A study on the roles of Helicobacter pylori in bile reflux gastritis and gastric cancer.

PURPOSE: To observe the infection rates of Helicobacter pylori (HP) in bile reflux gastritis (BRG) and gastric cancer and the clinical significance of HP eradication in BRG and gastric cancer patients complicated with HP. METHODS: 248 patients diagnosed with BRG and gastric cancer via gastroscopy were enrolled in this study. HP detection and infection rates of HP were evaluated. Then, BRG and gastric cancer patients complicated with HP were randomly divided into BRG group 1, BRG group 2, gastric cancer group 1 and gastric cancer group 2. BRG group 1 and gastric cancer group 1 were treated with conventional anti-inflammatory drugs for 10 days, and BRG group 2 and gastric cancer group 2 were treated with anti-HP drugs in addition to conventional anti-inflammatory drugs. One month after drug withdrawal, the infection rates of HP in each group were evaluated, and prognostic follow-up was performed to record the post-therapy patient conditions. RESULTS: HP infection rate was 35.8% (57/159) in the BRG group and 73.0% (65/89) in the gastric cancer group, with statistically significant difference (p<0.01). In patients treated with anti-HP drugs had the HP infection rate effectively reduced. The treatment effective rates of patients with BRG and gastric cancer complicated with HP infection after eradication of HP were 82.8 and 68.8%, respectively, while those of patients with non-eradicated HP were only 46.4 and 37.5 %, respectively. The differences between the two groups were statistically significant (p<0.05). CONCLUSION: HP is directly and closely related to the occurrence of gastric diseases, HP infection rate in patients with gastric cancer is significantly higher than that in patients with BRG, and the treatment of HP can effectively improve the rehabilitation rate in patients with gastric diseases.

The effect of laparoscopic cholecystectomy on the development of alkaline reflux gastritis and intestinal metaplasia.

BACKGROUND/AIMS: Laparoscopic cholecystectomy is the gold standard treatment for symptomatic gallstones. The goal of this study was to investigate the effect of cholecystectomy on alkaline reflux, histopathological changes in the gastric mucosa and H. pylori colonization. METHODOLOGY: Eighty five patients who had undergone laparoscopic cholecystectomy were included in this trial (20 males; 65 females; 44.97 ± 11.22 years). All the patients had an upper gastrointestinal endoscopy before and 6 months after the surgery and biopsies in the antrum and corpus were taken to investigate the mucosal changes and assay for the presence of H. pylori. RESULTS: At 6 months post-surgery, the presence of bile in the fasting gastric fluid and an increase in the endoscopic gastritis findings were detected. While none of the patients had chemical gastritis prior to surgery, 7 patients were diagnosed with this condition after surgery. Intestinal metaplasia was detected in 6 patients prior to surgery and 20 patients after surgery. H. pylori was observed in 64 patients before surgery and 52 patients after surgery. CONCLUSIONS: An increase in duodenogastric reflux, alkaline reflux gastritis and intestinal metaplasia, and a reduction in H. pylori colonization were observed to occur post-cholecystectomy.

Cholangitis: bacterial virulence factors that facilitate cholangiovenous reflux and tumor necrosis factor-alpha production.

In previous studies we noted that biliary bacteria produce slime and possess P1-fimbriae. The presence of gram-negative bacteria killed by complement correlated with serious biliary infections and induced more tumor necrosis factor-alpha (TNF-alpha) production in sera, suggesting a role for cytokine production and complement activation in biliary sepsis. This study examined bacterial virulence factors that facilitate cholangiovenous reflux (CVR) and TNF-alpha production in a rat model. Twenty-one biliary bacteria and two stool isolates were tested for slime production, sensitivity to complement killing, and hemolysin production. 10(7) Bacterial colony-forming units/ml (or saline control) were injected retrograde into the common bile ducts of Sprague-Dawley rats at a pressure of 30 cm H(2)O. Blood was obtained at 5 and 60 minutes after infusion for bacterial culture and TNF-alpha assay, respectively. The magnitude of slime production correlated inversely with the magnitude of bacterial CVR. Average bacterial colony-forming units were 1.4 x 10(5), 6.8 x 10(4), or 2.1 x 10(3) for bacteria with slime production 0 to 10, 11 to 99, or more than 100, respectively (P < 0.0001, analysis of variance). CVR was greater for serum-resistant bacteria (1.2 x 10(5) vs. 5.5 x 10(4) [P = 0.007, resistant vs. sensitive]), but TNF-alpha production was greater in serum-sensitive bacteria. TNF-alpha production as a function of bacterial reflux followed a logarithmic curve (R(2) = 0.75) for serum-sensitive bacteria but was linear (R(2) = 0.60) for serum-resistant bacteria. These data show how specific virulence factors explain why some bacterial species colonize without causing illness, whereas others colonize and cause sepsis. Although slime production was necessary for colonization, too much slime inhibited CVR. Although complement killing cleared bacteria from the circulation, it was also associated with increased TNF-alpha production, which can lead to septic manifestations. The most virulent bacterial species (from patients with sepsis) were killed by complement, but they still had significant CVR and were associated with increased TNF-alpha production.

