原发性十二指肠胃反流程度与胃部炎性反应关系的研究

目的探讨原发性十二指肠胃反流程度与胃部炎性反应关系。方法选择我院2009年3月-2011年3月60例原发性十二指肠胃反流患者及体检中心60例健康志愿者作为正常对照,通过24 h胃内胆红素监测分为低反流组及高反流组,分别检测血清及胃液中IL-1、IL-6、IL-8、IL-10及TNF-α浓度。结果与对照组比较,原发性十二指肠胃反流组IL-1、IL-6、IL-8、IL-10及TNF-α的血清浓度均随反流程度加重而显著升高;IL-1与IL-6在胃液中浓度升高较血清更为明显。结论 IL-1、IL-6在胃液中浓度增加程度能作为十二指肠胃反流严重程度的预测指标。     

伊托必利联合富马酸伏诺拉生片治疗胃食管反流病的疗效及对患者CGRP、5-HT水平变化的影响

目的:探讨伊托必利联合富马酸伏诺拉生片治疗胃食管反流病(GERD)的疗效及对患者降钙素基因相关肽(CGRP)、5-羟色胺(5-HT)水平变化的影响。方法:选取2018年12月—2020年12月收治的86例GERD患者进行前瞻性研究,以简单随机化法分为观察组(n=43)、对照组(n=43)。对照组给予伊托必利联合埃索美拉唑治疗,观察组给予伊托必利联合富马酸伏诺拉生片治疗。比较2组疗效、不良反应及治疗前后食管黏膜损伤程度、食管24 h pH值监测参数、血清炎性因子[白细胞介素6(IL-6)、IL-1β、肿瘤坏死因子α(TNF-α)]、CGRP、5-HT水平。结果:观察组总有效率高于对照组(97.67%vs 81.40%,P<0.05);治疗后2组食管黏膜损伤程度均改善,且观察组优于对照组(P<0.05);治疗后2组>5 min反流次数、4 h反流次数、pH值<4总时间百分比、最长反流时间低于治疗前,且观察组低于对照组(P<0.05);治疗后2组血清CGRP、5-HT、IL-6、IL-1β、TNF-α水平低于治疗前,且观察组低于对照组(P<0.05);2组...     

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.     

老年急性脑出血患者血清炎性因子水平变化及其临床意义

目的分析老年急性脑出血患者血清炎性因子水平变化及其临床意义。方法选取2013年3月—2016年3月东莞市第八人民医院收治的老年急性脑出血患者60例作为观察组,另选取同期体检健康者60例作为对照组。比较两组受试者及不同严重程度、预后急性脑出血患者血清炎性因子水平。结果观察组患者血清白介素1(IL-1)、白介素6(IL-6)、白介素10(IL-10)、超敏C反应蛋白(hs-CRP)、肿瘤坏死因子α(TNF-α)水平高于对照组(P0.05)。重度急性脑出血患者血清IL-1、IL-6、IL-10、hs-CRP、TNF-α水平高于轻度、中度急性脑出血患者,中度急性脑出血患者血清IL-1、IL-6、IL-10、hs-CRP、TNF-α水平高于轻度急性脑出血患者(P0.05)。死亡患者血清IL-1、IL-6、IL-10、hs-CRP、TNF-α水平高于存活患者(P0.05)。结论老年急性脑出血患者血清炎性因子水平升高,且其与患者病情严重程度及预后有关。     

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.     

体外膜肺氧合支持治疗中炎性因子变化的意义

目的:探讨体外膜肺氧合(ECMO)支持治疗期间炎性因子的变化特点及变化规律。方法:42例成人心脏术后心肺功能衰竭患者接受ECMO支持治疗。分别于ECMO建立前及建立1,6,24,48,72小时撤机前采集中心静脉血标本,分离血浆冻存,测定各时点炎性因子TNF-α、IL-6、IL-8、IL-10及hsCRP水平,观察其变化情况。同时按是否发生院内死亡将患者分为死亡组和存活组,比较两组各时点上述指标的差异。结果:ECMO前两组TNF-a、IL-6、IL-8及IL-10等炎性因子的浓度均高于正常值;存活组TNF-α水平在ECMO建立24小时后开始下降,至撤机前明显低于死亡组(P<0.05);存活组IL-6水平在ECMO建立6小时后就开始下降,至48小时后各时点与死亡组相比均明显降低(P<0.05)。存活组TNF-α水平在ECMO治疗24小时、IL-6水平在ECMO治疗6小时后开始下降,撤机前均较死亡组低(P<0.05);死亡组炎性因子支持治疗期间均处于高水平状态。结论:心脏术后心肺衰竭患者ECMO前已存在明显炎性反应。存活组炎性反应强度随病情改善逐渐下降。持续高水平的炎性因子提示预后不良。     

