肝硬化门脉高压性胃病镜下特征分析

目的：观察肝硬化门脉高压性胃病（ＰＨＧ）的内镜特征。方法：ＯｌｙｍｐｕｓＣＩＦ－Ｑ２型电子胃镜对８８角诊肝硬化门脉高压症及１００例非门脉高压症对照组进行镜下观察,结合病检综合分析。结果：ＰＨＧ发生率６１．３６％。Ｍｏｓａｉｃ病变达９８．１％,合并樱桃红斑者占４２．５％,位于底体合并者占４９．０５％,局限一胃底３０．１８％。而１００例对照组中无１例ｍｏｓｄａｉｃ病变。结论：肝硬化门脉高压并发胃粘膜病     

肝硬化并发门脉高压性胃病临床分析

目的:观察门脉高压性胃病(PHG)发病率与肝功能分级及食管静脉曲张(EV)严重程度的关系.方法:对200例肝硬化住院患者采用回顾性分析,将PHG的发病率与肝功能分级及EV严重程度进行比较.结果:200例肝硬化患者中,PHG 97例(48.5%),EV154例(77%).肝功能Child-Pugh分级与PHG发病率呈明显正相关(P<0.01),EV程度与PHG发病率亦呈明显正相关(P<0.01).结论:PHG的发病率与肝功能分级及EV严重程度之间呈正相关.     

肝硬化门脉高压性胃病相关因素分析

目的:探讨肝硬化门脉高压性胃病(portal hypertensive gastropathy,PHG)与肝功能、食管-胃底静脉曲张分级及其他相关因素的关系.方法:胃镜观察已确诊的107例肝硬化患者胃黏膜病变及食管-胃底静脉曲张程度,测定血清胆红素、白蛋白、凝血酶原时间、肌酐及腹水量,肝功能进行Child-Pugh及MELD分级,数据进行统计学分析.结果:PHG内镜表现以马赛克征、蛇皮样病变、猩红热样疹最为常见,多位于胃底及胃体,其发生与食管静脉曲张程度、肝功损害程度及酒精、胆汁等刺激性因素有关,与胃底静脉曲张无相关性.结论:肝硬化PHG内镜特征明显,门脉高压是PHG形成的必备条件,同时也有其他损伤因素的参与.     

肝硬化门脉高压性胃病临床分析

目的探讨肝硬化门脉高压性胃病的临床特点。方法回顾性分析41例临床诊断为乙型肝炎肝硬化患者的临床资料，依据胃镜下是否存在门脉高压性胃病，将其分为PHG组和非PHG组，对二组资料的血常规、肝脏生化、凝血功能、T淋巴细胞亚群、B超及胃镜检查结果进行统计学分析。结果41例肝硬化患者中PHG共14例，占34．1％。PHG组与非PHG组胃底静脉曲张程度（X^2=10．342，P=0．001），胃底静脉重度曲张伴红色征阳性（X^2=10．342，P=0．001），食管静脉重度曲张伴红色征阳性（X^2=3．873，P=0．049），食管胃底静脉重度曲张伴红色征阳性（X^2=3．873，P=0．049），RDW（t=-2．322，P=0．026），MPV（t=2．149，P=0．038），PIA（t=2．064，P=0．046），CD3＋计数（t=3．292，P=0．017）、CD4^＋计数（t=3．642，P=0．011）及脾脏厚度（t=-2．952，P=0．005）、脾长径（t=-2．241，P=0．031）、门静脉内径（t=-2．177，P=0．044）及脾静脉内径（t=-2．235，P=0．031）等差异具有显著性意义，而二组间白细胞计数、血小板计数、肝脏生化、Child-pugh评分及分级等差异无显著性（P〉0．05）。结论（1）门静脉高压与肝功能下降均是PHG发生的重要因素。（2）PHG常伴有机体免疫紊乱。（3）PHG与胃底静脉曲张程度相关。     

36例门脉高压性十二指肠病的临床及内镜特点分析

目的研究门脉高压性十二指肠病（PHD）的内镜及临床特点。方法回顾性分析门脉高压性十二指肠病患者的临床和胃镜资料。结果31例患者中腹水28例;食管胃底静脉曲张轻度8例,中度9例,重度19例;36例患者均有门脉高压性胃病;PHD轻度17例,中度13例,重度6例。且PHD与门脉高压性胃病及食管胃底静脉曲张相平行。结论PHD临床表现无特异,与普通十二指肠炎表现不同,常与门脉高压性胃病并存,发病机制与门脉高压有关。     

肝硬化门脉高压性胃病的相关性研究

目的探讨肝硬化门脉高压性胃病（PHG）的临床特点及其与肝功能分级、食管静脉曲张以及食管静脉曲张套扎术干预治疗的关系。方法对268例肝硬化患者进行肝功能及常规胃镜检查，并对其并发PHG及干预治疗后PHG情况进行分析。结果268例肝硬化患者有不同程度的食管静脉曲张246例（91．8％），PHG发生率为102例（38．1％），原为轻型PHG22例患者在接收套扎术治疗后6例（27．2％）转化为重型PHG。随肝功能分级积分（级别）的增加以及食管静脉曲张严重程度的增加，PHG发病率增加（P〈0．05）。结论肝硬化患者PHG发病率随肝功能分级、食管静脉曲张严重程度的增加以及多次干预食管静脉曲张治疗手段而上升。     

