more number, than in a gallbladder mucosa in patients, suffering ACCH.

[Gastroesophageal reflux disease in patients receiving chemotherapy: clinical, endoscopic, morphological and immunohistochemical features].

THE PURPOSE OF THE STUDY: Determine the pathogenetic significance of express molecules PCNA, Bcl-2, NF-Kb and tachykinins (substance P, neurokinin A) in patients with gastroesophageal reflux disease (GERD), receiving polychemotherapy (PCT). MATERIALS AND METHODS: In total 60 patients were examined with GERD time-divided into 2 equal groups on the receiving PCT Leukemia over standard dose for at least one year. The first group consisted of 30 subjects with non-erosive GERD (NEGERD) endoscopically positive form receiving PCT. The second group consisted of 30 subjects with erosive form of GERD (EFGERD) receiving PCT. Patients underwent endoscopy, morphological and immunohistochemical examination of the esophageal mucosa to the definition expression of molecules PCNA, Bcl-2, neurokinin A, substance P and factor Nf-Kb. In patients with refractory form of GERD to proton pump inhibitors therapy (PPIs), additionally imposed ursodeoxycholic acid. THE RESULTS: Patients with NEGERD receiving PCT in 33.3% of cases formed refractory to PPIs form of the disease, when EFGERD refractoriness occurs in 46.7% of patients, which is associated with slowing the proliferation of epithelial cells of the esophagus due to decreased expression of PCNA. Reduced expression of neurokinin A in patients receiving PCT is associated with less activity and intensity of inflammation of esophageal mucosa. Against the background of a high degree of PCT expression of Bcl-2 and factor Nf-Kb, which may explain the frequent detection of atrophic and meta- plastic changes in the esophageal mucosa. Appointment of ursodeoxycholic acid in the complex therapy of GERD can overcome resistance to PPIs and improve the performance of cell renewal. CONCLUSION: Due to the frequent development of GERD refractory to PPIs in patients suffering from diseases requiring the appointment of long-term courses of PCT requires the appointment of cytoprotective therapy, as that can be used ursodeoxycholic acid.

[Gastroesophageal reflux disease and connective tissue dysplasia in aspect of premorbid and comorbid disorders].

AIM: To investigate the phenotypic and visceral signs of connective tissue dysplasia (CTD) and comorbid diseases of the digestive system in gastroesophageal reflux disease (GERD) patients with different types of esophageal reflux as the predictors of its variants. MATERIAL AND METHODS: In 124 patients with GERD the clinical features, phenotypic and visceral signs of undifferentiated CTD were studied in details. RESULTS: In 82.0% of patients with GERD associated with gastroesophageal type of reflux (GER) phenotypic and especially visceral signs of STD were detected, mainly in the form of cardiochalasia and hiatal hernia. In patients with duodenogastroesophageal reflux symptoms (DGER) the signs of STD were marked in 42.0% of cases, mostly in the form of biliary tract structure abnormalities. The risk of GERD associated with prevalence of GER, was 11.9 times higher in the presence of diagnostically meaningful combination of 6 or more signs of STD than in patients with DGER. Realization of predictor options in GER occurs in the preference of sharp, acidic foods, spices, taking medications that reduce lower esophageal sphincter tone. GERD, associated with DGER, is formed in patients with family history of diseases of the biliary tract and in the preference of food rich of calories. CONCLUSION: Study of STD symptoms as predictors of structural development of GERD and its variants is prospective to predict disease, choice of profession and eating behavior, primarily in young adults.

The role of duodenogastric reflux in formation of precarcinogenic gastric lesions--an experimental study.

