抗胆汁反流治疗对胃内幽门螺杆菌感染的影响

体外研究发现胆汁可抑制幽门螺杆菌（H.pylori)的生长，但人体内胆汁反流对H.pylori的作用尚不清楚。目的：探讨抗胆汁反流治疗对胃内H.pylori感染的影响。方法：50例经胃镜检查确诊有胆汁反流的慢性胃炎患者纳入本研究。取胃窦黏膜活检标本行组织病理学检查和快速尿素酶试验（RUT），用改良Giemsa染色、RUT或血清H.pylori-IgG检测H.pylori感染情况。患者接受铝碳酸镁治疗（1000mg.tid,4周），治疗结束后复查胃镜和H.pylori感染情况。结果：治疗前患者的H.pylori感染率为66．0％，H.pylori感染者在I、Ⅱ、Ⅲ级胆汁反流性胃炎中的分布无显著差异。治疗后共有48例患者接受胃镜复查，结果显示胃内胆汗反流程度较治疗前明显减轻，H.pylori感染率为64．6％，与治疗前相比无显著差异。合并H.pylori感染者的胃黏膜炎症细胞浸润较非H.pylori感染者为重，且肠化发生率（39．4％）与非H.pylori感染者（11．8％）相比有显著差异（P＜0．05）。结论：合并H.pylori感染胆汁反流患者的胃炎和肠化均较单纯胆汁反流者为重。抗胆汁反流治疗可有效缓解胆汁反流性胃炎，但未能改善胃黏膜的H.pylori感染情况。     

以胃黏膜胆汁酸浓度评估胆汁反流对胃黏膜组织的作用

背景:胃黏膜胆汁酸水平可直接反映胃黏膜细胞胆汁酸暴露的程度,并体现胆汁酸对胃黏膜的损伤程度。目的:探讨以胃黏膜组织胆汁酸浓度评估胆汁反流对胃黏膜病理改变的影响。方法:选取经内镜检查和黏膜胆汁酸浓度确诊的40例胆汁反流性胃炎患者和20例无胆汁反流性胃炎患者,评估幽门螺杆菌(H.pylori)检出率,行组织病理学评分,并分析胃黏膜胆汁酸浓度与组织病理学评分的相关性。结果:与无胆汁反流性胃炎患者相比,胆汁反流性胃炎患者H.pylori检出率无明显差异;胃窦、胃体黏膜组织胆汁酸含量显著升高(P0.05);胃窦黏膜慢性炎症和肠化生评分显著升高(P0.05),胃体黏膜慢性炎症、炎症活动性、萎缩和肠化生评分均显著升高(P0.05)。胆汁反流性胃炎患者胃窦、胃体组织病理学改变均与胆汁酸浓度相关(P0.05)。结论:以胃黏膜胆汁酸浓度评估的胆汁反流与胃黏膜病理损伤严重程度呈正相关。与无胆汁反流性胃炎相比,胃内胆汁反流主要加重胃体部组织病理学损伤。     

根除幽门螺杆菌对胃黏膜病变的影响

幽门螺杆菌（H.pylori）被认为是导致胃黏膜病变的重要因子，根除H.pylori能使胃黏膜病变改善。目的：观察根除H.pylori对胃黏膜病变的影响。方法：予100例经胃镜和组织病理学检查确诊为萎缩性胃炎伴H．pylori感染患者抗H.pylori治疗，1年后复查胃镜和组织病理学，评定组织学变化。结果：所有患者均有不同程度的活动性炎症和慢性炎症。抗H.pylori治疗后，86例被根除。与根除前相比，根除后慢性炎症、活动性炎症、腺体萎缩程度评分均明显下降（P〈0．01），肠化生评分无显著改善。结论：根除H.pylori对胃黏膜病变具有临床治疗意义。     

