Helicobacter pylori induces gastritis and oxidative stress after distal gastrectomy

BACKGROUND/AIMS: Helicobacter pylori is a carcinogen for gastric cancer. There have been few reports on carcinogenesis about H. pylori infection in the gastric remnant after distal gastrectomy. The relationship between carcinogenesis and H. pylori infection was studied by means of inflammation and oxidative stress. METHODOLOGY: Ninety-seven patients who had undergone curative distal gastrectomy for gastric cancer were studied. All patients underwent endoscopic examination 3 months after surgery. The presence of H. pylori was determined using urease rapid test, hematoxylin-eosin staining, and immunohistochemical staining. Fifty-one patients were positive (group A) and 46 patients were negative (group B). The grades of remnant gastritis were scored by updated Sydney System. 8-Hydroxydeoxyguanosine (8-OHdG) as an oxidative stress marker, was analyzed immunohistochemically, and graded in 4 grades. RESULTS: Both the neutrophil infiltration score and 8-OHdG expression score was higher in group A than group B (p = 0.03 and 0.05). The correlation between the 8-OHdG expression score and the neutrophil infiltration score was significant (p = 0.02). CONCLUSIONS: As gastritis is related to oxidative stress, H. pylori infection is suspected to play an important role in carcinogenesis in the gastric remnant.     

Duodenogastric reflux eradicates Helicobacter pylori after distal gastrectomy

BACKGROUND/AIMS: Patients who undergo distal gastrectomy often develop duodenogastric reflux and preoperative H. pylori infection is eradicated spontaneously after distal gastrectomy in some patients. However, whether a causal relationship exists has not yet been studied. This report examines the correlation between H. pylori eradication and the amount of duodenogastric reflux following distal gastrectomy. METHODOLOGY: Among 72 consecutive patients who underwent curative distal gastrectomy with radical lymphadenectomy for gastric cancer, 37 patients had H. pylori infection preoperatively and were included in this study. The period of bile reflux (percent time) into the gastric remnant was measured with the Bilitec 2000 under standardized conditions on the 14th day after the surgery. Endoscopic examination was performed to determine the presence of H. pylori infection on week 12 after surgery. RESULTS: The percent time was higher in patients whose H. pylori infection had been eradicated after distal gastrectomy (58.1+/-9.2%) than in patients who had H. pylori infection after distal gastrectomy (33.8+/-5.7%). CONCLUSIONS: Duodenogastric reflux correlates with spontaneous eradication of H. pylori infection following distal gastrectomy.     

Effect of H. pylori on COX-2 expression in gastric remnant after distal gastrectomy

BACKGROUND/AIMS: Helicobacter pylori infection is known to induce gastritis, oxidative stress, and cyclooxygenase (COX)-2 expression in the gastric mucosa. However, the effect of H. pylori infection on remnant gastritis has not been studied. We investigated whether the severity of remnant gastritis and COX-2 expression were affected by H. pylori infection after distal gastrectomy. METHODOLOGY: The study included 97 patients with gastric cancer who underwent curative distal gastrectomy with lymphadenectomy in our department between May 1999 and April 2001. All patients underwent endoscopic examination 2 weeks before and 12 weeks after surgery. The presence of H. pylori infection was determined by urease activity, hematoxylin-eosin staining, and immunochemical staining. Histologic remnant gastritis was graded based on the degree of neutrophil infiltration using the updated Sydney System. COX-2 expression was estimated immunohistochemically. RESULTS: Both the degree of neutrophil infiltration and the level of COX-2 expression were significantly higher in patients with than without H. pylori (p<0.05). There was a significant correlation between the degree of neutrophil infiltration and the degree of COX-2 expression (p<0.001). CONCLUSIONS: H. pylori eradication may become a treatment for preventing both remnant gastritis as well as remnant gastric carcinoma after distal gastrectomy.     

