[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 associated with duodenogastroesophageal reflux in patients with biliary pathology: the specific features of the course and esophagogastroduodenal microbial biocenosis].

AIM: To study the specific features of the clinical course of gastroesophageal reflux disease (GERD) associated with duodenogastroesophageal reflux (DGER) in patients with chronic acalculous cholecystitis (CAC) and cholelithiasis (CL), as well as qualitative and quantitative characteristics. SUBJECTS AND METHODS: The clinical, morphological, motor tonic characteristics of the esophagogastroduodenal area, mucosal microbial biocenosis in the esophagus, stomach, and duodenum were studied in detail in 83 patients with GERD that was associated with DGER and ran concurrently with CAC or CL. RESULTS: Impaired duodenal propulsive activity as a concomitance of the signs of gastrostasis and duodenal dyskinesia with dyscoordination of both anthroduodenal and duodenojejunal propulsion and with the development of duodenogastric reflux and DGER, which in turn determine esophageal and gastric pH values is shown to be of importance in CAC and CL, which match GERD. Abnormal microbiocenosis in the upper digestive tract is characterized by the higher quantitative and qualitative content of the mucous microflora. Opportunistic microorganisms exhibit cytotoxic, hemolytic, lecithinase, caseinolytic, urease, and RNAase activities. CONCLUSION: The found specific features of the course of GERD associated with DGER in patients with biliary tract abnormalities lead us to search for novel therapeutic approaches based on the correction of digestive motor tonic disorders and abnormal microbiocenoses of the mucous flora in the esophagus, stomach, and duodenum.

[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.

[Characteristics of duodenogastric reflux in duodenal ulcer patients and its dynamics after Helicobacter pylori eradication].

UNLABELLED: Studying role of duodenogastric reflux (DGR) in pathogenesis and sanogenesis of duodenal ulcer (DU). MATERIAL AND METHODS: 233 DU patients (92 patients with a mild, 45--with modern and 96--with the complicated current of disease) are surveyed. Control group were 100 healthy volunteers. Clinical research, endoscopy and 24-hours pH-metria was carried out. In a year after eradication Helicobacter pylori (Hp) 30 patients are repeatedly surveyed. RESULTS: at healthy acidity more low, and DGR above and more for a long time, than at DU patients. DU was especially supressed at complicated current DU. Eradication Hp was accompanied by acidity normalization only at mild DU, and at complicated DU--is not present. CONCLUSION: at healthy people DGR arises in reply to antrum's acidification and has compensative value, and at DU there is the considerable suppression leading to insufficiency of antrum's alkalization. After eradication Hp normalization DGR is marked only at mild current DU.

[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.

[What contributes to the transformation of Helicobacter pylori from symbiont into the etiopathogenetical factor of duodenal ulcer?].

UNLABELLED: The aim was to study the relationship duodenogastral reflux (DGR) and Helicobacterpylori infection (Hp) at duodenal ulcer (DU). MATERIAL AND METHODS: Group 1-50 patients with uncomplicated course of DU, Group 2-75 patients with destructive complications of DU; Group 3-40 "healthy" volunteers. It was performed daily EGDS, pH meter, semi-quantitative assessment of contamination of the Hp. RESULTS: The acidity in the body of the stomach was highest in group 2, and lowest--in group 3, patients diagnosed DU night rush giperatsidnosti. In the night period patients from the 1st and 3rd groups were recorded an increase of antral pH, including the expense of growth duration of DGR, while in group 2 reflux was extremely short. The maximum Hp dissemination was in a bulb at fetomaternal of DU. CONCLUSIONS: in healthy individuals DGR intragastral involved in the regulation of pH, in patients with uncomplicated DU while reducing the duration of this resonance persists compensation of antral alkalization, and complications throughout the DGR sharply depressed, which is accompanied by severe decompensation alkalization of antrum. Bulbs semination with Hp inversely proportional to the intensity of this resonance.

[Pathogenic effects of primary duodenogastric reflux on gastric mucosa of children].