INTRODUCTION: Duodenogastric reflux, commonly encountered as an aftermath of gastroenteroanastomosis, with or without gastric resection (Billroth I, Billroth II), vagotomy and pyloroplastic surgery, is known to cause inflammatory-dystrophic-metaplastic lesions of gastric mucosa. Our objective was to determine the effects of surgery-induced duodenogastric reflux on the development of precarcinogenic lesions or carcinoma in correlation with the reflux duration. MATERIAL AND METHODS: The experiment was performed on three groups of Wistar rats with 1) Billroth II-induced reflux surgery, 2) resection of the Rouxr-en-Y type reconstruction, and 3) control group with no resection. The aim of the experiment was to study the effects ofduodenogastric reflux on the rat gastric mucosa in correlation with two different types of gastroenteroanastomosis 8, 16 and 24 weeks after the surgery. RESULTS: In Billroth II group, hyperplastic changes were observed as early as in week 16. Statistically significant results were recorded in week 24, with 6.7% of metaplastic alterations, including dysplasia of all three degrees, dominantly severe dysplasia in 66.67%, early carcinoma in 20% and gastric carcinoma in 6.67%. In the Roux-en-Y group, gastric mucosa remained predominantly normal (60%), with somewhat increased frequency ofgastritis and dysplasia in week 24. In the control group, the finding of normal gastric mucosa was constant. CONCLUSION: The experiment confirms that direct contact of duodenal juice with gastric mucosa associated with Billroth II resection causes precarcinogenic lesions. Development of adenocarcinoma caused solely by duodenogastric reflux, excluding a carcinogenic agent is possible 20 weeks after the experiment--earlier than suggested by previous researchers.

A flow visualization model of duodenogastric reflux after esophagectomy with gastric interposition.

BACKGROUND: Our goal was to verify surgical factors that affect duodenogastric reflux (DGR) after esophagectomy through the use of a flow visualization model that would mimic an intrathoracic gastric tube. METHODS: Transparent gastric tube models for different routes (retrosternal space [RS] and posterior mediastinum [PM]) were fabricated. Various distal pressures were applied to the experimental model filled with water, and the flow was recorded with a high-speed camera. The volume and maximum height of the refluxate through the pylori of two different sizes (7.5 mm, 15 mm) in two different postures (upright, semi-Fowler) was measured by analyzing the video clips. RESULTS: For the large pylorus setting, when the pressures of 20, 30, and 40 mmHg were applied in the upright position, the volumes of the refluxate in the RS/PM tubes were 87.7 ± 1.1/96.4 ± 1.7 mL, 150.8 ± 1.1/158.0 ± 3.2 mL, and 156.8 ± 3.3/198.0 ± 4.7 mL (p < 0.05), and the maximum heights were 101.6 ± 4.8/113.4 ± 2.9 mm, 151.4 ± 2.2/165.4 ± 1.5 mm, and 166.1 ± 1.7/193.7 ± 6.6 mm (p < 0.05). The data for the small pylorus setting or in the semi-Fowler position showed similar tendencies. For any given route, posture or pressure setting, DGR in the large pylorus model was definitively higher than that for small one. CONCLUSIONS: This fluid mechanics study demonstrates posterior mediastinal gastric interposition or pyloric drainage procedure, or both, is associated with high reflux of duodenal contents.

[Lymph node metastasis in superficial squamous carcinoma of the esophagus]. / Lymphknotenmetastasen bei Plattenepithelfrühkarzinomen des Ösophagus.

The definition of early carcinoma of the esophagus has changed with time on the basis of new data. As from 2007 an early carcinoma is defined as an intramucosal carcinoma with or without metastasis. In the subclassification based on invasion depth, m1 and m2 squamous cell carcinomas have no metastasis and are considered curable by endoscopic resection alone, whereas less than 10% of m3 carcinomas and some 20% of sm1 squamous cell carcinomas have lymph node metastasis. In this article the relationship between various histopathological findings and the incidence of lymph node metastasis is reviewed. The m3 and sm1 superficial squamous cell carcinomas showing 0-I and 0-III types, large tumors over 50 mm in size or those showing vessel permeation have higher incidences of lymph node metastasis. In the field of gastrointestinal surgical pathology pathologists are now expected to not only diagnose the presence or absence of malignancy but also to investigate in detail many of the histological factors related to the prevalence of lymph node metastasis.