Reconstructive procedure after distal gastrectomy to prevent remnant gastritis

BACKGROUND/AIMS: Gastroduodenostomy (Billroth I) or gastrojejunostomy (Billroth II) after distal gastrectomy is associated with duodenogastric reflux and remnant gastritis. This study sought to determine which reconstructive procedure is least likely to cause remnant gastritis and to determine the correlation between duodenogastric reflux and remnant gastritis. METHODOLOGY: Sixty patients who underwent curative distal gastrectomy for gastric cancer were classified into three groups by reconstructive procedure: group A, Roux-Y (n=18); group B, Billroth I (n=25); group C, Billroth II (n=17). Intragastric bile reflux was monitored using the Bilitec 2000 14 days after surgery, and endoscopy was performed and a patient questionnaire was completed 12 weeks after surgery. RESULTS: Bile reflux occurred in 23.9%, 40.4%, and 73.4% of the time (p<0.001), and remnant gastritis developed in 33%, 76%, and 100% of patients (p<0.001), in groups A, B, and C, respectively. Helicobacter pylori infection did not correlate with remnant gastritis (p=0.57). Symptoms following Roux-Y reconstruction were comparable to those following Billroth I and II reconstructions. CONCLUSIONS: Roux-Y reconstruction following distal gastrectomy is superior to Billroth I and II reconstruction in preventing remnant gastritis because it reduces duodenogastric reflux.     

胆汁反流和幽门螺杆菌感染在远端胃切除术后残胃炎发生中的作用

胆汁反流和幽门螺杆菌（H．pylori）感染是远端胃切除术后残胃炎发生的致病因素，但其确切的作用机制尚未明了。目的：明确胆汁反流和H．pylori感染与远端胃切除术后残胃黏膜炎症的相关性。方法：调查281例胃远端切除术后1年以上接受内镜随访的患者，除外胃镜检查发现恶性肿瘤者。内镜下观察残胃炎严重程度；根据炎症和活动性等指标评估残胃黏膜组织学严重程度。观察胆汁反流和H．priori感染对残胃炎内镜下表现和组织学炎症的影响。结果：81．1％的患者具有1级和1级以上程度的内镜下残胃炎，其H．pylori感染率和胆汁反流发生率均显著高于内镜下无明显炎症的患者（分别为20．6％对1．9％，P〈0．01和88．6％对24．5％，P〈0．0001）。有明显胆汁反流的各级残胃炎患者，胃黏膜慢性炎症和活动性程度与无明显胆汁反流的患者相比无显著性差异（P均〉0．05）；但伴有H．pylori感染的各级残胃炎患者，炎症和活动性分数均显著高于H．pylori阴性患者（P均〈0．05）。结论：远端胃切除术后胆汁反流发生率高，而H．pylori感染率降低。胆汁反流加重残胃炎内镜下炎症，而H．pylori感染与残胃炎内镜下和组织学炎症均相关。     

Role of bile reflux and Helicobacter pylori infection on inflammation of gastric remnant after distal gastrectomy

OBJECTIVE: The influence of the main pathogenic factors on remnant gastritis is still to be evaluated. The aim of this study was to investigate the role of bile reflux and Helicobacter pylori infection on endoscopic inflammation and histological changes of gastric remnant after distal gastrectomy. METHODS: A total of 281 patients with a more than 1‐year history of distal gastrectomy were retrospectively involved after excluding those with tumors and ulcers on endoscopy. The severity of endoscopic remnant gastritis and bile reflux were recorded during the endoscopy. The histological changes including chronic inflammation, activity, atrophy, intestinal metaplasia and H. pylori were evaluated independently. RESULTS: An endoscopic inflammation of remnant gastric mucosae was found in 81.1% (228/281) of the patients. The prevalence of H. pylori infection and bile reflux in patients with endoscopic remnant gastritis was more common than in those without gastritis (21.5%vs 0%, 88.6%vs 24.5%, P < 0.0001). The score of histological chronic inflammation was significantly higher in patients with bile reflux than in those without obvious bile reflux (1.65 vs 1.45, P = 0.02). Chronic inflammation (1.82 vs 1.57), activity (0.78 vs 0.34), atrophy (0.67 vs 0.41) and intestinal metaplasia (0.67 vs 0.27) in H. pylori‐positive patients were all significantly more severe than in H. pylori‐negative patients. CONCLUSION: Bile reflux and H. pylori infection exacerbates the severity of endoscopic remnant gastritis and chronic histological inflammation.     

