原发性胆汁反流性胃炎胃黏膜ghrelin的表达

目的:探讨原发性胆汁反流性胃炎患者胃黏膜ghrelin的表达变化.方法:选取我院2007-06/2007-11就诊的原发性十二指肠胃返流患者96例,分为低反流组和高反流组,同时选取胃镜检查大致正常,没有胆汁反流者30例为对照组.免疫组化法检测胃黏膜ghrelin的表达.结果:ghrelin在浅表性胃炎组、肠上皮化生组、不典型增生组和萎缩性胃炎组中的表达均低于正常对照组(653.822±99.303,98.913±14.079,65.875±13.844,52.290±11.463VS 9 884.420±1 26.362,均P＜0.05).浅表性胃炎组、萎缩性胃炎组和肠上皮化生组中的Hpylori阳性组的ghrelin表达与H pylori阴性组比较均有显著性差异(599.320±87.300 VS 721.950±67.836,47.157±9.582 VS 55.283±11.580,92.700±10.372 VS 107.600±17.560,均P＜0.05).结论:胆汁反流是造成胃黏膜损伤的危险因素,随着胆汁反流程度加重,胃黏膜萎缩程度加重,ghrelin表达减少.     

老年人原发性胆汁反流性胃炎病理特征分析

目的：探讨原发性胆汁反流对老年人胃黏膜组织损伤的病理特点。方法回顾性地分析2013年1月～2014年8月于我院经胃镜检查诊断的77例老年原发性胆汁反流性胃炎（BRG）患者为观察组,同时取同期诊断为幽门螺杆菌（Hp）感染的非BRG慢性胃炎的78名老年患者为对照组,分析两组患者胃黏膜组织的病理变化特点。结果原发性BRG患者Hp感染率为19.5%。胆汁反流组与Hp感染的非BRG慢性胃炎病理组织特征比较：轻、中、重慢性炎分别为32.5% vs 11.5%、58.4% vs 34.6%和9.1% vs 53.8%,中性粒细胞浸润分级（无、轻、中、重）分别为83.1% vs 41.0%、11.7% vs 20.5%、5.2% vs 32.1%和0.0% vs 6.4%。淋巴滤泡、肠上皮化生和胃黏膜萎缩检出率分别为4.3%vs 26.9%、5.2%vs 17.9%和6.5%vs 25.6%;胆汁反流组中,Hp阳性和Hp阴性患者轻、中、重度慢性炎分别为：13.3% vs 37.1%、53.3% vs 59.7%和33.3% vs 3.2%,中性粒细胞浸润分级（无、轻、中、重）分别为53.3%vs 41%、20.0%vs 9.7%、20.0%vs 0.0%和6.7%vs 0.0%,淋巴滤泡、肠上皮化生和胃黏膜萎缩检出率分别为53.3%vs 4.8%、0.0% vs 6.5%和0.0%vs 8.1%。结论原发性胆汁反流可引起老年患者胃黏膜组织慢性炎症反应、肠上皮化生、腺体萎缩,但其发生率低于Hp感染的慢性胃炎。中性粒细胞浸润和淋巴滤泡形成主要与Hp感染相关,Hp感染并未增加原发性胆汁反流患者胃黏膜萎缩、肠化生不良结局的发生。     

胆汁反流与幽门螺杆菌感染和消化性溃疡的关系

目的探讨胆汁反流与消化性溃疡和幽门螺杆菌感染的关系。方法选择行胃镜检查的患者400例,并同时行幽门螺杆菌检测。根据胃镜下是否存在胆汁反流分为胆汁反流阳性组和胆汁反流阴性组,比较两组间幽门螺杆菌感染率和消化性溃疡的发生率。结果胆汁反流阳性组消化性溃疡发生率9.88%(8/81),胆汁反流阴性组22.26%(71/319),胆汁反流阳性组消化性溃疡发生率低于胆汁反流阴性组(P<0.05);胆汁反流阳性组幽门螺杆菌感染率30.86%(25/81),胆汁反流阴性组51.72%(165/319),胆汁反流阳性组幽门螺杆菌感染率明显低于胆汁反流阴性组(P<0.01)。结论胆汁反流可能通过抑制幽门螺杆菌感染而减少了消化性溃疡的发生。     