糖尿病合并卒中患者血清炎性因子水平的临床价值

目的探究糖尿病合并卒中患者血清炎性因子水平在糖尿病患者卒中风险中的临床价值。方法选取2017年2月—2018年8月正常组(60例)、单纯脑卒中组(60例)、单纯糖尿病组(74例)、糖尿病合并脑卒中组(66例),共260例。对患者空腹血糖、糖化血红蛋白(HbA1c%)、炎性因子指标进行检测。结果 4组炎性因子比较糖尿病合并卒中组的血清hs-CRP、sICAM-1、sVCAM-1、MCP-1、IL-6、IL-1β、TNF-α水平显著高于其余3组(P0.05)。选择hs-CRP、IL-6、IL-1β、TNF-α对糖尿病合并卒中进行Logistics回归分析,IL-6、IL-1β、TNF-α是糖尿病合并卒中的独立危险因素,随着血清炎症因子水平的增加,糖尿病合并卒中的危险增加(P0. 05)。结论糖尿病患者体内炎性因子水平升高,提示糖尿病卒中患者较单纯卒中与单纯糖尿病患者存在更为严重的炎性反应,炎性因子水平能够反映患者血管炎性病变的程度,对心脑血管并发症有预测价值。     

胃黏膜胆色素染色对原发性病理性十二指肠胃反流的诊断价值

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的诊断价值.方法 86例原发性病理性十二指肠胃反流病人和 42例正常志愿者对照胃黏膜胆色素染色后进行定量分析,应用便携式胆汁监测仪(Bilitec 2000)监测胃内24 h胆汁反流情况,以胆红素吸收值≥0.25的时间百分比作为评价胆汁反流程度的主要观察指标.结果 病例组中胃窦、胃角和胃体部黏膜胆色素沉积显著高于正常对照组(P＜0.01),胃窦和胃角部黏膜胆色素沉积显著高于胃体部(P＜0.01);病例组中胃窦和胃角部黏膜胆色素沉积与胃窦和胃角部黏膜新悉尼系统病理积分均呈正相关(r=0.521,P=0.000和r=0.468,P=0.002),胃体部黏膜胆色素沉积与胃体部黏膜新悉尼系统病理积分无相关性(r=0.185,P=0.236);病例组中胃窦和胃角部黏膜胆色素沉积与胆红素吸收值≥0.25的时间百分比均呈正相关(r=0.458,P=0.002和r=0.334,P=0.028),胃体部黏膜胆色素沉积与胆红素吸收值≥0.25的时间百分比无相关性(r=0.092,P=0.556).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,对原发性病理性十二指肠胃反流有诊断价值,可用于原发性病理性十二指肠胃反流的辅助诊断.     

急性冠状动脉综合征患者血清炎性细胞因子水平及临床意义

目的通过对急性冠状动脉综合征患者血清炎性细胞因子水平的测定及比较,分析炎症及细胞因子在急性冠状动脉综合征发生发展过程中的作用及临床意义。方法选择急性心肌梗死(AMI)患者44例(AMI组),不稳定性心绞痛(UAP)患者44例(UAP组),稳定性心绞痛(SAP)患者43例(SAP组),无冠心病患者35例(对照组),分别检测各组患者血清白细胞介素6(IL-6)、白细胞介素8(IL-8)、白细胞介素10(IL-10)、TNF-α、C反应蛋白(CRP)和基质金属蛋白酶9(MMP-9)浓度并进行比较。结果 AMI组患者血清IL-6、IL-8、IL-10、TNF-α、CRP和MMP-9水平均明显高于SAP组和对照组(P<0.01);AMI组患者血清IL-10、TNF-α、CRP、MMP-9水平明显高于UAP组(P<0.05);UAP组患者血清IL-6、IL-8、IL-10水平明显高于SAP组和对照组;MMP-9和CRP与IL-6呈正相关(r=0.308,r=0.384,P<0.01)。结论冠心痛与炎性反应密切相关,多种细胞因子参与了动脉粥样硬化斑块的形成和进程,血清炎性细胞因子水平的升高是冠状动脉粥样硬化斑块不稳定的标志。     