The affect of Helicobacter pylori and bile acids as the pathogenesis of gastritis of the remnant stomach after distal partial gastrectomy]

AIMS: After distal partial gastrectomy with Billroth I reconstruction, gastritis of the remnant stomach was previously considered to be caused by bile reflux. However, since in 1982, Helicobacter pylori (HP) was discovered and it was found that this organism caused for many types of stomach diseases. The affect of HP must also be examined in the remnant stomach. In a current study, we examined the existence of HP and explored bile reflux as a pathogenesis of gastritis of the remnant stomach after distal partial gastrectomy. PATIENTS AND METHODS: The subjects were 56 patients who underwent gastrectomy. The existence of HP was investigated before and after gastrectomy. At postoperative gastroscopy, we examined histological findings of remnant gastritis and total bile acid (TBA) concentration in the gastric juice. Then we assessed the effect of HP and TBA on gastritis regarding the time after gastrectomy. RESULT: HP was positive in 75% of the patients before the operation and in 37.5% after the operation. The HP positive ratio was significantly lower in patients more than 5 years after gastrectomy than in those within 5 years. Inflammatory cell infiltration of the remnant gastric mucosa was more prominent in HP positive patients than in HP negative patients. In HP positive remnant stomachs, the TBA concentration of the gastric juice was lower than in HP negative remnant stomachs. CONCLUSION: Within 5 years after distal partial gastrectomy, gastritis of the remnant stomach was mainly caused by HP.     

Inflammation of the gastric remnant after gastrectomy: mucosal erythema is associated with bile reflux and inflammatory cellular infiltration is associated with Helicobacter pylori infection

Background Controversy exists concerning the role of bile reflux and Helicobacter pylori (H. pylori) infection in the development of inflammation of the gastric remnant after gastrectomy. This study was designed to investigate association of bile reflux and H. pylori infection or both with inflammatory changes in the gastric remnant.Methods A questionnaire on GI symptoms was returned by 200 gastrectomy patients, and 24-h bilirubin monitoring in the gastric remnant was performed on 55 patients with Bilitec 2000. Upper GI endoscopy evaluated reflux gastritis in the gastric remnant, and the presence of H. pylori infection and chronic, active inflammatory cellular infiltration in the biopsy specimens were examined microscopically with the updated Sydney system.Results No difference in the incidence of GI symptoms was observed among individual gastrectomy patients. Bile reflux was lower in patients who had undergone a gastrectomy with jejunal interposition, a pylorus-preserving gastrectomy, and a gastrectomy with Roux–Y anastomosis than those who had undergone a Billroth-II (B-II) anastomosis (P < 0.05). Endoscopy showed positive correlation between mucosal erythema and bile reflux (P < 0.001). No correlation was observed between the mucosal erythema and chronic and active inflammatory cellular infiltration. Infection of H. pylori correlated with chronic and active inflammatory cellular infiltration (P < 0.001). Bile reflux did not correlate with the severity of chronic and active inflammatory cellular infiltration or H. pylori infection.Conclusions Bile reflux into the gastric remnant was observed by Bilitec 2000. Mucosal erythema and chronic, active inflammatory cell infiltration in the gastric remnant after gastrectomy may be caused by bile reflux or H. pylori infection, respectively.     

Gastro-oesophageal reflux and duodenogastric reflux before and after eradication in Helicobacter pylori gastritis

OBJECTIVE: Helicobacter pylori and duodenogastric reflux (DGR) are both associated with chronic gastritis, peptic ulcer and gastric cancer. The nature of their interrelationship remains unclear. H. pylori eradication has also been reported to result in new or worsening acid gastro-oesophageal reflux (GOR). The aim of this study was to investigate the relationship between GOR, DGR and H. pylori infection. METHOD: 25 patients with H. pylori gastritis underwent ambulatory 24-hour oesophageal and gastric pHmetry and gastric bilirubin monitoring before and 12 weeks after H. pylori eradication, confirmed by 14C urea breath testing (UBT). Ten healthy subjects served as a control group. RESULTS: There were no differences between patient and control groups for gastric alkaline exposure or gastric bilirubin exposure (P> 0.25 in all categories). Oesophageal acid reflux was higher in the study group (P< 0.02). No differences were detected in oesophageal acid reflux, gastric alkaline exposure, or gastric bilirubin exposure (P = 0.35, 0.18 and 0.11, respectively) before and after eradication. CONCLUSIONS: Acid GOR is not increased by H. pylori eradication. DGR in patients with H. pylori gastritis is similar to that in healthy, non-infected subjects. H. pylori eradication produces no change in GOR or DGR. In patients with chronic gastritis, H. pylori infection and DGR appear to be independent of each other.     