OBJECTIVE: Duodenogastric reflux (DGR) is a reverse flow of duodenal juice into stomach through pylorus composed of bile acid, pancreatic secretion, and intestinal secretion. The increased entero-gastric reflux results in mucosal injury that may relate not only to reflux gastritis but also esophagitis, gastric ulcers, carcinoma of stomach and esophagus. However, the exact mechanisms of gastric mucosal damage caused by DGR are still unknown. The objective of the present study is to investigate the pathogenic effect of primary DGR on gastric mucosa in children, and to explore the correlation of DGR with clinical symptoms, Hp infection and intragastric acidity. METHOD: Totally 81 patients with upper gastrointestinal manifestations were enrolled and they were graded according to the symptom scores and underwent endoscopic, histological examinations and 24-hour intra-gastric bilirubin was monitored with Bilitec 2000. Of the 81 cases, 51 underwent the 24-hour intra-gastric pH monitoring by ambulatory pH recorder simultaneously. The total fraction time of bile reflux was considered as a marker to evaluate the severity of DGR. The total fraction time of bile reflux was compared between the patients with positive and negative results under endoscopy and histologically, respectively. The correlations of the total fraction time of bile reflux with clinical symptom score, Hp infection, intragastric acidity were analyzed respectively. RESULT: The total fraction time of bile reflux in the patients with hyperemia and yellow stain gastric antral mucosa under endoscopy was significantly higher than that without those changes [17.1% (0.5% approximately 53.2%) vs. 6.5% (0 approximately 58.6%), Z = -1.980, P < 0.05; 19.8% (0.5% approximately 58.6%) vs. 8.8% (0 approximately 38.0%), Z = -2.956, P < 0.01 respectively]. Histologically, the cases with intestinal metaplasia had significantly higher total fraction time of bile reflux than in the cases without intestinal metaplasia [29.0% (1.9% approximately 58.6%) vs. 14.3% (0 approximately 53.7%), Z = -2.026, P < 0.05], but no significant difference was found either between the cases with and without chronic inflammation (P > 0.05) or between the cases with and without active inflammation (P > 0.05). The severity of bile reflux was positively correlated with the score of abdominal distention (r = 0.258, P < 0.05), but no correlation with either the severity of intragastric acid (r = -0.124, P > 0.05), or Hp infection (r = 0.016, P > 0.05) was found. CONCLUSION: Primary DGR could cause gastric mucosal lesions manifested mainly as hyperemia and bile-stained gastric antral mucosa under endoscopy and the gastric antral intestinal metaplasia histologically in children. There was no significant correlation between DGR and gastric mucosal inflammatory infiltration. DGR had no relevance to Hp infection and intragastric acidity. We conclude that DGR is probably an independent etiological factor and might play a synergistic role in the pathogenesis of gastric mucosal lesions along with gastric acid and Hp infection.

Bile reflux index after therapeutic biliary procedures.

BACKGROUND: Therapeutic biliary procedures disrupt the function of the sphincter of Oddi. Patients are potential "bile refluxers". The aim of this study was to assess how these procedures affect the histology-based bile reflux index (BRI), which can be used to reflect duodenogastric reflux (DGR). METHODS: Gastric antrum and corpus biopsies were collected from 131 subjects (56 men, 75 women; mean age, 55.9 +/- 15.6 years). Group 1 (Biliary group-BG; n = 66) had undergone endoscopic sphincterotomy, endoscopic stenting, or choledochoduodenostomy for benign pathology; Group 2 (n = 20) had undergone cholecystectomy alone; and Group 3 (n = 6) Billroth II gastroenterostomy. Group 4 (no cholecystectomy; n = 39) had upper endoscopy with normal findings and served as controls. BRI > 14 indicated DGR (BRI [+]). To eliminate confounding effects of Helicobacter pylori (Hp) infection, comparisons were made according to Hp colonization. RESULTS: Fifty-nine subjects (45%) were Hp (+). The frequencies of BRI (+) status in antrum and corpus specimens from Hp (-) BG patients were 74.3% and 71.4%, respectively (85.7% for both antrum and corpus for choledochoduodenostomy). Corresponding results were 60% and 60% for Group 2, 100% (only corpus) for Group 3, and 57.1% and 38.1% for controls (BG, Group 2, and Group 3 vs controls - p > 0.05 antrum, p < 0.05 corpus). Fifty-four BG patients had previously undergone cholecystectomy. Excluding those, the rates of BRI (+) in Hp (-) BG patients were 75% antrum and 62.5% corpus (p > 0.05 for both vs. Group 2). CONCLUSION: Patients who had undergone biliary procedures showed similar bile-related histological changes in both corpus and antrum biopsies, but the changes seen in controls were more prominent in the antrum than corpus. Therapeutic biliary procedures increase the rate of BRI (+) especially in the case of choledochoduodenostomy. Therapeutic biliary procedures without cholecystectomy also increase the rate of BRI (+) similar to that observed in patients with cholecystectomy.

Effect of duodenogastric reflux on N-methyl-N'-nitro-N-nitrosoguanidine-induced glandular stomach tumorigenesis in Helicobacter pylori-infected Mongolian gerbils.

