Correlation between duodenogastric reflux and remnant gastritis after distal gastrectomy

BACKGROUND/AIMS: Many patients who undergo distal gastrectomy develop remnant gastritis. This report describes the correlation between remnant gastritis and the amount of duodenogastric reflux and looks at the relationship between Helicobacter pylori infection and duodenogastric reflux in remnant gastritis. METHODOLOGY: Sixty-two patients who underwent curative distal gastrectomy for gastric cancer with radical lymphadenectomy were studied. The period of bile reflux (percent time) into the gastric remnant was measured with the Bilitec 2000 under standardized conditions. Remnant gastritis was semi-quantified using the neutrophil infiltration score based on the updated Sydney System, and the presence of H. pylori infection was determined 12 weeks after the surgery. RESULTS: Overall, the correlation was not significant between the neutrophil infiltration score and the percent time (p=0.08). Similarly, the correlation was not significant in patients with H. pylori infection (p=0.30), but it was significant in patients without H. pylori infection (p=0.03). CONCLUSIONS: Duodenogastric reflux after distal gastrectomy can cause remnant gastritis in patients without H. pylori infection. Reconstruction with biliary diversion is protective against the development of remnant gastritis.     

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.     

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。     

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.     

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.     

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 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.     

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.     

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.     

251例残胃胃镜、病理和幽门螺杆菌检查结果分析

本文对251例胃部分切除术后病例,进行胃镜和病理组织学分析,发现85.65％病例可发生残胃炎,且具有炎症轻微,粘膜水肿、表面上皮增生反应强烈和易有腺体扩张的组织学特点。残胃的Hp感染率仅为24.3％,与非手术的慢性胃炎组相比具有高度显著性差异(P<0.01)。本文提示残胃的低Hp阳性率,可能与残胃腔内胆汁酸含量较高,pH值升高,造成不利于Hp生长的环境有关。     

Cyclooxygenase-2 expression in gastric antral mucosa before and after eradication of Helicobacter pylori infection

OBJECTIVE: Helicobacter pylori (H. pylori) causes chronic gastritis. The inducible prostaglandin synthetase cyclooxygenase 2 (COX-2) plays an important role in inflammatory conditions. We hypothesized that H. pylori-associated chronic gastritis would express COX-2 protein. Our aim was to evaluate the effect of eradication of H. pylori infection on COX-2 expression in the antral mucosa of patients before and after antibiotic therapy. METHODS: Tissues were obtained from patients with non-ulcer dyspepia undergoing H. pylori eradication. Ten patients with proven H. pylori infection and subsequent successful eradication were studied. Three biopsies of antral mucosa were evaluated before and after H. pylori eradication. The amount of acute and chronic inflammation was quantitated. Immunohistochemical staining for COX-2 was expressed as a percentage of the total number of cells and correlated with the degree of chronic inflammation. RESULTS: Specific immunostaining for COX-2 was observed in antral mucosa of patients infected with H. pylori. Patchy cytoplasmic staining was seen in surface epithelial cells and strong cytoplasmic staining for COX-2 was seen in parietal cells. Spotty cytoplasmic staining for COX-2 was also seen in lamina propria plasma cells, as well as there being macrophages present in the germinal centers of lymphoid aggregates. COX-2 expression could be detected both before and after eradication of H. pylori. The mean percentage of cells staining for COX-2 was significantly higher in H. pylori-infected mucosa, compared with mucosa after successful H. pylori eradication (33.4% +/- 5.4 vs 18.9% +/- 3.3, p = 0.038). COX-2 immunostaining correlated best with the chronic inflammation score (r2 = 0.78, p < 0.001). There was a strong correlation for those subjects who were H. pylori infected, as well as for those who had successful H. pylori eradication. CONCLUSIONS: H. pylori associated acute and chronic antral inflammation was associated with immunohistochemical detection of COX-2 protein in epithelial cells, in addition to associated mononuclear cells and parietal cells. Expression was reduced, but not eliminated, in the epithelium after successful eradication of H. pylori. Despite the reduction in COX-2 expression after H. pylori eradication, expression of COX-2 in epithelial cells remained and strongly correlated with the extent of the chronic inflammatory cell infiltrate. The clinical implications of H. pylori-associated induction of COX-2 expression for patients on selective COX-2 inhibitors, in addition to the role of COX-2 in gastric carcinogenesis, deserve further study.     