Mucosal changes in the gastric remnant: long-term effects of bile reflux diversion and Helicobacter pylori infection

OBJECTIVE: Bile reflux is thought to be responsible for reflux gastritis and stump carcinoma occurring after partial gastrectomy for peptic ulcer. Gastritis and gastric carcinoma are also correlated with Helicobacter pylori. The aim of this study was to investigate whether diversion of enteric reflux and the presence of H. pylori infection alter long-term histological developments in the gastric remnant. METHODS: Twenty-nine patients partially gastrectomized for peptic ulcer were reoperated on with re-resection and a Roux-en-Y reconstruction because of reflux gastritis (12 patients) or severe dysplasia/early gastric cancer (17 patients). The resected specimens and subsequent biopsies from the new anastomotic region taken at endoscopies 5-17 years after reoperation were evaluated regarding the presence of H. pylori, the grade of active and non-active chronic gastritis, and the premalignant changes--atrophy, intestinal metaplasia and dysplasia. RESULTS: A progression of active chronic gastritis, atrophy, intestinal metaplasia and dysplasia was seen after re-resection and Roux-en-Y reconstruction. Non-active chronic gastritis remained unchanged. The development was, in general, independent of H. pylori infection. CONCLUSIONS: Enteric reflux may perhaps induce a histological transformation of the gastric mucosa that cannot be reversed, even if the reflux is diverted. In our study, H. pylori infection had no impact on the histological development. Factors other than enteric reflux and H. pylori infection might also be of importance.     

Expression of 8-hydroxydeoxyguanosine in the gastric remnant after distal gastrectomy

BACKGROUND/AIMS: The correlation between remnant gastritis after distal gastrectomy for gastric cancer and expression of 8-hydroxydeoxyguanosine (8-OHdG) and inducible oxide synthase (iNOS) as a marker of oxidative DNA damage was investigated. METHODOLOGY: Ninety-seven patients who had undergone curative distal gastrectomy for gastric cancer were studied. Reconstructive procedures included Billroth I, Billroth II, and Roux-Y reconstruction in 42, 27, and 28 patients, respectively. Histologic and immunohistochemical analyses were performed on biopsy specimens of the gastric mucosa obtained endoscopically within 2 weeks before and 12 weeks after surgery. The grades of remnant gastritis were evaluated according to the updated Sydney System. 8-OHdG and iNOS expression levels, detected immunohistochemically, were graded. RESULTS: Neutrophil infiltration correlated with expression of 8-OHdG (p = 0.02). Expression of iNOS also correlated with 8-OHdG (p = 0.02). The ratio of postoperative to preoperative infiltration of neutrophils was less in patients who underwent Roux-Y reconstruction than in others (p = 0.04). CONCLUSIONS: These results suggest that remnant gastritis possibly causes DNA damage. Excess production of reactive oxygen species correlates with carcinogenic DNA changes. Roux-Y reconstruction may reduce carcinogenesis in the gastric remnant.     

Helicobacter pylori in gastric corpus of patients 20 years after partial gastric resection

AIM: To determine the long-term prevalence of Helicobacter pylori (H pylori) gastritis in patients after partial gastric resection due to peptic ulcer, and to compare the severity of H pylori-positive gastritis in the corpus mucosa between partial gastrectomy patients and matched controls. METHODS: Endoscopic biopsies were obtained from 57 patients after partial gastric resection for histological examination using hematoxylin/eosin and Warthin-Starry staining. Gastritis was graded according to the updated Sydney system. Severity of corpus gastritis was compared between H pylori-positive partial gastrectomy patients and H pylori-positive duodenal ulcer patients matched for age and gender. RESULTS: In partial gastrectomy patients, surgery was performed 20 years (median) prior to evaluation. In 25 patients (43.8%) H pylori was detected histologically in the gastric remnant. Gastric atrophy was more common in H pylori-positive compared to H pylori-negative partial gastrectomy patients (P<0.05). The severity of corpus gastritis was significantly lower in H pylori-positive partial gastrectomy patients compared to duodenal ulcer patients (P<0.01). There were no significant differences in the activity of gastritis, atrophy and intestinal metaplasia between the two groups. CONCLUSION: The long-term prevalence of H pylori gastritis in the gastric corpus of patients who underwent partial gastric resection due to peptic ulcer disease is comparable to the general population. The expression of H pylori gastritis in the gastric remnant does not resemble the gastric cancer phenotype.     

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.     