胆汁反流、胃酸和幽门螺杆菌感染共同作用对胃黏膜损伤程度和分布的影响

背景:胆汁反流、胃酸和幽门螺杆菌（H.pylori）感染均是胃黏膜损伤的独立致病因素。然而,它们共同存在时有无协同致病作用尚不清楚。目的:探讨胆汁反流、胃酸和H.pylori感染共同作用对胃黏膜损伤程度和分布的影响。方法:37例胃镜检查疑有十二指肠胃反流者均经24h胃内胆汁监测证实,同时行胃内PH监测。胃体和胃窦黏膜有或无活动性炎症、萎缩、肠化和不典型增生分别记2分或1分。分别以胃体和胃窦黏膜的各项病理学改变为应变量,以胃内胆红素吸收值>0.14的时间百分比、pH<4的时间百分比和H.pylori感染状态指标为自变量进行多变量逐步Logistic回归分析。结果:37例患者胃内胆红素吸收值>0.14的时间百分比为34.49％±22.69％,pH<4的时问百分比为78.68％土 9.91％,H.pylori阳性率为29.73％。胆汁反流出现在以胃体和胃窦黏膜肠化以及胃体黏膜活动性炎症为应变量的Logistic回归模型中,H.pylori出现在以胃体黏膜活动性炎症为应变量的回归模型中。结论:胆汁反流是胃黏膜肠化的危险因素;胃内有胆汁反流存在时,H.pylori感染是导致胃体新膜炎症的重要病因。     

NSAIDs在幽门螺杆菌相关性胃黏膜病变中的作用

目的 了解NSAIDs与Hellicobecter pylori感染在胃黏膜病变中的作用。方法 患者190例，①病例选择：连续服用NSAIDs治疗2周-12周190例。男性121例，女性69例。平均年龄55岁。②均经胃镜检查和病理组织学检查。对糜烂性胃炎的胃镜诊断和病理诊断胃黏膜炎症分级。③进行H．pylori感染的检测。分为H．pylori感染组与H．prlori阴性组。分析两组的病理组织学改变的特点，了解是否有显著性差异。结果 ①胃镜检查，轻度糜烂106例（55．8％，106／190）。中．重度糜烂84例（44．2％，84／190）。糜烂性胃炎的轻重程度与服药的剂量时间无明显的相关性。②H．pylori感染组46例（24．2％）。H．prlori阴性组144例（75．8％）。③两组病人胃镜诊断的糜烂性胃炎程度无显著性差异（P〉0．05）。④病理情况：H．prlori感染组黏膜中．重度胃炎明显多于H．prlori阴性组（P〈0．01）。⑤病理改变中有淋巴组织增生56例。其中H．prlori感染组有淋巴组织增生22例（47．8％），H．prlori阴性组34例（23．6％）。134例未见淋巴组织增生，其中H．pylori感染组24例（52．2％），H．pylori阴性组110例（76．4％）。两组相比，有显著性差异（P〈0．01）。结论 服用NSAIDs2周以上对胃黏膜有不同程度的损伤。服用NSMDs同时合并H．pylori感染的患者的胃黏膜损伤的严重程度远远高于非感染组。NSAIDs与H．pylori感染是导致胃黏膜损伤的独立危险因子，它们对胃黏膜的损伤作用是叠加的。NSAIDs相关性胃病合并H．pylori感染，根除H．prlori治疗是必要的。     

内镜下均一胃黏膜颗粒样改变的临床特征及治疗效果分析

目的探讨内镜下均一胃黏膜颗粒样改变的临床及病理特点,分析各种药物的治疗效果。方法通过对比胃黏膜颗粒样改变与普通慢性非萎缩性胃炎的临床表现、病理表现、H.pylori感染率、胆汁反流内镜检出率等分析胃黏膜颗粒样改变的临床特点。127例接受过内镜检查的胃黏膜颗粒样改变患者按治疗方式的不同分为三组,分别采用单纯质子泵抑制剂、质子泵抑制剂为主的四联根除H.pylori、质子泵抑制剂加抗胆汁反流药物治疗,并比较各组治疗效果。结果胃黏膜颗粒样改变组患者上腹痛、反酸烧心、纳差等症状发生率显著高于对照组(P0.05),病理表现中肠上皮化生发生率、淋巴细胞浸润发生率显著高于对照组(P0.05),H.pylori感染率显著高于对照组(P0.05),胆汁反流发生率显著高于对照组(P0.05)。41例胃黏膜颗粒样改变患者经质子泵抑制剂为主的四联根除H.pylori治疗10 d后继续质子泵抑制剂治疗3周,27例患者临床症状消失,8周后复查胃镜发现17例原黏膜隆起病变显著减轻或消失。42例患者经单纯质子泵抑制剂治疗4周后14例症状消失,8周后复查胃镜仅6例黏膜隆起病变显著减轻或消失。44例患者经质子泵抑制剂联合抗胆汁反流药物治疗4周后23例症状消失,8周后复查胃镜11例黏膜隆起病变显著减轻或消失。结论胃黏膜颗粒样改变作为一种特殊类型的胃炎,临床表现具有一定的特征性,根据H.pylori感染情况行根治H.pylori治疗联合抗胆汁反流治疗是该病有效的治疗方法,值得临床推广。     

