疏肝和胃法治疗胆汁反流性胃炎24例

自1995年以来，笔者应用疏肝和胃法治疗胆汁反流性胃炎24例．并与对照组对比观察．疗效满意．现报告如下。1资料与方法1．1一般资料：本组44例全部为门诊患者．其中治疗组24例．男15例．女9例：年龄26～50岁．平均32岁；病程6个月～3年。其中并发胆囊炎9例，慢性胃十M指肠病变6例．无并发症9例。对照组20例．一般情况与治疗组相近。诊断标准参照文献「1」。两组病例临床表现均有上腹部持续胀痛、灼痛．进食后不能缓解．纳差．恶心．暖气．吐酸苦水。均行纤维胃镜检查见胆汁反流．或胃壁附有含胆汁粘液。胃粘膜充血水肿糜烂。并发十二指肠炎…     

原发性胆汁反流性胃炎与胃食管反流病的关系

目的:探讨原发性胆汁反流性胃炎(primary bile reflux gastritis,PBRG)与胃食管反流病(gastroesophageal reflux disease,GERD)之间的相关性.方法:选取我院确诊为PBRG的患者1060例为观察组,无痛胃镜下未查见有PBRG的体检者1060例为对照组,比较两组GERD的发生率;依据内镜下PBRG的诊断标准,将260例PBRG伴有GERD的患者分为轻度、中度及重度3组,对比各组食管黏膜损伤的程度以及GERD症状积分的分布.结果:PBRG组GERD的发生率高于对照组(24.5%vs9.8%,P<0.05).食管黏膜损伤程度加深的发生率随着PBRG程度的加重而增加.PBRG的程度与GERD症状分级无相关性.结论:PBRG与反流性食管炎(refluxe sophagitis,RE)形成存在正性相关,PBRG并非是引起GERD症状的主要原因.     

胆汁反流性胃炎胃排空和胃窦平滑肌电改变的研究

目的；本文着重探讨了胃排空改变以及胃窦平滑肌电节律紊乱在胆汁反流性胃炎发病中的可能机制，方法：１８例胆汁反流性胃炎患者（ＢＲＧ组）；１７例非胆汁反流性胃炎患者（ＮＲＧ组）和１０名健康志愿者（ＨＣ组）用双核纱记标的固，液体混合标准餐用γ照相机以１帧／２分钟连续动态照相１２０分钟检测胃排空，根据胃排空拟合曲线计算固体相延滞期（ＳＬＰ）和滞后期半排空时间（ＨＳＥＴ），以及液体相半排空时间（ＨＬＥＴ），其     

原发性胆汁反流性胃炎诊断的探讨

目的　探讨原发性胆汁反流性胃炎的诊断方法及十二指肠胃反流 (DGR)的临床意义。方法　用便携式胆红素监测仪 (Bilitec2 0 0 0 )对 2 0例健康人及 42例有腹痛、腹胀、恶心及呕吐胆汁等症状的非溃疡性消化不良患者进行 2 4h胃内胆红素监测、临床症状评分、胃镜检查及组织活检。分析DGR的严重度与症状、内镜所见和组织学改变之间的关系。结果　 2 4h胆汁反流总时间百分率在健康组和有症状组中分别为 (2 92± 2 39) %及 (1 7 68± 1 7 89) % (P <0 0 1 ) ,病理性DGR的检出率为55 %。内镜下黏液湖胆染、胃窦黏膜糜烂、胆染伴胃窦黏膜糜烂、胆染伴中度以上的充血者中病理性DGR的检出率分别为 86 %、88%、8/8、85 %。内镜检查发现黏液湖胆染和胃窦黏膜糜烂和 (或 )中度以上充血并被Bilitec2 0 0 0证实存在病理性DGR的胆汁反流性胃炎 (BRG)者共有 1 1例。幽门螺杆菌(Hp)阴性的BRG者 ,组织学上活动性炎症比生理性DGR组Hp阴性者严重 (P <0 0 5)。各项临床症状的发生率在各组间差异无显著性 (P值均 >0 0 5) ,但BRG组腹胀、恶心及呕吐胆汁等症状的严重程度显著重于生理性DGR组 (P值均 <0 0 5)。结论　完整胃内镜检查发现黏液湖胆染同时伴胃窦黏膜糜烂和 (或 )中度以上充血并被Bilitec2 0 0 0证实存在病理性DG     