Helicobacter pyloriin gastric corpus of patients 20 years after partial gastric resection

AIM:To determine the long-term prevalence of Helicobacterpylori(H pylori)gastritis in patients after partial gastricresection due to peptic ulcer,and to compare the severityof Hpylori-positive gastritis in the corpus mucosa betweenpartial gastrectomy patients and matched controls.METHODS:Endoscopic biopsies were obtained from 57patients after partial gastric resection for histologicalexamination using hematoxylin/eosin and Warthin-Starrystaining.Gastritis was graded according to the updatedSydney system.Severity of corpus gastritis was comparedbetween Hpylori-positive partial gastrectomy patients andHpylori-positive duodenal ulcer patients matched for ageand gender.RESULTS:In partial gastrectomy patients,surgery wasperformed 20 years(median)prior to evaluation.In 25patients(43.8%)Hpyloriwas detected histologically inthe gastric remnant.Gastric atrophy was more common inH pylori-positive compared to H pylori-negative partialgastrectomy patients(P<0.05).The severity of corpusgastritis was significantly lower in Hpylori-positive partialgastrectomy patients compared to duodenal ulcer patients(P<0.01).There were no significant differences in theactivity of gastritis,atrophy and intestinal metaplasiabetween the two groups.CONCLUSION:The long-term prevalence of Hpylorigastritisin the gastric corpus of patients who underwent partialgastric resection due to peptic ulcer disease is comparableto the general population.The expression of Hpylorigastritisin the gastric remnant does not resemble the gastric cancerphenotype.     

Duodenal ulcer, Helicobacter pylori, and gastric secretion.

Patients with chronic dyspepsia were categorised by macroscopic appearance at oesophagogastroduodenoscopy as having duodenal ulceration (DU), other diagnosed lesions such as reflux oesophagitis, carcinoma of stomach, etc, or no organic lesion (non-ulcer dyspepsia, NUD). Material was collected to identify gastric infection with Helicobacter pylori (H pylori) by CP urease test, culture, and histological examination and to make the microscopic diagnosis of active chronic gastritis. Each patient in the DU and NUD categories was then invited to volunteer for a gastric secretion study in which maximal gastric secretion in response to histamine was measured. Sixty two gastric secretion tests were performed (31 DU, 31 NUD). The presence of H pylori was associated with active chronic gastritis (100%). DU patients secreted more acid than the NUD patients. H pylori positivity was associated with decreased maximal gastric secretion in both groups. There was a positive correlation between smoking and maximal acid output shown only in H pylori negative but not in H pylori positive patients. These findings were clear cut when all corrections of maximal gastric secretion were made for pyloric loss, duodenogastric reflux, and stature. This study failed to show any aetiological link between H pylori and DU by increased maximal gastric secretion.     

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.     

Correlation between CD4, CD8 cell infiltration in gastric mucosa, Helicobacter pylori infection and symptoms in patients with chronic gastritis

AIM: To evaluate the correlation between CD4, CD8 cell infiltration in gastric mucosa, Helicobacter pylori(H pylori) infection and symptoms or the assemblage of symptoms in cases with chronic gastritis. METHODS: Biopsy samples at the gastric antrum were obtained from 62 patients with chronic gastritis. CD4 and CD8 cell infiltration was evaluated by immunohistochemical assays on frozen sections of the biopsy samples. Fifteen symptoms referring to digestion-related activity and non-digestion related activity were observed. The correlation between lymphocyte infiltration and each symptom or symptom assemblage was analyzed by logistic regression and K-mean cluster methods. RESULTS: CD4 cell infiltrations in gastric mucosa were much more in patients with H pylori infection, while CD8 cell infiltrations were similar in patients with or without H pylori infection. Logistic regression analysis showed that the symptoms including heavy feeling in head or body (t = 2.563), and thirst (t = 2.478) were significantly related with CD4 cell infiltration in gastric mucosa (P<0.05), and cool limbs with aversion to cold were related with CD8 cell infiltration (t = 2.872, P<0.05). Further analysis showed that non-digestive related symptom assemblage could increase the predicted percentage of CD4 and CD8 cell infiltration in gastric mucosa, including lower CD4 infiltration by 12.5%, higher CD8 infiltration by 33.3%, and also non-H pylori infection by 23.6%. K-means cluster analysis of all symptoms and CD4 and CD8 cell infiltration in gastric mucosa showed a similar tendency to increase the predicted percentage of CD4, CD8 cell infiltration and H pylori infection. CONCLUSION: Based on correlation between the gastric mucosa lymphocyte infiltration, H pylori infection and clinical symptoms, symptoms or symptomatic assemblages play an important role in making further classification of chronic gastritis, which might help find a more specific therapy for chronic gastritis.     