阿魏酸钠对溃疡性结肠炎模型小鼠炎性因子及免疫功能的影响

目的探讨阿魏酸钠对溃疡性结肠炎(ulcerative colitis,UC)模型小鼠炎性因子及免疫功能的影响。方法选择32只实验小鼠,随机分为空白对照组、模型组、阿魏酸钠低剂量组、阿魏酸钠高剂量组,每组8只,模型组、阿魏酸钠组采用5%葡聚糖硫酸钠制作UC小鼠模型,建模成功后,阿魏酸钠低剂量组经胃管灌胃50 mg/kg阿魏酸钠,阿魏酸钠高剂量组灌灌胃10 mg/kg阿魏酸钠。比较4组血清炎性因子、免疫功能。结果模型组血清白介素1β(IL-1β)、肿瘤坏死因子(TNF-α)明显高于对照组,白介素4(IL-4)明显低于对照组(P0.05),阿魏酸钠干预组血清IL-1β、TNF-α明显低于模型组,IL-4明显高于模型组(P0.05),阿魏酸钠高剂量组血清IL-1β、TNF-α明显低于阿魏酸钠低剂量组,IL-4明显高于阿魏酸钠低剂量组(P0.05);模型组血清免疫球蛋白Ig A、Ig G、Ig M明显高于对照组,补体C3明显低于对照组(P0.05);阿魏酸钠干预组血清Ig A、Ig G、Ig M明显低于模型组,补体C3明显高于模型组(P0.05);阿魏酸钠高剂量组血清Ig A、Ig G、Ig M明显低于阿魏酸钠低剂量组,补体C3明显高于阿魏酸钠低剂量组(P0.05)。结论阿魏酸钠可能通过降低炎性反应、调节体液免疫达到治疗UC的目的,且大剂量阿魏酸钠干预效果更好。     

From gastric inflammation to gastric cancer

The majority of gastric adenocarcinomas are related to chronic inflammation induced by Helicobacter pylori infection. For intestinal-type gastric cancer, a multistep process of mucosal alterations leading from gastritis via glandular atrophy, intestinal metaplasia and dysplasia to invasive carcinoma is well recognized. Ongoing clinical studies focus on a 'point of no return'. It is defined as a situation when certain alterations are no longer reversible by H. pylori eradication and progression to gastric cancer may continue. H. pylori affects the mucosal as well as the systemic immune response by secretion of cytokines and the recruitment of distinct inflammatory cells. The immune response is characterized by a balance between a Th1-dominated response and the recruitment of antigen-specific regulatory T cells that allow the bacteria to persist in human gastric mucosa. Besides immune-mediated effects, H. pylori induces cellular alterations as well as genetic alterations in genes that are essential for the epigenetic integrity and mucosal homeostasis. These genetic alterations during gastric cancer development are in focus of intensive research and should ultimately allow the identification of risk factors involved in gastric carcinogenesis. The detection of individuals at high risk for gastric cancer would help to design appropriate strategies for prevention and surveillance.     

Control of gastric emptying by gastric tone

During ingestion of food, the stomach relaxes to accommodate the meal and, subsequently, a progressive gastric contraction parallels gastric emptying. Intestinal nutrients trigger feedback relaxatory mechanisms that regulate gastric tone and, hence, the nutrient load delivered into the small intestine. This regulation of gastric tone is mediated, at least in part, via the vagus. Defective gastric tone is associated with impaired gastric emptying, as seen in patients with postsurgical gastroparesis. However, increased intragastric pressure, corresponding with defective gastric accommodation, induces abdominal symptoms, but does not alter the gastric emptying pattern. These data indicate that gastric emptying is controlled by complementary mechanisms: gastric tone exerts an emptying force, but gastric outlet resistance is also an important regulator.     

胃起搏对胃动力紊乱犬胃排空及胃肌电活动的影响

目的　研究胃起搏对胃动力紊乱犬胃排空及胃电参数的影响。方法　采用双侧迷走神经干切断术联合应用胰高血糖素建立胃动力紊乱犬模型 ;采用 4导联胃肠电系统微机分析仪记录胃肠浆膜肌电活动 ;99mTc 植酸钠标记的半固体试餐 ,单光子计算机断层显像技术 (SPECT)检测胃半排空时间(GEt1/ 2 ) ;采用适宜起搏参数从胃体、胃窦在腹部投影部位输入起搏信号驱动胃电节律。结果　迷走神经干切断术后犬的GEt1/ 2 为 (79.4 2± 1.91)min ,较术前 (5 6 .35± 2 .99)min明显延迟 (P <0 .0 0 1) ,但行胃起搏治疗后GEt1/ 2 为 (6 4 .94± 1.75 )min ,较治疗前明显加快 (P <0 .0 0 1) ;胃起搏治疗前迷走神经干切断犬餐后的胃电频率为 (0 .0 81± 0 .0 0 7)Hz、胃电幅度为 (2 .32± 0 .35 )mV、慢波的传播速度为 (4 .0 6± 0 .4 0 )cm/s ,均较正常对照犬显著降低 [(0 .0 90± 0 .0 0 6 )Hz ,(4 .2 5± 0 .12 )mV ,(6 .92± 0 .2 4 )cm/s,(P <0 .0 5 ) ],治疗后其餐后胃电频率 (0 .0 92± 0 .0 0 5 )Hz、胃电幅度 (3.97± 0 .19)mV和慢波的传播速度 (5 .5 7± 0 .4 8)cm/s均明显高于治疗前 (P <0 .0 5 )。结论　采用适宜起搏参数输入起搏信号可完全触发胃电慢波 ,改善胃电参数 ,纠正药物导致的异常胃电节律 ,加速胃排空 ,恢     