调胃降逆胶囊治疗胆汁反流性胃炎70例

目的观察调胃降逆胶囊对胆汁反流性胃炎的疗效。方法按《中药新药临床研究指导原则》设立治疗组和对照组,治疗组70例,药用调胃降逆胶囊,每次6粒,每日3次;对照组30例,药用吗丁啉,每次10mg,每日3次,均饭前服,疗程1个月。结果治疗组总有效率为92.9％,对照组为76.7％,经统计学处理,两组疗效有显著性差异。结论调胃降逆胶囊治疗胆汁反流性胃炎疗效优于吗丁啉。     

胆汁反流性胃炎病因分析

胆汁反流性胃炎（bile reflu gasritis,BRG）又称碱性反流性胃炎,是一种常见的胃部疾病,是由于含有胆汁的十二指肠液反流人胃内引起的胃黏膜炎症,胆汁反流性胃炎的病因对该病的治疗有着重要的临床意义,笔者通过我院明确诊断150例胆汁反流性胃炎,对其病因做初步分析和探讨。     

中医药治疗胆汁反流性胃炎概况

慢性胆汁反流性胃炎是临床常见病,以病程长、反复发作、缠绵难愈为其临床特点.现代医学认为,本病多因幽门功能不全、胃排空能力低下、十二指肠压力增高、反流液中胆酸盐等物质反复刺激胃黏膜屏障,从而导致胃黏膜的慢性炎症、糜烂及溃疡的发生.近年来,随着胃肠动力系列药相继问世,胃动力药与制酸剂及黏膜保护剂联合应用对治疗胆汁胃食管反流病虽取得了一定进展,但对病程较长、病情较重者,疗效较差,至今尚缺少行之有效的方法.积极寻求有效方法,提高疗效,降低其复发率,是临床医家亟待解决的难题,亦是当前研究之热点.现将近10年来中医治疗胆汁反流性胃炎疡情况综述如下.     

胃力康治疗胆汁反流性胃炎50例

本文回顾性研究2 0 0 1年3月～2 0 0 2年2月我院门诊用中药胃力康治疗的胆汁反流性胃炎患者5 0例,并与同期用吗丁啉者作比较,现报告如下。1　资料与方法1 .1　临床资料:90例患者中男68例,女2 2例,年龄1 8～70岁,平均39.5岁。均有胸骨后烧灼感、上腹部疼痛、腹胀、嗳气反酸、口干口苦等临床表现,病史3个月以上。胃镜检查均有明显的胆汁反流现象和胃粘膜炎症改变。随机分成两组,治疗组5 0例,对照组40例,两组患者性别、年龄及临床表现差异无显著性意义( P >0 .0 5 ) ,具有可比性。1 .2　治疗方法:治疗组给予胃力康(组方:柴胡、枳壳、川黄连、…     

Ursodeoxycholic acid treatment of bile reflux gastritis

Intractable epigastric pain associated with nausea and bilious vomiting often follows gastric surgery and has been attributed to reflux of bile and the irritating effects of endogenous bile acids on the gastric remnant. To test the effect of changing bile acid composition of the refluxed material on the symptoms and gastric mucosal histology, 12 patients with symptomatic alkaline reflux gastritis were treated for 1 mo with placebo and for 1 mo with ursodeoxycholic acid, 1000 mg/day. Before treatment, all patients were symptomatic and manifested epigastric pain, nausea, and bilious vomiting. The gastric mucosa was erythematous, friable, and bile stained, and the histology revealed chronic inflammation. No significant change in symptoms was noted during administration of placebo. In contrast, ursodeoxycholic acid treatment resulted in a profound decrease in the intensity and frequency of pain and almost abolished nausea and vomiting. During bile acid therapy the proportion of ursodeoxycholic acid in gastric bile rose to 50% of total bile acids, whereas cholic and deoxycholic acids decreased and chenodeoxycholic acid remained unchanged. The macroscopic and microscopic appearance of the gastric mucosa, however, did not change after 1 mo of ursodeoxycholic acid treatment. These results suggest that increasing the proportion of ursodeoxycholic acid in refluxed gastric bile reduces the pain and frequency of symptoms associated with bile reflux.     