Bile acid reflux and possible inhibition of Helicobacter pylori infection in subjects without gastric surgery.

Bile acids are generally known to inhibit growth of Helicobacter pylori in vitro, but whether they do so in humans with no gastric surgery has been uncertain. The present study addresses this issue. Among healthy control subjects with preserved acid secretion, H. pylori-positive subjects were older and had lower gastric bile acid concentrations than H. pylori-negative subjects (P < 0.05). Among gastric ulcer patients with preserved acid secretion, H. pylori-positive patients had a higher basal acid output than H. pylori-negative patients (P < 0.05). Among H. pylori-positive subjects with preserved acid secretion, duodenal ulcer patients had a higher basal and maximum acid output than healthy control subjects (P < 0.01). In conclusion, gastric bile acids may suppress initial stages of H. pylori infection in subjects without gastric surgery. However gastric bile acids may have little effect on peptic ulcer disease, once H. pylori infection is established.

Gastric pathology in cholecystectomy patients: role of Helicobacter pylori and bile reflux.

The data regarding the role of Helicobacter pylori infection in patients with bile reflux are conflicting. Bile reflux is often observed after cholecystectomy. This study focuses on the role of H. pylori in gastric pathology of patients who had undergone cholecystectomy. Eighty-seven consecutive patients were included in the study. An upper gastrointestinal endoscopy was performed, and biopsy specimens were taken in the antrum, incisura angularis, and in the gastric body. The presence of bile reflux in gastric fluid at endoscopic examination was recorded. The overall H. pylori infection rate was 62%, with no difference between patients with (59.7%) and without (64%) endoscopic bile reflux (p = 0.67). The intestinal metaplasia rate in gastric mucosa was significantly higher in patients with both H. pylori and bile reflux than in patients without infection and bile reflux (36.4% vs. 5.6%, p = 0.02). Moreover, the mean number of years after cholecystectomy in patients with intestinal metaplasia was significantly higher than in those without metaplasia (21.1 +/- 7 vs. 11.5 +/- 8 years, p < 0.0001), whereas mean age did not differ significantly between groups (60.3 +/- 12 vs. 55.8 +/- 11 years, p = 0.14). Furthermore, we found four cases of gastric cancer, three with H. pylori infection. The mean number of years after cholecystectomy was significantly higher in patients with gastric cancer than in other patients (21.8 +/- 4 vs. 12.2 +/- 8 years, p = 0.009). This study found that H. pylori infection is frequent in cholecystectomized patients, also in the presence of endoscopic bile reflux. Bile reflux seems to act synergistically with H. pylori infection on gastric pathology.

Routes of spread of pathogens into the pancreas in a feline model of acute pancreatitis.

The routes of spread of pathogens into the pancreas in acute pancreatitis were investigated. Four experiments were performed: (1) cats with and without acute pancreatitis were given 10(7) Escherichia coli (E coli) intravenously, (2) in cats with acute pancreatitis 10(8) E coli was placed in the colon. In half of them the colon was then enclosed in an impermeable bag to prevent transmural spread. (3) E coli (10(4)) was placed in the pancreatic duct in cats with and without acute pancreatitis. (4) In cats with acute pancreatitis 10(5) E coli was placed in the gall bladder. In half of them the common bile duct was ligated to prevent biliary-pancreatic reflux. After 24 hours, intravenous E coli infected the pancreas in six of nine cats with acute pancreatitis and three of 10 controls. After 72 hours E coli spread to the pancreas from the colon in six of nine cats with acute pancreatitis. This was prevented by enclosing the colon in an impermeable bag (p = 0.02). In five of six cats with acute pancreatitis and five of six controls E coli placed in the pancreatic duct colonised the pancreas within 24 hours. Pancreatic colonisation from the gall bladder occurred in five of six cats with a patent common bile duct and in three of six with an obstructed common bile duct. In conclusion, in cats E coli can spread to the pancreas by the blood stream, transmurally from the colon, and by reflux into the pancreatic duct.