Both Helicobacter pylori (Hp) and bile acids are gastric carcinogens. An experimental model of duodenogastric reflux in Mongolian gerbils was developed and was used to study the effects of Hp infection and duodenogastric reflux on N-methyl-N'-nitro-N-nitrosoguanidine (MNNG)-induced glandular stomach tumorigenesis independently and synergistically. Male Mongolian gerbils underwent both inoculation with Hp, and had duodenogastric reflux (DR) induced, or neither, followed by MNNG administration. Animals were sacrificed at week 40, and histopathological examination of their excised stomachs and serological investigation were performed. Glandular stomach adenocarcinomas were observed in animals that underwent Hp inoculation and/or induction of DR after MNNG administration, and glandular stomach adenomas were found in animals inoculated with Hp after MNNG administration. The incidence of glandular stomach tumors was significantly higher in animals inoculated with Hp after MNNG administration and in animals undergoing combined Hp inoculation, DR induction and MNNG administration than in animals only administered MNNG. These findings indicate that Hp infection has a stronger tumorigenic effect than the exposure to duodenal contents, and duodenal contents may attenuate the effect of Hp on glandular stomach tumorigenesis.

Relationship between enterogastric reflux estimated by scintigraphy and the presence of Helicobacter pylori.

The aim of the study is assessment of the relationship between enterogastric reflux and the presence of Helicobacter pylori infection as factors that cause gastritis, peptic ulcer and adenocarcinoma ventriculi. The study was performed in 52 patients with different digestive disorders, using gamma camera, during 90 min (1 frame/min) after intravenous injection of 185 MBq 99mTc-dietil IDA in the cubital vein. According to time/activity curves from the region of hepatobiliary system and stomach, index of enterogastric reflux (EGR) was assessed. There was no correlation between the presence of Helicobacter pylori and EGR (r = 0.181, df = 52, p > 0.05). However, Helicobacter pylori was present more frequently in the patients with positive EGR (p < 0.01), but there were no significant differences (p > 0.05) in reflux value in patients with either positive or negative findings of Helicobacter pylori.

[The presence and significance of Helicobacter pylori in patients with enterogastric reflux]. / Prisustvo i znacaj helikobaktera pilori kod bolesnika sa enterogastricnim refluksom.

The aim of the study is assessment of the relationship between enterogastric reflux and the presence of Helicobacter pylori infection as a factors that cause gastritis, peptic ulcer and adenocarcinoma ventriculi. The study was performed in 52 patients with different digestive disorders, using gamma camera, during 90 minutes (1 frame/min) after intravenous injection of 185 MBq 99mTc-dietil IDA in cubital vein. According to time activity curves from the region of hepatobiliary system and gaster, index of enterogastric reflux was assessed (EGR). There is no correlation between the presence of Helicobacter pylori and EGR (r = 0.181, DF = 52, P < 0.05). However, Helicobacter is present more frequently in the patients with positive EGR (p 0.01). However, there is no significant difference (p < 0.05) in reflux value in patients with both positive and negative finding of Helicobacter.

Refluxo duodenogástrico em portadores de colecistolitíase, antes e após a colecistectomia, e prevalência do "Helicobacter pylori" no antro gástrico / Duodenal gastric reflux in cholecystoletiasis carrier state, before and after cholecystectomy, and prevalence of helicobacter pylori in gastric antrum

Foram estudados 34 portadores de litíase vesicular. Verificou-se a prevalência do refluxo duodenogástrico e da colonizaçäo pelo Helicobacter pylori no antro gástrico, antes e após a colecistectomia. No somatório dos casos do pré e pós-operatório foi determinado se a presença de bile refluída para o estômago portador do Helicobacter pylori modificava a prevalência deste no antro gástrico. Concluiu-se que, quando havia bile no estômago, houve diminuiçäo significante na prevalência do Helicobacter pylori no antro gástrico (p<0,05).

Prevalence of Helicobacter pylori infection in 190 control subjects and in 236 patients with gastroesophageal reflux, erosive esophagitis or Barrett's esophagus.