肝硬变并发门脉高压性胃病的研究

目的　探讨肝硬变并发门脉高压性胃病的情况。方法　对 390例门诊及住院的肝硬变患者常规进行胃镜检查 ,并对不同肝功能水平患者门脉高压性胃病发生情况进行回顾分析。结果　 390例肝硬变患者中 ,食管 胃底静脉曲张 330例 (84 .6 % ) ;门脉高压性胃病发生率 4 9.2 % (192例 )。根据Child Pugh分级将肝功能分为A、B、C 3级 ,随肝功能级别增加门脉高压性胃病发生率随之增加 ,随食管 胃底静脉曲张严重程度上升 ,门脉高压性胃病发生率亦呈上升趋势 (P <0 .0 5 )。结论　门脉高压性胃病随肝功能分级增加而上升 ,随食管 胃底静脉曲张严重程度的增加而上升 ,对肝硬变患者应常规胃镜检查。     

肝硬化门脉高压性胃病98例临床分析

各种原因引起的肝硬化是门脉高压的重要原因。门脉高压性胃病是门脉高压症的重要并发症，它不同于非门脉高压患者的胃炎，其特征为胃镜下胃黏膜出现特殊病变伴有黏膜和黏膜下微细血管、毛细血管的明显扩张、扭曲．组织学上表现为血管扩张，黏膜下层动静脉短路开放和固有膜水肿，伴或不伴有炎性细胞浸润。笔者对2001～2004年98例确诊为肝硬化门静脉高压性胃病的患者做出以下临床分析。     

肝硬化门脉高压性胃病45例临床分析

目的 探讨肝硬化门脉高压与胃粘膜病变的关系。方法 对45例肝硬化门脉高压患者进行电子胃镜检查，仔细观察胃粘膜及食道病变。结果 门脉高压性胃部（PHG）占57.78%；门脉高压性胃病直接导致出血占26.09%。结论 (1)肝硬化门脉高压患者胃粘膜病变较一般人群明显增多。(2)门脉高压性胃病是肝硬化出血的重要原因。     

肝硬化门脉高压性胃病与幽门螺杆菌感染

肝硬化门静脉高压症最危险的并发症是上消化道出血，以往通常把出血原因归咎于食管或胃底曲张静脉破裂。但近10余年来，广泛开展的胃镜调查发现，其中10％～60％是由门静脉高压性胃病（portal hypertensive gastropathy，PHG）引起，PHG出血的临床意义已引起学术界的高度重视。幽门螺杆菌感染是慢性胃炎的主要致病因素，但其与以乙型肝炎肝硬化为病因的PHG相关关系，目前尚缺乏细致、系统的研究。为此，本文旨在探讨幽门螺杆菌感染与PHG的相关关系，以指导临床治疗。     

血清胃蛋白酶原1、2在胃癌诊断中的价值

目的 探讨血清胃蛋白酶原（PG）检测对胃癌诊断价值.方法 采用胶乳增强免疫比浊法对36例非萎缩性胃炎、39例胃溃疡、31例萎缩性胃炎及42例胃癌患者血清PG1、PG2水平进行了检测.结果 非萎缩性胃炎组、胃溃疡组、萎缩性胃炎组及胃癌组中血清PG1水平及PG1/ PG2比值（PGR）逐渐降低,以胃癌组降低最为明显,显著低于其他三组患者（P〈0.01）,胃溃疡组血清PG2水平显著高于其他三组（P〈0.01）,其他三组血清PG2水平无统计学差异（P〉0.05）,以PG1〈70 μg/L,且PGR〈3.0为判断界值,其诊断胃癌的敏感性为78.6%,特异性为85.8%.结论 血清PG1及PGR明显降低可作为胃癌及癌前病变的一项血清学诊断指标,对于提高胃癌早期诊断率和早期治疗率,从而降低病死率具有积极意义.     

Clinical relevance of colonic lesions in cirrhotic patients with portal hypertension

BACKGROUND AND STUDY AIMS: This prospective study was conducted in order to evaluate whether the colonic lesions previously described in cirrhotic patients may be of clinical relevance. PATIENTS AND METHODS: Eighty-five patients with cirrhosis of the liver, but without colonic or systemic diseases unrelated to the liver disease, underwent colonoscopy and were followed up for at least 2 years. RESULTS: Colonic varices were observed in 31 % of the patients, portal hypertensive colopathy (PHC; defined as diffuse hyperemia, edema, spider angiomas, and spontaneous bleeding of the colonic mucosa) in 54 %, and normal colonic findings in 18 %. Colonic varices and PHC were present simultaneously in 27 % of the patients. Previous sclerotherapy or band ligation treatment for esophageal varices had been carried out in 27 % and 23 % of the patients, respectively. Portal hypertensive gastropathy was observed in 42 % of the patients. Polyps were found in 12 % of the cirrhotic patients and cancer in 3 %. All of the patients were followed up for at least 2 years; 34 % of them developed upper gastrointestinal hemorrhage (81 % from esophageal varices, 19 % from the stomach), while only 6 % developed lower gastrointestinal bleeding. CONCLUSIONS: Colonic lesions are frequent in cirrhotic patients, but statistical analysis showed that these lesions are not specific for the disease and do not correlate with the etiology and degree of cirrhosis, with the endoscopic treatment of esophageal varices, or with the risk of bleeding from the lower gastrointestinal tract.     