Prospective comparative study of the influence of postoperative bile reflux on gastric mucosal histology and Campylobacter pylori infection.

Biopsies of 17 peptic ulcer patients, randomly treated by partial gastrectomy with either Billroth-II (n = 9) or Roux-en-Y (n = 8) anastomosis were studied before and six months after surgery to determine the role of bile reflux in the early postoperative histological alterations of the gastric mucosa. After BII-gastrectomy bile acid reflux (median 16.1 mumol/h) was significantly higher (p less than 0.0001) than after RY-gastrectomy (0.1 mumol/h). Campylobacter pylori was present in the preoperative biopsies of all 17 patients. After RY-gastrectomy biopsies of all eight patients were positive for Campylobacter pylori, but was detected in only five of the nine patients with BII-gastrectomy. Preoperative scores of gastritis grading were similar in both groups and no significant differences were found postoperatively. Gastritis scores of the anastomotic mucosa in patients with BII-gastrectomy were significantly higher (p less than 0.02) than in the RY-gastrectomy group. Moreover, the reflux gastritis score in the four BII-gastrectomy patients cleared from Campylobacter pylori was significantly higher (p less than 0.02) than in the postgastrectomy patients harbouring Campylobacter pylori. The results suggest that reflux gastritis and Campylobacter pylori related gastritis are distinct microscopic entities and that bile reflux may play a role in the eradication of Campylobacter pylori after gastrectomy.     

Apoptosis in Helicobacter pylori gastritis and residual gastritis after distal gastrectomy

BACKGROUND/AIMS: Active gastritis, accelerated cell turnover followed by apoptosis, DNA damage and hyperplasia are often seen in the anastomosis area after gastrectomy. Recently, it has been reported that H. pylori induces apoptosis on gastric cells. Until now, the surgical effect itself and H. pylori infection have not been well differentiated as causes of apoptosis associated with gastritis. Our aim is to clarify the relationship of residual gastritis after gastrectomy and H. pylori gastritis. METHODOLOGY: Residual gastritis model using the Mongolian gerbil has been established with microsurgical technique. Residual gastritis with and without H. pylori infection was studied by histopathological examination and quantitated by Rauws' score. Elevation of pH in gastric juice after surgery was confirmed. Stimulation of downstream events leading to apoptosis, cleavage of poly-ADP-ribose polymerase as a result of activation of caspase-3, was evaluated using Western blotting. RESULTS: Histopathologically, H. pylori infection led to deterioration after surgery. The postoperative Rauws' score with infection was higher than without infection. Cleavage of poly-ADP-ribose polymerase was increased after surgery in gerbils with and without H. pylori infection. Densitometric study showed a greater increase in the animals with H. pylori infection than those without infection that was enhanced after surgery (0.59 vs. 1.04, 0.73 vs. 1.17, respectively). CONCLUSIONS: Apoptosis is increased both in residual gastritis and H. pylori gastritis. Both enterogastric reflux and H. pylori infection may be linked to tumorigenesis in anastomosis sites followed by accelerated epithelial cell turnover followed by apoptosis.     

十二指肠胃反流性疾病内镜诊断及相关因素分析

目的探讨十二指肠胃反流性疾病的内镜表现、相关病因及与幽门螺杆菌的关系。方法选取2011年3月-2011年9月在我院消化内镜中心胃镜检查确诊的206例十二指肠胃反流性疾病患者的内镜下表现、幽门螺杆菌(Helicobacter pylori,H.pylo-ri)检测结果进行分析。结果 206例十二指肠胃反流性疾病患者的病因有手术史49例(毕I式46例,毕II式3例)占23.79%,合并胆囊疾患60例(胆囊切除术后32例,胆结石18例,慢性胆囊炎10例)占29.13%,不明原因97例占47.09%,H.pylori阳性者90例,阳性率43.69%。内镜以胃黏膜充血为主伴有不同程度胆汁附着。结论十二指肠胃反流性疾病呈逐年增高趋势,胆囊疾患和胃大部分切除术是主要病因,胆汁反流性胃炎的临床表现无特异性,胆汁反流性胃炎患者中H.pylori阳性检出率较高。