935例胆汁反流性胃炎临床和内镜分析

目的探讨胆汁反流性胃炎临床表现，中医证型，胃镜胃黏膜病变和幽门螺杆菌（Hp）感染的情况。方法对符合诊断的935例胆汁反流性胃炎的临床表现，中医证型，胃镜胃黏膜病理及Hp感染情况进行分析。结果935例胆汁反流性胃炎Hp感染率为36．6％，与中医证型存在一定的相关性。胆汁反流性胃炎与萎缩，肠化生等病理改变有关。结论胆汁反流性胃炎Hp感染率低于非胆汁反流性慢性胃炎。Hp感染率在脾胃湿热型及肝胃不和型较高。胆汁反流性胃炎肠化生和萎缩性病变在脾胃湿热型和肝胃不和型中较高，而异型增生的发生在脾胃虚寒型中较高。     

原发性十二指肠胃反流程度与胃黏膜炎性反应关系的研究

目的 分析原发性病理性十二指肠胃反流(DGR)患者胃黏膜病变、幽门螺杆菌(Hp)感染及胆汁反流变化以及相互间的关系.方法 对58例原发性病理性DGR患者进行24 h胃内胆汁监测,以反流时间百分23.60%为界,将患者分为高反流组(29例)和低反流组(29例).并行胃镜检查及胃黏膜活检.分析原发性病理性DGR患者胃黏膜炎性反应、Hp感染、胆汁反流间的关系.结果 高反流组及低反流组的Hp阳性率分别为20.7%(6/29)和48.3%(14/29),差异有统计学意义(P＜0.05).高反流组胃窦和胃角部黏膜肠上皮化生检出率高于低反流组(P＜0.05).胃窦、胃角部黏膜新悉尼系统病理积分Hp阳性组高于Hp阴性组(P＜0.05),高反流组高于低反流组(P＜0.05).Hp阳性组胆红素吸收值≥0.25的时间百分比低于Hp阴性组(P＜0.05),HP阳性组短时间反流频率、长时间反流频率、最长反流时间、吸收值最大值、平均值和中位值与Hp阴性组间差异无统计学意义(P＞0.05).Hp阳性组和阴性组胆红素吸收值≥0.25的时间百分比与胃窦、胃角部黏膜新悉尼系统病理积分均呈正相关(P＜0.05).结论 原发性病理性DGR导致胃窦黏膜损伤的主要因素可能为胆汁反流,胆汁反流可抑制HP在胃内定植,Hp感染可能与胆汁反流协同作用导致胃黏膜损伤.     

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。     

青年人生理性十二指肠胃反流的相关因素

目的:探讨生理性十二指肠胃反流的反流特点,反流与胃黏膜组织学改变的关系.方法:选取20名青年健康志愿者,分别接受常规胃镜检查,24 h动态胃内pH和胆汁反流监测,HE染色行常规组织病理学检查以及改良Giemsa染色行幽门螺杆菌检查.结果:胃镜与胃黏膜组织检查多为正常黏膜或轻度浅表性炎症,仅2名胃镜下有胆汁反流,6名H pylori阳性.未见溃疡、糜烂、萎缩及肠化生.胆红素监测均有不同程度的十二指肠胃反流,abs>0.14的时间百分比为12.5%±8.8%,短时间反流频率62.8±36.0次、长时间反流频率5.9±3.8次、最长反流时间53.5.0±50.3min,其中立位反流时间显著性长于卧位(P=0.017).胃内pH>4的时间百分比为13.91%±10.1%,与胃内abs>0.14的时间百分比比较无相关性.结论:正常生理条件下均存在生理性十二指肠胃反流,不同个体、不同体位其反流程度不一,但这种反流不引起胃黏膜的病理性改变,也不引起胃内pH的变化.     

原发性病理性十二指肠胃反流致病的因素分析

目的 探讨原发性病理性十二指肠胃反流(DGR)胃黏膜病变、幽门螺杆菌(Hp)感染、胆汁反流之间的关系.方法 应用便携式胆汁监测仪监测86例原发性病理性DGR患者胃内24 h胆汁反流情况;另取胃黏膜组织活检,分别行快速尿素酶试验、改良Giemsa染色和HE染色,判断有无Hp感染,并观察胃黏膜慢性炎症、活动性、萎缩、肠化等组织学特征.结果 ①将患者根据有无Hp感染分为Hp阳性组和Hp阴性组,Hp阳性组胃窦部黏膜病理积分、胆红素吸收值≥0.25的时间百分比均显著低于Hp阴性组(P均＜0.05);两组胆红素吸收值≥0.25的时间百分比和胃窦、胃角部黏膜病理积分均呈显著正相关(P均＜0.05).②将患者根据胆汁反流程度分为高反流组和低反流组,高反流组Hp阳性率显著低于低反流组(P＜0.05),胃窦和胃角部黏膜肠上皮化生的检出率、胃窦部黏膜病理积分均显著高于低反流组(P均＜0.05).结论 原发性病理性DGR导致胃窦黏膜损伤的主要因素可能为胆汁反流,随胆汁反流程度加重,胃窦黏膜损伤程度加重;胆汁反流可能抑制Hp在胃窦部定植,Hp感染可能与胆汁反流协同作用导致胃体部黏膜损伤.     