Helicobacter pylori of the remnant stomach and its eradication.

BACKGROUND/AIMS: Many authors have reported that Helicobacter pylori (H. pylori) is one of the major causes of gastritis and peptic ulcer. This study was conducted to evaluate the incidence of H. pylori infection and the curative effects of amoxicillin and omeprazole on H. pylori in the remnant stomach. METHODOLOGY: Biopsy specimens were obtained from 70 patients who underwent gastrectomy for gastric cancer. H. pylori was subsequently diagnosed by CLO test and culture of H. pylori. Gastritis was assessed by the scoring of four characteristic pathological parameters. Patients with positive H. pylori were eligible for the eradication study. Amoxicillin, 750 mg per day for 2 weeks, and omeprazole, 20 mg per day for 8 weeks, were administered to them. Endoscopic reexamination was performed 12 weeks after the initiation of treatment. RESULTS: The overall positive rate of H. pylori was 37.1%; 39.6% in Billroth I reconstruction, 0% in Billroth II reconstruction, and 55.6% in pylorus preserving gastrectomy, respectively. The positive H. pylori rate of Billroth II reconstruction was significantly low. However, there was no association of positive rate of H. pylori with time. There was no significant difference of gastritis scores between H. pylori infected patients and non-infected patients. The eradication rate was 70.0%. CONCLUSIONS: H. pylori was present in 37.1% of patients who underwent gastrectomy. Gastritis was not significantly severe in H. pylori infected patients. The treatment with amoxicillin and omeprazole was effective for these patients.     

Helicobacter pylori of remnant stomach and optimal dose of amoxicillin for eradicating Helicobacter pylori

BACKGROUND/AIMS: The optimal dose of antibiotics for Helicobacter pylori eradication is not known. The aim of this study was to evaluate optimal dose of antibiotics (amoxicillin) for eradication of H. pylori in the remnant stomach. METHODOLOGY: Biopsy specimens were obtained from 77 patients who underwent gastrectomy for gastric cancer. H. pylori was subsequently diagnosed by rapid urease test and culture. Gastritis was assessed by scoring. Patients with positive H. pylori were eligible for the eradication study. Amoxicillin 750 mg per day for 2 weeks and omeprazole 20 mg per day for 8 weeks were administered to them. Endoscopic reexamination and 13C-urea breath test were performed 12 weeks after the initiation of treatment. RESULTS: The positive rate of H. pylori was 38.9% in the remnant stomach. Eradication rate was 50.0%. Mean dose of amoxicillin in effective cases was 14.1 +/- 1.5 mg/kg/day. This was significantly higher than that in non-effective cases (12.5 +/- 1.5 mg/kg/day). Remnant gastritis was significantly improved after complete eradication. CONCLUSIONS: H. pylori was present in 38.9% of patients who underwent gastrectomy for gastric cancer. The optimal dose of amoxicillin was 15.6 mg/kg/day for 14 days with omeprazole-amoxicillin therapy.     

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.     