兰索拉唑对糜烂性食管炎及非糜烂性胃食管反流病胃电节律影响

目的研究糜烂性食管炎及非糜烂性胃食管反流病患者胃电节律,以及兰索拉唑对其症状及胃电节律的影响。方法采取反流性疾病问卷分析20例糜烂性食管炎（EE组）及20例非糜烂性胃食管反流病（NERD组）4周及8周兰索拉唑30mg／a治疗前后的症状程度,并使用体外胃电图描述方法记录10名健康志愿者（对照组）胃电节律,以及EE组及NERD组患者4周及8周兰索拉唑30mg／d治疗前后的胃电节律。结果EE组和NERD组均存在胃电节律的异常,且与对照组有明显差异（P〈0．05）,并且EE组与NERD组之间无明显差异（P〉0．05）。经过兰索拉唑30mg／d治疗后,EE组及NERD组RDQ评分均较前好转,并且治疗8周后的RDQ评分小于治疗4周时（P〈0．05）,且两组之间无明显差异。治疗4周时EE组的餐前及餐后的正常慢波百分率较治疗前明显升高（P〈0．05）,而NERD组治疗4周时正常慢波百分率较治疗前无明显变化（P〉0．05）。当兰索拉唑30mg／d疗程满8周时两组餐前、餐后的正常慢波百分率均较治疗前明显升高（P〈0．05）,并且与对照组比较无差异（P〉0．05）。结论EE及NERD均存在胃电节律异常,兰索拉唑不仅能缓解EE及NERD的症状,也能使其胃电节律恢复正常。     

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.     

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.     

Enhanced postprandial gastric myoelectrical activity after moderate-intensity exercise

OBJECTIVE: The aim of this study was to investigate the change of postprandial gastric myoelectrical activity and its relation with vagal activity after exercise. METHODS: Nine subjects were studied in two sessions. In the control session, gastric myoelectrical activity was recorded using electrogastrography (EGG) for 30 min in the fasting state and 60 min after a test meal. In the exercise session, after the baseline recording of both the EGG and electrocardiogram (ECG), the subject was put on a cycle ergometer for exercise until reaching 50% of the maximum age-predicted heart rate for 10 min. The test meal was then given and the recording was resumed for 60 more minutes. Spectral analyses were performed on both the EGG and the heart rate variability derived from the ECG. RESULTS: The postprandial increment of the dominant power (p<0.05) and the percentage of the 2-4 cpm slow waves (p = 0.01) were significantly higher with exercise. The standard deviation of the postprandial dominant frequency was significantly decreased (more stable slow waves) with exercise (p<0.04). While cardiac vagal activity was significantly decreased after the meal, exercise did not significantly affect the postprandial change. CONCLUSIONS: Gastric slow waves become more regular, more stable, and of higher amplitude after exercise, and this enhancement is probably not mediated via the vagal pathway.     

康复新液治疗儿童胆汁反流性胃炎临床研究

[目的]探讨康复新液对儿童胆汁反流性胃炎的治疗效果。[方法]2006年1月-2008年6月胃镜诊断为胆汁反流性胃炎患儿82例,随机分为治疗组和对照组,2组均予达喜0．5g／次,3次／d,多潘立酮5mg／d,3次／d口服治疗,治疗组在此基础上加用康复新液5ml／次,3次／d口服,疗程均1个月,比较分析2组临床症状评分、胃镜下评分及有效率。[结果]治疗组有效率92．6％,对照组65．8％,2组有效率、治疗后临床症状评分和胃镜下评分比较差异均有统计学意义（均P〈0．05）。[结论]康复新液对儿童胆汁反流性胃炎有较好疗效。     

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.     