十二指肠胃反流与胆囊切除术关系的临床研究

目的　通过对胆石症和胆囊切除术后出现胆汁反流性胃炎患者的血清胃动素 (MTL)和胆囊收缩素 (CCK)检测 ,探讨十二指肠胃反流 (DGR)的发生机制。方法　对确诊胆汁反流性胃炎的胆囊切除术后患者 (A组 ,30例 )和胆石症合并胆汁反流性胃炎患者 (B组 ,2 2例 ) ,以及对照组 (C组 ,2 0例 )即胃镜无胆汁反流现象 ,病理示慢性浅表性胃炎患者 ,分别抽血测空腹血清MTL和CCK含量。结果　A组血清CCK为 5 86pg/mL± 2 .78pg/mL ,较C组 3 80pg/mL± 1.10pg/mL有显著性升高 ,A组血清MTL为310 31pg/mL± 118 2 1pg/mL ,较C组 32 6 0 0pg/mL± 5 8 0 0pg/mL的降低无显著性差异 ,B组与C组相比CCK变化无显著性差异 ,MTL较C组有显著性降低 ,值为 2 2 8 30pg/mL± 72 2 0pg/mL。结论　DGR是胆道疾患的多见病理现象。胃运动功能障碍和幽门括约肌功能不全是病理性DGR的一个重要原因 ,胃十二指肠收缩不协调可导致DGR发生。MTL和CCK对胃排空和十二指肠运动起重要调节作用 ,胆囊切除术后和胆石症患者发生病理性DGR时存在CCK和MTL分泌不协调 ,调节紊乱的现象     

二甲基硅油治疗胆汁反流的临床实验室研究

我们曾发现二甲基硅油能使反流的胆汁减少。为进一步确定此发现,我们测定胃液中的胆红素浓度以评价二甲基硅油对胆汁反流的疗效。65例慢性胃炎病人接受此项测定,其中45例伴胆汁反流,并将其进步分成2组:治疗组(30例)在测定前服二甲基硅油 硫糖铝;对照组(15例)单服硫糖铝。用胆红素氧化酶法测定胆红素浓度。结果:治疗组在服二甲基硅油前后均值分别为16±12.0097μmol/L和6.6± 4.9454μmol/L(P<0.01),而对照组则分别为14.6±12.3320μmol/L和15.9±19.8035μmol/L(P>0.05);胆红素浓度减少30％以上者治疗组中占80.0％,对照组中占26.7％,两组间有极显著差异(X2=12.1008,P<0.01)。结论:测定胃液中胆红素有助于判断胆汁反流,并肯定二甲基硅油可减少胆汁反流,由此而减轻胆汁反流性胃炎。     

二甲基硅油对胃液中反流胆红素的影响

目的测定胃液中的胆红素浓度以评价二甲基硅油对胆汁反流的疗效．方法慢性胃炎患者６５例，其中伴胆汁反流４５例，进一步分成２组：治疗组（３０例）在测定前服二甲基硅油＋硫糖铝；对照组（１５例）单服硫糖铝．用胆红素氧化酶法测定胆红素浓度．结果无胆汁反流的２０名患者中，胃液中胆红素浓度分别检测１５例为０，５例为０４μｍｏｌ／Ｌ～０８μｍｏｌ／Ｌ；治疗组在服二甲基硅油前后均值分别为（１６０±１２０）μｍｏｌ／Ｌ和（６６±４９）μｍｏｌ／Ｌ（Ｐ＜００１），而对照组则分别为（１４６±１２３）μｍｏｌ／Ｌ和（１５９±１９８）μｍｏｌ／Ｌ（Ｐ＞００５）；胆红素浓度减少３０％以上者治疗组中占８００％，对照组中占２６７％，两组间有高度显著差异（χ２＝１２１００８．Ｐ＜００１）．结论测定胃液中胆红素有助于判断胆汁反流，并肯定二甲基硅油可减少胆汁反流，从而减轻胆汁反流性胃炎．     