胃微生态与胃癌的研究进展

胃微生态平衡是人体健康的重要前提,幽门螺杆菌(Helicobacter pylori,Hp)是目前已发现的与胃癌相关的关键病原体之一,普遍存在于人胃黏膜上皮。Hp感染可引起胃内其他菌群的改变,还可引起长期慢性的胃黏膜损伤,导致一系列胃黏膜上皮恶性进展和胃癌的发生。本文就胃微生态与Hp感染的关系、Hp感染在胃癌发生中的作用、胃内其他菌群在胃癌发生中的作用及微生态制剂在胃癌治疗的作用进行综述。进一步揭示Hp感染对胃微生态平衡的影响,胃微生态平衡和Hp感染在胃癌发生发展中的作用及微生态制剂在胃癌治疗中的意义。     

The relationship between gastric microbiota and gastric disease

Traditionally, the stomach was believed to be a sterile organ unsuitable for microbiota growth. However, the discovery of H. pylori subverted this conception. With the development of molecular techniques, an abundance of microbiota of great diversity was found in the stomach. In addition, various lines of evidence suggest that the gastric microbiota plays a critical role in the development and progression of the gastric disease.The gastrointestinal microbiome plays an important role in various physiologic and pathologic processes.     

Endoscopy,gastric ulcer,and gastric cancer

The practice of following benign-appearing gastric ulcers until healing was critically evaluated in a retrospective manner by reviewing all gastric ulcers that were followed with serial endoscopy and all gastric cancers diagnosed at the University of Alabama at Birmingham. The stated purpose of following ulcers to healing is to detect those gastric cancers that may be masquerading as benign ulcer and were not correctly diagnosed at initial endoscopy. Over a five-year period, 148 gastric ulcers were followed with serial endoscopy and in no case was an unsuspected carcinoma found at follow-up endoscopy. In addition, of 67 gastric cancers diagnosed between 1979 and 1986, 62 were suspected of being malignant by the endoscopist at initial examination for an accuracy of 92%. The accuracy rate based solely on biopsy and/or brush cytology was 94%. When endoscopic and biopsy and/or cytology impressions were combined, only one case of gastric carcinoma was not suspected. The overall accuracy was 99%. These results suggest that if either the endoscopic impression or the biopsy and cytology is suspicious for malignancy, then follow-up endoscopy until healing should be done. On the other hand, if, at the initial examination, the ulcer appears benign and biopsy plus cytology are negative, then serial endoscopy has a low benefit relative to its cost.     

The role of gastric microbiota in gastric cancer

ABSTRACT

Gastric cancer represents one of the leading causes of cancer deaths worldwide. Helicobacter pylori (H. pylori) infection is the strongest risk factor associated with gastric cancer. Due to new molecular techniques allowing greater identification of stomach microbes, investigators are beginning to examine the role that bacteria other than H. pylori play in gastric cancer development. Recently, researchers have investigated how the composition of the gastric microbiota varies among individuals with various stages of gastric disease. Specific microbes residing in the stomach have been preferentially associated with gastric cancer patients compared to individuals with a healthy gastric mucosa. Studies conducted on the insulin-gastrin (INS-GAS) transgenic mouse model have provided additional insight into the association between the gastric microbiota and gastric cancer. The purpose of this article is to review the current state of literature on the relationship between the gastric microbiota and gastric cancer based on clinical studies performed to date.     

Relationship between gastric mucosal hemodynamics and gastric motility

Continuous measurement of gastric mucosal hemodynamics (the index of mucosal hemoglobin concentration, the index of oxygen saturation and blood flow) in rats showed oscillatory changes. The mechanism of the oscillations was investigated using a probe specially designed for simultaneous measurement of hemodynamics and intragastric pressure. A hemodynamics-measuring probe for either reflectance spectrophotometry or laser-Doppler flowmetry was tied to a pressure microtransducer, inserted through an incision in the forestomach, and brought into gentle contact with the corpus mucosa. Synchronous oscillatory changes (4-6 cycles/min) in hemodynamics and motility were observed in the resting state (mean blood pressure: 120 mmHg). During moderate hemorrhagic hypotension (mean: 81 mmHg), oscillations in the hemodynamics increased in both amplitude and frequency, while motility remained constant. Oscillations in the hemodynamics were also affected by fluctuations in blood pressure and by topical application of norepinephrine to the corpus serosa. In water-immersion restraint rats, changes in the oscillations in the hemodynamics and motility were virtually synchronous; frequency decreased and amplitude increased. These findings suggest that oscillatory changes in gastric mucosal hemodynamics are regulated not only by gastric motility but also by arteriolar vasomotion of the gastric wall.