Clinical characteristics of bile reflux gastritis

Thirty patients with bile reflux gastritis, proven by gastroscopy and Milk 99mTc-EHIDA Test, were studied and their clinical features were compared with those of patients with non-bile reflux gastritis. The symptoms were similar in both groups of patients, whereas histologically in bile reflux gastritis there were more hyperemia of mucosa, more obvious edema in lamina propria and more polymorphonuclear infiltration. Furthermore, in bile reflux gastritis the histological changes were more severe in the antrum and decreased in severity toward the cardia. Acid secretion was significantly lower in patients with bile reflux gastritis than in patients with non-bile reflux gastritis while the serum gastrin level was significantly higher in the former than in the latter group. The authors suggest that there may be a vicious cycle among duodenogastric reflux, low level of gastric acidity and high level of serum gastrin. When duodenogastric reflux occurs, not only the bile salts damage the gastric mucosa and subsequently cause the back diffusion of hydrogen ion but also the alkaline duodenal juice neutralizes the gastric acid, resulting in decrease of gastric acidity. The bile salts and low acidity can stimulate the release of serum gastrin which antagonizes the effects of cholecystokinin and secretin on pyloric tone and aggravates the duodenogastric reflux.     

Prevalence of Helicobacter pylori, gastric myoelectrical activity, gastric mucosal changes and dyspeptic symptoms before and after laparoscopic cholecystectomy

BACKGROUND/AIMS: Cholecystectomy may lead to anatomic and functional alterations which eventually induce reflux of duodenal contents with its sequlae. The aim of this study is to evaluate the prevalence of Helicobacter pylori (H. pylori), gastric myoelectrical activities and gastric mucosal changes before and after laparoscopic cholecystectomy. METHODOLOGY: This prospective study has been carried out on 46 patients (20 M & 26 F) with mean age 41.7+/-0.2 years for whom laparoscopic cholecystectomy for gallstones was carried out. Prior to the operation and 1 year after, all patients were subjected to clinical assessment, upper gastrointestinal endoscopy, histopathology of antral mucosa, reflux gastritis score, detection of H. pylori and electrogastrography. RESULTS: There was an increase in the postoperative suggestive symptoms of reflux gastritis compared to the preoperative: epigastric pain increased from 8 (17.4%) to 11 (23.39%) patients, nausea increased from 6 (13%) to 12 (26.1%) and bilious vomiting increased from 3 (6.5%) to 11 (23.9%) patients. Mild antral gastritis was detected endoscopically before laparoscopic cholecystectomy in 20 patients (43.5%) and increased to 27 patients (58.7%) after surgery. Meanwhile, severe antral gastritis and erosions were only detected after the operation in 10 (21.7%) patients, respectively. The histological results showed an increase of the histopathologic score of reflux gastritis after cholecystectomy from 4.28 (+/-1.56) to 9.28 (+/-1.99) (p<0.001). Active chronic superficial gastritis decreased from 23 (50%) to 13 (28.2%) patients while the inactive form increased from 15 (32.6%) to 23 (50%) patients. Also, chronic atrophic gastritis, intestinal metaplasia and dysplasia were detected postoperatively in 4 (8.6%) patients. The incidence of H. pylori infection was decreased from 32 (69.6%) to 19 (41.3%) patients (p<0.0001). Electrogastrography abnormal frequency decreased in fasting from 26.1% to 8.7% (p<0.001), and postprandial from 16.9% to 4.4% recording (p<0.002). On the other hand, there was an increase in the number of patients with decreased electrogastrography amplitude after a meal from 4.3% to 28.3% (p<0.0001). CONCLUSIONS: Our study shows that dyspeptic symptoms, endoscopic and histologic gastric changes as well as electrogastrography abnormalities are present before and increase after cholecystectomy; meanwhile H. pylori colonization in gastric mucosa is decreased after cholecystectomy.