反流性食管炎患者血浆血管活性肠肽、胃动素变化及其意义

测定反流性食管炎患者血浆血管活性肠肽、胃动素浓度,及下食管括约肌压力,以探讨反流性食管炎的发病机制。方法：采用液体灌注体外传感器法测定２８例反流性食管炎患者下食管括约肌压力。采用放射免疫法测定其血浆ＶＩＰ及胃动素浓度。     

胃黏膜胆色素染色在诊断原发性病理性十二指肠胃反流中的意义

目的 探讨胃黏膜胆色素染色对原发性病理性十二指肠胃反流（DGR）的辅助诊断价值.方法 选择2007年1月至2008年4月因上消化道症状就诊的原发性病理性DGR患者纳入原发性病理性DGR组,另选择同期健康志愿者作为正常对照组.对2组患者进行24 h胃内胆汁监测,以胆红素吸收值0.25为界值,取反流时间百分比的中位数（23.60%）作为分界将原发性病理性DGR组进一步分为低反流（反流时间百分比＜23.60%）组和高反流（反流时间百分比≥23.60%）组.所有患者行胃镜检查及胃黏膜活检,对胃黏膜胆色素染色后进行定量分析.结果 原发性病理性DGR组中胃窦、胃角和胃体部黏膜胆色素沉积均明显高于正常对照组（P均＜0.05）.高反流组胃窦部黏膜萎缩及肠上皮化生的检出率均明显高于低反流组（P均＜0.05）,高反流组胃窦、胃角和胃体部黏膜胆色素沉积的腺体数均明显高于低反流组（P均＜0.05）,高反流组胃窦、胃角部黏膜新悉尼系统病理积分均明显高于低反流组（P均＜0.05）.原发性病理性DGR组胃窦部胃黏膜胆色素沉积的腺体数与新悉尼系统病理积分呈明显正相关（r=0.59,P=0.041）,胃角部两因素亦呈明显正相关（r=0.73,P=0.038）,胃体部两因素无明显相关性（r=-0.33,P=0.072）.结论 胃窦部黏膜胆色素染色能够反映胆汁反流程度,并与黏膜损伤程度呈正相关,可有效辅助原发性病理性DGR诊断.     

Oesophagitis and bile reflux gastritis—clinical and histological assessments

BACKGROUND AND AIMS: Little is known concerning the relationship between oesophagitis and bile reflux (chemical) gastritis despite the numerous studies on gastritis related to Helicobacter pylori. Given the importance of bile in the pathogenesis of both gastric and oesophageal disorders, we aimed at assessing the chemical gastritis score in patients with or without oesophagitis. METHODS: Chemical/bile reflux gastritis score and bile reflux index were assessed in gastric biopsies taken from patients with oesophagitis and gastric surgery (group 1, n=9), gastric surgery without oesophagitis (group 2, n= 11), and oesophagitis without gastric surgery (group 3, n= 10). Endoscopic oesophageal damage was also graded on a 0-5 scale. RESULTS: Group 1 had a median (interquartile range) chemical score of 6 (4-9) compared with 8 (6-10) in group 2, and 1 (0-2) in group 3 (p=0.001; Kruskal-Wallis test for multiple group comparisons). Both the reflux gastritis score and bile reflux index were lowest in patients with intact stomachs. However, the oesophageal scores were 2 (1-2) in group 1 compared with 3 (2-5) in group 3 (p=0.01). CONCLUSION: Patients with post-surgical stomachs have similar chemical and related scores regardless of the presence or absence of oesophagitis. Despite the higher chemical gastritis scores, patients with gastric surgery, exposed mainly to bile reflux, have milder oesophagitis than those with intact stomachs, exposed to both gastric acid and bile.     

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.     