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。     

铝碳酸镁咀嚼片联合奥美拉唑治疗活动性胃溃疡组织学愈合质量的评价

背景：随着质子泵抑制剂的广泛应用，以及根除幽门螺杆菌（H．pylori）感染作为治疗消化性溃疡的主要手段，极大地提高了消化性溃疡的临床愈合率，但复发的难题仍待解决。溃疡愈合质量，尤其是组织学愈合质量受到许多学者关注。目的：观察活动性胃溃疡患者应用铝碳酸镁咀嚼片联合奥美拉唑与单用奥美拉唑治疗前后胃黏膜组织学变化。比较两组患者组织学溃疡愈合质量。方法：88例经胃镜检查证实伴有H．pylori感染的活动性胃溃疡患者随机分成治疗组和对照组。治疗第1周，两组患者均予H．pylori根除三联疗法，治疗组同时加服铝碳酸镁咀嚼片；第2～6周，治疗组给予铝碳酸镁咀嚼片联合奥美拉唑胶囊，对照组仅用奥美拉唑胶囊治疗；第7～8周，治疗组继续给予铝碳酸镁咀嚼片，对照组则停药。8周疗程结束后，两组患者复查胃镜。内镜下取胃溃疡周围黏膜（相当于原取材点处）组织2～4块，重新观察两组患者治疗后的胃黏膜组织学变化，着重从炎性细胞浸润程度和黏膜形态结构两个方面观察胃黏膜组织学恢复情况。结果：治疗组胃黏膜腺体密度和腺管形态改善程度较对照组好，且有统计学差异（P值分别为0．0351和0．0176）。结论：治疗活动期胃溃疡患者在根除H．pylori感染＋抗溃疡治疗后的第8周时点上．同时加用兼有抗酸和吸附胆汁作用的胃黏膜保护剂——铝碳酸镁咀嚼片，能更好地恢复胃黏膜形态结构，增强溃疡愈合的组织学质量．并有可能降低溃疡的远期复发率。     

幽门螺杆菌阴性消化性溃疡的病例对照研究

背景：幽门螺杆菌（H．pylori）感染是消化性溃疡（PU）的重要病因，但H．pyZori阴性溃疡在PU中仍占有一定比例。目的：分析总结H．pyfori阴性PU的临床特点。方法：回顾性分析2004年1月-2007年3月北京大学第三医院住院PU患者的病例资料。从H．pylori阳性患者中以l：l的比例为H．pylori阴性组随机选取性别相同、年龄相近的对照，分析比较两组临床特点。结果：共纳入480例PU患者，男女比例为3．62：1；HpyZori阴性120例，阳性360例，阴性患者中位年龄显著高于阳性患者（P〈0．001）。病例对照研究显示，Hpylori阴性组首发症状存在腹痛者显著少于对照组，有恶心、呕吐症状以及有PU史和非甾体抗炎药（NSAIDs）服用史者显著多于对照组（P〈0．05）。H．pyZori阴性组胃溃疡显著多于对照组，十二指肠溃疡显著少于对照组（P〈0．05）；内镜下慢性非萎缩性胃炎显著少于对照组，息肉显著多于对照组（P〈0．05）：组织学上胃黏膜炎症、炎症程度和活动性显著轻于对照组，淋巴组织增生和肠化生显著少于对照组（P〈0．05）。结论：H．pyfo矗阴性PU占本组PU总数的25．O％，患者年龄相对较大，临床多表现为无痛性溃疡，多有PU史和NSAIDs服用史。溃疡多发生于胃部，黏膜炎症程度较轻，活动性炎症少见。     

胆汁反流性胃炎胃动力及幽门螺杆菌感染情况的临床研究

目的研究原发性胆汁反流性胃炎的胃动力及幽门螺杆菌(H.pylori)感染情况,以探讨其发病机理。方法将原发性胆汁反流性胃炎118例作为试验组,慢性非萎缩性胃炎120例作为对照组,所有病例分别利用13C-辛酸呼气试验进行胃动力检查,利用13C-尿素呼气试验进行H.pylori检查,对比研究原发性胆汁反流性胃炎的胃动力及H.pylori感染情况。结果与慢性非萎缩性胃炎相比,原发性胆汁反流性胃炎的胃排空明显延迟(P0.05);原发性胆汁反流性胃炎H.pylori的阳性率为33.1%,慢性非萎缩性胃炎H.pylori的阳性率为55.8%,有统计学差异(P0.05)。结论原发性胆汁反流性胃炎存在胃动力障碍,反流的胆汁可能对幽门螺杆菌有抑制和杀灭作用。     

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.     