[Diagnostic aspects of chronic cholangitis after cholecystectomy].

AIM: To determine the chronic cholangitis risk factors and to provide a practically significant diagnostic criteria of chronic cholangitis in patients after cholecystectomy. MATERIALS AND METHODS: Were examined the clinical, anamnestic data, clinical laboratory and instrumental studies of the condition of the hepatobiliary system in 127 patients with chronic cholangitis after cholecystectomy. The determination of microbial contamination of bile was performed during the duodenal intubation. RESULTS: In the bile microbial landscape study were noted the violation of biliary system microbiota in 92.1% of cases. Herewith identified a combination of bacterial factors with parasitic invasion (mixed infection) in 28 (22.0%) patients. Cholangitis develops in the presence of duodeno biliary reflux, duodenal motility disorders and hypotonia of Oddi's sphincter in the early postoperative period. In the late periods after cholecystectomy, cholangitis chronization defines outflow obstruction and cholestasis due to functional or organic causes in most patients. CONCLUSIONS: Risk factors for chronic cholangitis should be referred to long history of gallstone disease, performance of cholecystectomy in the emergency order against the inflammatory process of thehepatobiliary system, absence of adequate correction of postoperative hypertension of bile duct, destruction of sphincter apparatus major duodenal papilla during surgery.

Effect of PPI (rabeprazole) on reflux esophagitis after total gastrectomy.

BACKGROUND/AIMS: Esophagitis after total gastrectomy has been associated with biliary and pancreatic reflux into the esophagus. The aim is to clarify the effect of PPI (rabeparazole) on these factors in esophagitis. METHODOLOGY: Sixteen 8-week old male Wistar rats underwent total gastrectomy and esophagoduodenostomy to induce esophageal reflux of duodenal juice. In 5 rats, the sham operation induced a midline laparotomy alone. One week following surgery, they were treated with control (saline) or PPI (rabeprazole) (30mg/kg) ip. Three weeks after operation, all rats were euthanized and the esophagus was evaluated histologically. Esophageal injury was evaluated by macroscopic and microscopic findings, and expression of COX2 and PGE2. Esophageal washing was aspirated for the evaluation of bile acid activity. RESULTS: At 3 weeks after surgery, duodenal reflux induced esophageal erosions and ulcer formation as well as marked thickening of esophageal wall. The macroscopic ulcer score and histological ulcer length were significantly reduced by treatment with rabeprazole. The enhanced expression of COX2 and PGE2 in the control group was also markedly inhibited in the rabeprazole treated group. The bile acid activity in the esophageal lumen was significantly increased in the control group and this increase was significantly inhibited in the rabeprazole treated group. CONCLUSIONS: Rabeprazole significantly reduces inflammation and hyperplasia in esophageal mucosa. These results indicate that bile acid, inhibited by rabeprazole, plays an important role in mucosal damage induced by duodenal reflux.

[Clinico-endoscopic peculiarities of gastric ulcer of type I and II].

A detailed analysis of clinico-endoscopic peculiarities of gastric ulcer type I and II was presented. The peculiarities of a clinical course and the complications character of differently localized gastric ulcers were determined. There was shown the connection between concomitant disorders of esophagogastroduodenal motor-evacuation function and gastric ulcer localization and type. While tactics of treatment and operative procedure choosing it is mandatory to take into account the clinical course peculiarities and the results of endoscopic investigation.

Use of selective serotonin reuptake inhibitors and upper gastrointestinal disease.