雷贝拉唑和铝碳酸镁治疗胆囊切除术后伴胆汁反流的胃炎作用比较

目的 观察雷贝拉唑、铝碳酸镁及两药联合对胆囊切除后伴有胆汁反流的胃炎的疗效.方法 胆囊切除后,经24 h胃内胆红索监测证实伴有胆汁反流的胃炎患者随机分为4组:空白对照组(n=30)、雷贝拉唑组(n=30,雷贝拉唑20 mg,1次/d)、铝碳酸镁组(n=29,铝碳酸镁1.0 g,3次/d)及联合用药组(n=31,雷贝拉唑+铝碳酸镁,用法同上),疗程8周.观察各组患者腹痛、腹胀、烧心、口苦等症状改善情况,并于治疗结束后2周复查胃镜及组织学检查并再次进行24 h胃内胆红素监测,进行胃镜下黏膜炎性反应程度(充血、水肿),组织学炎性反应程度(炎性反应、活动性)量化评分以及24 h胆红索吸收值(ABS)>0.14总时间百分比、十二指肠内容物反流次数、长反流次数(>5 min)的变化比较.结果 治疗后三组治疗组患者症状均有所改善,联合用药组内镜下水肿程度(2.11±0.77比1.50±0.67,P<0.05)及HE染色组织学活动性评分(2.87±0.72比1.97±0.78,P<0.05)均明显改善,长时间十二指肠内容物反流次数明显减少(18.26±1.80比9.70±1.20,P<0.05),雷贝拉唑组和铝碳酸镁组上述指标治疗前后差异无统计学意义;三组治疗组患者ABS>0.14的时间治疗前后差异均有统计学意义(P<0.05).结论 雷贝拉唑和铝碳酸镁联用可有效治疗伴有胆汁反流的胃炎.     

Gastro-oesophageal reflux and alcoholic cirrhosis. A reappraisal

The oesophageal pH was recorded for 3 h after a test-meal in 27 healthy control subjects (group I), 40 patients with alcoholic cirrhosis (group II), and 22 patients with a normal liver and symptoms of gastro-oesophageal reflux (control refluxers). Gastro-oesophageal reflux was observed in 10 of the cirrhotic patients. Marked reflux episodes lasted longer in cirrhotic refluxers than in control refluxers (P less than 0.05). The frequency of ascites, bleeding from ruptured oesophageal varices, peripheral neuropathy and hepatic encephalopathy were not significantly different according to presence or absence of reflux. Plasma concentrations of gastrin, somatostatin, motilin and vasoactive intestinal peptide (VIP) were measured in groups I and II. Fasting plasma motilin levels, and the release of motilin and of VIP after the meal were higher in group II than in group I. Basal levels and post-prandial profiles of the four peptides tested did not differ between cirrhotics with or without gastro-oesophageal reflux. We conclude that in patients with alcoholic cirrhosis: gastro-oesophageal reflux is frequent (25%) and characterized by prolonged reflux episodes; reflux is not correlated with the degree of liver failure and plays no significant role in the rupture of oesophageal varices; and raised plasma motilin and VIP levels cannot account for the high incidence of reflux in cirrhotics.     

Bile reflux gastritis and Barrett's oesophagus: further evidence of a role for duodenogastro-oesophageal reflux?

BACKGROUND: There is increasing evidence that reflux of bile plays a part in the pathogenesis of Barrett's oesophagus. Bile injury to the gastric mucosa results in a "chemical" gastritis in which oedema and intestinal metaplasia are prominent. AIM: To determine if patients with Barrett's oesophagus have more bile related changes in antral mucosa than patients with uncomplicated gastro-oesophageal reflux disease (GORD) or non-ulcer dyspepsia (NUD). PATIENTS AND METHODS: Patients were identified by a retrospective search of pathology records and those with a clinically confirmed diagnosis of either Barrett's oesophagus or reflux oesophagitis who had oesophageal and gastric biopsies taken at the same endoscopy and had no evidence of Helicobacter pylori infection entered the study. Control biopsies were taken from H pylori negative NUD patients. Antral biopsies were examined "blind" to clinical group and graded for a series of histological features from which the "reflux gastritis score" (RGS) and "bile reflux index" (BRI) could be calculated. The reproducibility of these histological scores was tested by a second pathologist. RESULTS: There were 100 patients with Barrett's, 61 with GORD, and 50 with NUD. The RGSs did not differ between groups. BRI values in the Barrett's group were significantly higher than those in GORD subjects (p=0.014) which in turn were higher than those in NUD patients (p=0.037). Similarly, the frequency of high BRI values (>14) was significantly greater in the Barrett's group (29/100; 29%) than in the GORD (9/61; 14.8%) or NUD (4/50; 8%) group. However, agreement on BRI values was "poor", indicating limited applicability of this approach. CONCLUSION: Patients with Barrett's oesophagus have more evidence of bile related gastritis than subjects with uncomplicated GORD or NUD. The presence of bile in the refluxate could be a factor in both the development of "specialised" intestinal metaplasia and malignancy in the oesophagus.