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.     

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.     

Influence of bile reflux and Helicobacter pylori infection on gastritis in the remnant gastric mucosa after distal gastrectomy

Background Two main pathogenic factors, bile reflux and Helicobacter pylori infection, have been identified in the remnant stomach, but it is still unclear which factor is important in the pathogenesis of gastritis in the remnant stomach after distal gastrectomy.Methods In 184 patients who had had distal gastrectomy performed using the Billroth-I procedure (B-I; n-106), Billroth-II procedure (B-II; n-36), and jejunal interposition (J-I; n-42) we examined the severity of remnant gastritis endoscopically and carried out examinations for H. pylori infection and histological examination.Results The endoscopic severity of remnant gastritis was grade 1 or more in 101 of the 106 B-I patients (95.3%) and in all 36 B-II patients (100%). But, of the 42 J-I patients, the grade was 0 in 33 (78.6%). The endoscopic severity of remnant gastritis was significantly milder for J-I than for B-I (P < 0.001) and B-II (P < 0.001). H. pylori infection was confirmed in 59 of the 106 B-I patients (55.6%), 21 of the 36 B-II patients (58.3%), and 32 of the 42 J-I patients (76.1%). The rate of H. pylori infection was higher for J-I patients than for B-I (P < 0.05), but not for B-II patients (P = 0.1495). The severity of chronic and active inflammatory cellular infiltration tended to be inverse proportional relation with the endoscopic severity of the remnant gastritis. Furthermore, the histological inflammation and activity scores of H. pylori-positive patients were higher than those of H. pylori-negative patients, without regard to the endoscopic grade of gastritis.Conclusions Reconstruction techniques play an important role in the prevention of bile reflux, and we found that endoscopically more severe remnant gastritis was associated with a lower rate of H. pylori infection and with a lower degree of inflammatory cellular infiltration.     

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.     

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.     

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.     

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.     

Effects of bile reflux on gastric mucosal lesions in patients with dyspepsia or chronic gastritis

AIM: To investigate the influences of bile reflux on profiles of gastric mucosal lesions in patients with dyspepsia or chronic gastritis. METHODS: A total of 49 patients diagnosed with dyspepsia and chronic gastritis underwent 24-h ambulatory and simultaneous monitoring of intragastric bilirubin absorbance and pH values, and then they were divided into bile reflux positive group and bile reflux negative group. Severity of pathological changes in gastric mucosa including active inflammation, chronic inflammation, intestinal metaplasia, atrophy and dysplasia as well as Helicobacter pylori (H pylori) infection at the corpus, incisura and antrum were determined respectively according to update Sydney system criteria. The profiles of gastric mucosal lesions in the two groups were compared, and correlations between time-percentage of gastric bilirubin absorbance >0.14 and severity of gastric mucosal lesions as well as time-percentage of gastric pH >4 were analyzed respectively. RESULTS: Thirty-eight patients (21 men and 17 women, mean age 44.2 years, range 25-61 years) were found existing with bile reflux (gastric bilirubin absorbance >0.14) and 11 patients (7 men and 4 women, mean age 46.2 years, range 29-54 years) were bile reflux negative. In dyspepsia patients with bile reflux, the mucosal lesions such as active inflammation, chronic inflammation, intestinal metaplasia, atrophy or H pylori infection in the whole stomach, especially in the corpus and incisura, were significantly more severe than those in dyspepsia patients without bile reflux. Moreover, the bile reflux time was well correlated with the severity of pathological changes of gastric mucosa as well as H pylori colonization in the near-end stomach, especially in the corpus region. No relevance was found between the time of bile reflux and pH >4 in gastric cavity. CONCLUSION: Bile reflux contributes a lot to mucosal lesions in the whole stomach, may facilitate H pylori colonization in the corpus region, and has no influence on acid-exposing status of gastric mucosa in patients with dyspepsia or chronic gastritis.