BACKGROUND: Selective serotonin reuptake inhibitors (SSRIs) are the most widely used antidepressants in the world. Recent studies, however, have raised the concern that SSRIs increase the risk of gastrointestinal dysfunction. Therefore, we conducted a case-control study on gastrointestinal symptoms and endoscopic findings in patients who were taking SSRIs in Japan. METHODS: Forty-one patients who were taking SSRIs (SSRI-treated group) and 82 age- and sex-matched patients who were not taking antidepressants (control group) were selected from the population of patients who underwent endoscopic examination from January 1, 2005 to March 31, 2010 in our institution, and their subjective symptoms and endoscopic findings were analyzed. Patients who were taking proton pump inhibitors (PPIs) and/or histamine H(2)-receptor antagonists (H2RAs) were excluded from this study. RESULTS: The chief complaints at the endoscopic examination were classified into the following 4 categories: reflux symptoms, dysmotility symptoms, ulcer-like symptoms, and no upper abdominal symptoms. No significant difference was found in the complaint rate of each category between the SSRI-treated and the control groups. No significant differences were found between the groups in endoscopic findings, the LANZA score and the rate of chief complaints in patient classes stratified by the endoscopic finding. CONCLUSION: It was not evident that SSRIs induced mucosal damage of the upper gastrointestinal tract. And, it is considered that SSRIs do not increase the risk of upper gastrointestinal symptoms in patients treated with SSRIs for 1 month or longer. The present study suggests that SSRI medication does not have a bad influence on gastrointestinal symptoms and gastrointestinal organic diseases.

[Duodenogastral reflux burden gastroesophageal reflux disease].

The article presents research data of duodenogastral reflux (DGR) role in patients with gastroesophageal reflux disease. It is shown that in the presence DGR, the reflux esophagitis is detected at a higher frequency and outside of esophageal manifestations of the disease. The comorbidities of hepatobiliary zone and pancreas contributes to the DGR development, as well as the syndrome of bacterial overgrowth in the small intestine.

[Morphological features and esophago-gastroduodenal zone microbiocenose in patients with syndrome postcholecystectomic syndrome].

Endoscopical and histological features of oesophagogastroduodenal zone, parameters of pH-metry and electrogastroenterography, qualitative and quantitative characteristics of microbiocenosis were studied in 80 female persons with postcholecystectomy syndrome more then a year after cholecystectomy. In the presence of duodenogastral reflux the most natural is the combination of distal oesophagitis, antral atrophic gastritis and duodenitis, accompanied with low level of gastric acidity, gastric hypokinesis and duodenal dyskinesis, dysbacteriosis of mucosal microflora with its quantitative increase and appearance of bacteria with expressed pathogenicity non-typical for this biotope. These data should be taken into consideration for determination of pre- and postoperative treatment tactics for patients with gallstones.

[The clinical and functional status of the stomach and small intestine in patients with chronic inflammatory bowel diseases concurrent with chronic opisthorchiasis].

To study the impact of Opisthorchis infestation on the upper digestive tract and small bowel in chronic inflammatory bowel diseases, the authors examined 164 patients with inflammatory bowel diseases, including 71 patients with ulcerative colitis and 45 with Crohn's disease without parasitosis and 48 with chronic opisthorchiasis (31 with ulcerative colitis and 17 with Crohn's disease). A control group consisted of 20 healthy individuals and 20 patients with chronic opisthorchiasis. A diagnosis was established by colonofibroscopy and a morphological study of colonic biopsy specimens. Gastric mucosal atrophic changes and motor evacuatory disorders as duodenogastric reflux were significantly more frequently encountered in inflammatory bowel diseases concurrent with chronic opisthorchiasis. The presence of Opisthorchis infestation significantly worsened fat and carbohydrate malabsorption in the small bowel in inflammatory bowel diseases.

[Condition of the gastric mucosa in patients with duodeno-gastric reflux].

The article examines the state of the antral mucosa of the stomach in 43 young patients with duodeno-gastric reflux without any clinical manifestations. In 69.9% of investigated revealed changes in the gastric mucosa, characteristic of reflux gastritis. The comparative characteristic of stereometric indicators of cellular elements, infiltrated own plate of a mucous membrane of a stomach is spent at a reflux-gastritis and the mixed gastritis (at presence Helicobacter pylori). Article is illustrated by 2 tables.