A prospective study was performed in 190 control subjects and in 236 patients with different degrees of endoscopic esophagitis in order to determine the prevalence of Helicobacter pylori infection at duodenal gastric and esophageal mucosa and its correlation with histological findings. All patients with pathologic gastroesophageal reflux had 24-h pH monitoring studies confirming the presence of acid reflux into the esophagus. Besides the endoscopic findings, biopsies were taken from the duodenal bulb, gastric antrum, gastric fundus and distal esophagus or at the specialized columnar epithelium in patients with Barrett's esophagus. Patients with pathological gastroesophageal reflux were divided into three groups: 55 with absence of endoscopic esophagitis (gastroesophageal reflux), 81 patients with erosive esophagitis and 100 patients with Barrett's esophagus. There was no H. pylori infection present at duodenal or esophageal mucosa or at the specialized columnar epithelium of the distal esophagus in any case. The prevalence of H. pylori infection at gastric antrum was similar in controls and in any group of patients with reflux disease (20-25% of H. pylori infection). No differences in age and sex distribution were seen. H. pylori infection at gastric fundus was very low (less than 5%). The presence of HP infections was correlated with the finding of chronic active superficial or athrophic gastritis while, in the absence of H. pylori infection, gastric mucosa was normal. In the presence of intestinal metaplasia, no H. pylori infection occurred. Based on these findings, it seems that there is no significant evidence for an important pathogenic role for H. pylori infection in the development of pathologic chronic gastroesophageal reflux, erosive esophagitis or Barrett's esophagus, and the presence of antral gastritis in patients with Barrett's esophagus is closely related to the presence of H. pylori infection, and probably not related to an increased duodenogastric reflux.

Helicobacter pylori may induce bile reflux: link between H pylori and bile induced injury to gastric epithelium.

Helicobacter pylori and duodenogastric reflux are both recognised as playing aetiological roles in chronic gastritis. This study investigated whether H pylori colonisation of the antral mucosa and duodenogastric reflux are independent phenomena or have a causal relationship. Thirty eight patients (15 men, 23 women) aged (mean (SD)) 48 (17) years participated. Each patient underwent gastroscopy. Antral biopsy specimens were taken to investigate H pylori colonisation. In addition BrIDA-99mTc/111In-DTPA scintigraphy was used to quantify duodenogastric reflux. H pylori positive patients who were found to have duodenogastric reflux were treated with amoxycillin (1 g/d) and metronidazole (1.5 g/d) for seven days and four tablets of bismuth subcitrate daily for four weeks. Follow up antral biopsies and scintigraphy were repeated at six months. Duodenogastric reflux could not be found in 18 patients, including eight (44%) who were H pylori positive. Ten of the 11 patients who had duodenogastric reflux (reflux % 11.6 (9.2)), however, were H pylori positive (chi 2 = 6.26, p = 0.01). These 10 patients were given eradication treatment. At six months, in six patients who became H pylori negative, duodenogastric reflux was significantly reduced from a pretreatment value of 14.3% to 3.3% (two tail, paired t = 2.57, p = 0.016). These data suggest that H pylori may induced duodenogastric reflux which may be important in the pathogenesis of H pylori gastritis or carcinogenesis, or both.

Postoperative alkaline reflux gastritis following vagotomy.

This study was undertaken to evaluate the incidence and severity of postoperative alkaline reflux gastritis in 798 symptomatic duodenal ulcer patients who had undergone vagotomy. The condition was identified on the basis of the unique endoscopic and histological findings in 116 (14.5%) of them. It was more frequent and severe in patients with truncal vagotomy and gastrojejunostomy than in those with truncal vagotomy and pyloroplasty, while it was not at all observed in cases with proximal gastric vago-tomy, the symptoms depended on the preoperative history of the ulcer disease and the patient's age at the time of surgery, but did not always correspond with the degree of histological findings. The location of the gastrojejunostomy and the size of the pyloroplasty stoma had an influence on the incidence of the syndrome. Helicobacter pylori was found more frequently in biopsy specimens from patients with severe symptoms (30.3%), but was present in only 14.6% of the total number of the patients with postoperative alkaline reflux gastritis after vagotomy.

Gastroduodenal dysfunction and bacterial colonisation of the ventilated lung.

The source of ventilator-associated pneumonia (gastric or oropharyngeal flora) remains controversial. We investigated the source of bacterial colonisation of the ventilated lung in 100 consecutive intensive-care patients. Gram-negative bacilli were isolated from the lower respiratory tract in 19 patients. Bacteria isolated from the stomach contents either previously or at the same time were identical to lower respiratory isolates in 11 patients. No gram-negative oropharyngeal isolate was identical to a lower respiratory tract isolate. Gastric bacterial overgrowth with gram-negative bacilli was associated with the presence of bilirubin in the stomach contents. Detectable bilirubin was also associated with subsequent acquisition of gram-negative bacilli in the lower respiratory tract. Only 5 gastric aspirate specimens with pH < 3.5 contained gram-negative bacilli. These results establish a relation between duodenal reflux and subsequent bacterial colonisation of the lower respiratory tract. Restoration of normal gastroduodenal motility might help prevent pneumonia in intensive-care patients.