环氧合酶-2表达与幽门螺杆菌相关性胃十二指肠疾病的研究

目的　探讨环氧合酶 2表达与幽门螺杆菌Helicobacterpylori ,H .pylori相关性胃十二指肠疾病的关系 ,并通过抗菌治疗评价根除H pylori感染对胃窦黏膜中COX 2表达的影响。方法　用免疫组化方法半定量检测 2 64例经胃镜和组织病理学检查患有十二指肠球部溃疡、胃溃疡、复合性溃疡、胃癌、单纯性慢性胃炎及胃黏膜正常者的胃窦黏膜COX 2蛋白的表达 ,比较H pylori感染与非感染者之间的差异。对检出的 3 5例H pylori的单纯慢性胃炎进行H pylori抗菌根除治疗 ,比较根除前后胃窦黏膜COX 2蛋白的表达变化。根据 2 0 0 0年 5月全国慢性胃炎研讨会共识意见 (江西 井冈山 )对胃黏膜炎症、活动性、异型增生、肠化生和H pylori密 ,度进行半定量测定。结果　胃黏膜表面上皮、腺上皮细胞和固有层间质细胞的浆中可见COX 2蛋白表达 ,但阳性染色细胞多集中在表层上皮。 2 53例中 ,14 3例H pylori者 (56 52 % )COX 2平均阳性细胞率显著高于 110例H pylori者 (43 48% ) ,(P =0 ) ,各疾病组H pylori患者的COX 2平均阳性细胞率均显著高于H pylori者 (P =0 ) ,各疾病组H pylori患者COX 2平均阳性细胞率也均显著高于正常对照组 (P <0 0 5)。 2 7例H pylori根除后的胃黏膜COX 2平均阳性细胞率明显下降 (P =0 ) ,但仍明显高于正     

根除Hp前后胃窦粘膜COX-2表达的变化

目的检测胃窦粘膜在根除Hp前后环氧化酶-2(Cyclooxygenase-2,COX-2)表达水平的变化,探讨COX-2表达与急、慢性炎症的关系.方法对我院1999.6-2000.3胃镜诊断为慢性胃炎、胃粘膜活组织尿素酶试验和14C尿素呼气试验均证实Hp阳性的14例住院病人,在根除Hp前后取胃粘膜活检组织,HE染色显示组织结构和炎性细胞浸润情况,用免疫组织化学方法(SP法)显示COX-2表达情况.结果感染区域的胃窦上皮细胞和相应的壁细胞、单核细胞均可检测到COX-2的阳性表达,与根除Hp后比较,COX-2的表达明显减少而不完全消失(P＜0.005),COX-2阳性表达率与胃粘膜的急性炎症程度无关,而与慢性炎性细胞浸润密切相关(r=0.74 P＜0.05).结论COX-2的高表达可能是Hp相关性胃炎发生的重要机制.     

Effects of cyclooxygenase-2 inhibitor on gastric acid secretion in Helicobacter pylori-infected C57BL/6 mice.

BACKGROUND: Helicobacter pylori-associated body gastritis inhibits gastric acid secretion. The aim of this study was to determine the effects of H. pylori infection on gastric acid secretion and further determine whether cyclooxygenase-2 was involved. METHODS: C57BL/6 mice (n = 40) were inoculated with the Sydney strain of H. pylori. Control mice (n = 40) were treated with vehicle only. Half of the infected and control mice were fed an experimental diet containing etodolac (10 mg/kg/day) from 1 week after inoculation until the end of the experiment. Before, 12 and 24 weeks after inoculation, the gastric acid secretion, prostaglandin E2 (PGE2) levels in the gastric mucosa, and gastritis scores according to the updated Sydney system were determined. Immunohistochemical staining of COX-2 protein was also performed. RESULTS: No significant changes in gastric acid secretion, gastritis scores or PGE2 levels in the gastric mucosa were observed in uninfected groups with or without etodolac treatment during the study period. In the H. pylori-infected group without etodolac treatment, gastric acid secretion was significantly decreased with increases in PGE2 levels in the gastric mucosa 24 weeks after inoculation compared with the controls. Gastritis score for activity was significantly higher, and strong staining for COX-2 protein was observed in the H. pylori-infected group. In the H. pylori-infected group with etodolac treatment, PGE2 in the gastric mucosa was decreased and acid secretion was restored to the same level as in the control group. CONCLUSION: One of the mechanisms by which H. pylori infection inhibits gastric acid secretion is increased release of PGE2 produced by COX-2, which is induced by H. pylori infection.     