Observations on gastric histology, endoscopy appearance and Helicobacter pylori after corrective surgery for bile reflux gastritis.

This study was designed to look for the presence of Campylobacter pylori in patients who had Roux-en-Y procedure to control symptoms of severe alkaline reflux gastritis (ARG) and to correlate findings with endoscopy and histology. Twenty five patients, who had been operated on for ARG during the last 15 years, were recruited into this study (mean age: 53 years). Surgical procedures were performed by a single surgeon (K.B.). Clinical symptoms of ARG improved after corrective surgery in all cases, but endoscopic pictures remained abnormal in 14 of 25 patients and histological gastritis was observed in all cases. Helicobacter pylori were detected in 8 patients using an urease test performed on gastric mucosa biopsies (CLO-Gistbrocades test). All 8 patients had their biliary diversion 10 or more years earlier, suggesting that H-pylori colonisation of the gastric mucosa develops only slowly once the bile reflux has been stopped. Longitudinal studies, looking for the presence of H-pylori in postoperative stomachs, may help in determining whether they have a role in the aethiology of the peptic ulcer and gastritis, or whether it really is only an innocent bystander.

Effect of Roux-en-Y biliary diversion on Campylobacter pylori.

To assess the effect of biliary diversion on gastric colonization by Campylobacter pylori, we undertook a retrospective histologic study of 24 patients with symptomatic bile reflux after peptic ulcer surgery, who had endoscopic gastric biopsies performed before and after a Roux-en-Y operation. The time interval between the preoperative and postoperative endoscopic examinations ranged from 0.8 to 9.8 yr (mean 4.7 yr). The partial gastrectomy specimen, which had been resected at the initial operation, was available for assessment in 12 patients (50%). Biopsy specimens were assessed for the presence of C. pylori and scored for severity of reflux gastritis by the use of a histologic grading system. Ten of the 12 partial gastrectomy specimens (83%) were C. pylori-positive. Only 13 of the 24 patients (54%) were C. pylori-positive before the Roux-en-Y operation, rising to 22 (92%) after biliary diversion (p = 0.008). The median reflux score was 6 in the partial gastrectomy specimens; it rose to 11 before the Roux-en-Y operation and fell again to 6 after biliary diversion (p less than 0.001). These results suggest that C. pylori may recolonize the gastric remnant after biliary diversion.

Campylobacter-like organisms and gastritis: histopathology, bile reflux, and gastric fluid composition.

We studied a prospective series of 107 randomly chosen dyspepsia patients without gastric ulcer for the association of spiral Campylobacter-like organisms (CLO) with features of antral and fundal gastritis and duodenogastric reflux. CLO were observed in 38% of the patients. The scores for all classes of inflammatory cells in both antral and body mucosa were significantly higher in the CLO-positive patients than in the CLO-negative ones (p less than 0.001), and foveolar hyperplasia was also associated with CLO (p less than 0.05). Metaplasia and glandular atrophy in the antral mucosa were significantly commoner in the CLO-positive group (p less than 0.05 and p less than 0.01, respectively). The body gastritis score correlated significantly with age in the CLO-negative patients (R = 0.33, p less than 0.01) but not in the CLO-positive ones. There were no significant differences between the groups with regard to duodenogastric reflux or intragastric pH. The results confirm that CLO are associated with gastritis, most notably superficial gastritis in the body and atrophic gastritis in the antrum, but their aetiological significance remains to be proved.

Reflux gastritis syndrome. Role of upper gastrointestinal microflora.

Bacteriologic samplings of the upper gastrointestinal tract bile acids profile of the intestinal contents were performed in eight patients with reflux gastritis syndrome and three asymptomatic patients who had had gastric surgery. All symptomatic patients showed colonization of the gastric and/or intestinal samples with strains of enteric Gram-negative bacteria and Pseudomonas. However, no single specific group or species was consistently associated with reflux gastritis syndrome. The concentration of total and conjugated bile acids was significantly greater in symptomatic patients. Presence of free bile acids was correlated with heavier bacterial colonization. To evaluate the effect of antibiotic therapy on bacterial flora and symptoms, patients were studied for three separate four-week evaluation periods. Following the first evaluation period, they were assigned to receive either doxycycline or placebo in a crossover fashion during the second and third periods. Total symptom scores did not differ significantly and no specific patterns were evident in the bacterial flora. These observations support the hypothesis that microbial flora is an associated factor in reflux gastritis syndrome and may play an important role only in certain individual patients.