Influence of gastritis on cyclooxygenase-2 expression before and after eradication of Helicobacter pylori infection

OBJECTIVES: Helicobacter pylori infection causes chronic gastritis and induces cyclooxygenase (COX)-2 expression. The relationship between gastritis and COX-2 expression is not well understood, especially long after the organism has been eradicated. We designed a study to elucidate this relationship. METHODS: Four endoscopic gastric biopsies from each of 118 H. pylori-infected subjects were assessed for COX-2 expression immunohistochemically, gastritis, by an updated Sydney System. In the 107 successfully eradicated subjects, the assessment was repeated once yearly, for 3 years. RESULTS: After successful eradication, COX-2 expression was reduced significantly regardless of site. Atrophy improved significantly and intestinal metaplasia improved but not in the antrum greater curvature. After 1 year COX-2 expression was not significantly different in the epithelia with and without intestinal metaplasia. Correlation between COX-2 expression and neutrophil score in the antrum (r = 0.214, P = 0.042) and inflammation in the corpus (r = 0.234, P = 0.025) disappeared after eradication. COX-2 expression correlated well with atrophy and metaplasia before and after eradication. No significant reduction in COX-2 or improvement in gastritis was found in subjects with eradication failure. CONCLUSION: H. pylori infection is associated with the enhancement of COX-2 expression in the gastric mucosa. Eradication therapy reduces COX-2 expression and hence may reduce the risk of cancer development.     

Prevalence of Helicobacter pylori in the residual stomach after gastrectomy for gastric cancer

BACKGROUND/AIMS: In recent years, the role of Helicobacter pylori in gastritis of the residual stomach has attracted much attention. We investigated the prevalence of Helicobacter pylori in the residual stomach after distal gastrectomy for gastric cancer, as well as the correlations between Helicobacter pylori positivity and clinical characteristics or the severity of gastritis in the residual stomach. METHODOLOGY: The subjects were 66 patients with gastric cancer who underwent distal gastrectomy with Billroth I reconstruction at our department. Helicobacter pylori was detected by the 13C-urea breath test, and patients were considered to be Helicobacter pylori-positive if the delta 13C value was > 2.5@1000. RESULTS: The overall Helicobacter pylori positivity rate of the gastrectomy patients was a high 80.3%, with the rate being especially high in patients under 60 years of age and in those tested less than 5 years after surgery. There was a close relationship between Helicobacter pylori positivity and the severity of gastritis. CONCLUSIONS: Helicobacter pylori infection appears to cause the development of gastritis. Helicobacter pylori eradication needs to be taken into consideration in the management of Helicobacter pylori-positive patients after gastrectomy.     

Roles of Helicobacter pylori infection and cyclooxygenase-2 expression in gastric carcinogenesis

AIM: Cyclooxygenase (COX)-2 is over expressed in gastrointestinal neoplasm. Helicobacter pylori (H pylori) infection is causally linked to gastric cancer. However, the expression of COX-2 in various stages of H pylori-associated gastric carcinogenesis pathway has not been elucidated. Therefore, the aim of this study was to clarify the role of H pylori induced COX-2 expression during carcinogenesis in the stomach. METHODS: Gastric biopsies from 138 subjects (30 cases of chronic superficial gastritis (CSG), 28 cases of gastric glandular atrophy (GA), 45 cases of gastric mucosal intestinal metaplasia (IM), 12 cases of moderate gastric epithelial dysplasia and 23 cases of gastric cancer) were enrolled. H pylori infection was assessed by a rapid urease test and histological examination (modified Giemsa staining). The expression of COX-1 and COX-2 in human gastric mucosa was detected by immunohistochemical staining. RESULTS: H pylori infection rate was 64.3% in GA and 69.5% in gastric cancer, which was significantly higher than that (36.7%) in CSG (P<0.05). The positive expression rates of COX-2 were 10.0%, 35.7%, 37.8%, 41.7% and 69.5% in CSG, GA, IM, dysplasia and gastric cancer, respectively. From CSG to GA, IM, dysplasia and finally to gastric cancer, expression of COX-2 showed an ascending tendency, whereas COX-1 expression did not change significantly in the gastric mucosa. The level of COX-2 expression in IM and dysplasia was significantly higher in H pylori-positive than in H pylori-negative subjects (P<0.01). CONCLUSION: COX-2 expression induced by H pylori infection is a relatively early event during carcinogenesis in the stomach.