Improvement of portal hypertension and hepatic blood flow in cirrhotic rats by oestrogen

BACKGROUND: In this study, we investigated the effects of oestrogen on nitric oxide synthase activity and nitric oxide production using the cirrhotic rat liver. MATERIAL AND METHODS: Cirrhosis was induced by dimethylnitrosamine. Estradiol valerate was subcutaneously injected twice at week 4 after dimethylnitrosamine treatment. Furthermore, subcutaneous injection of an oestrogen receptor antagonist, ICI-182.780, was performed 2 days before administration of estradiol valerate. Portal pressure and hepatic blood flow were measured. Nitric oxide synthase activity was assessed by l-citrulline generation. Sinusoidal endothelial cells were isolated from the cirrhotic rat liver and cultured. The cells were incubated with estradiol and/or ICI-182.780 for 24 h. Images for nitric oxide in sinusoidal endothelial cells were obtained using diaminofluorescein-2 diacetate. RESULTS: Cirrhotic rats treated with estradiol valerate showed a significant decrease in portal pressure and a significant increase in hepatic blood flow compared with those of control cirrhosis rats. However, in cirrhotic rats treated with ICI-182.780, the reduction of portal pressure and elevation of hepatic blood flow were completely inhibited. In cirrhotic rats treated with estradiol valerate, nitric oxide synthase activity was increased compared with that in control cirrhotic rats. The fluorescent level of intracellular nitric oxide in estradiol-stimulated, cultured, sinusoidal endothelial cells was higher than that in nontreated sinusoidal endothelial cells. CONCLUSIONS: The present study indicated that oestrogen plays an important role in the enhancement of nitric oxide production in sinusoidal endothelial cells of cirrhotic liver and reduces the portal pressure in cirrhotic rats.     

糖尿病视网膜病变时TXB2及6-Keto-PGF1α的动态变化及临床意义

目的探讨TXA2及PGI2在糖尿病视网膜病变时的变化规律及临床意义.方法运用放射免疫方法对35例糖尿病视网膜病变临床前期患者、36例糖尿病视网膜病变背景期患者、32例糖尿病视网膜病变增殖期患者以及35例健康人进行TXB2及6-Keto-PGF1α的定量检测.结果各期糖尿病视网膜病变患者的TXB2及6-Keto-PGF1α检测值与对照组均有显著性差异,糖尿病视网膜病变临床前期、背景期及增殖期之间的TXB2及6-Keto-PGF1α水平亦显著不同.结论检测糖尿病患者的TXB2及6-Keto-PGF1α水平对糖尿病视网膜病变的早期诊断和预防以及临床治疗具有重要意义.     

Association of serum pepsinogen with degree of gastric mucosal atrophy in an asymptomatic population

BACKGROUNDAtrophic gastritis is a precancerous lesion of the stomach. It has been reported that pepsinogen (PG) can reflect the morphology and function of the gastric mucosa, and it is therefore used as a marker for the early diagnosis of atrophic gastritis.AIMTo evaluate the diagnostic value of serum PG for degree of gastric mucosal atrophy in asymptomatic Chinese upon physical examination.METHODSMedical data were collected from subjects who underwent transnasal gastroscopy between October 2016 and October 2018. For each study subject, serum PG levels and presence of Helicobacter pylori (H. pylori) infection were investigated. Pathology was evaluated using the Operative Link for Gastritis Assessment (OLGA) classification and Operative Link on Gastric Intestinal Metaplasia Assessment (OLGIM) systems. All statistical analyses were carried out using SPSS statistical software.RESULTSA total of 2256 subjects were enrolled and 1922 cases were finally included in the study. Based on the OLGA grading system, the levels of PGI were slightly decreased, while those of PGII were slightly increased. The PGI/PGII ratio (PGR) was reduced with increasing atrophy. The association between PG and OLGA grading was higher compared with that between PG and the OLGIM grading system. Compared with the OLGA-0 group, a statistically significant difference was observed in the mean age of OLGA-I, III, and IV groups (P < 0.05). In the H. pylori-positive subjects, the PGR levels were notably lower in the OLGA-I, II, and III groups compared with the OLGA-0 group (P < 0.05). H. pylori-positive subjects exhibited significantly higher PGI and PGII serum levels and a significantly lower PGR compared with H. pylori-negative patients in different OLGA groups (P < 0.05). CONCLUSIONSerum PG levels may represent a non-invasive screening marker for gastric mucosal atrophy in asymptomatic subjects.     

阿米洛利预处理对浸水束缚应激模型大鼠胃黏膜损伤的影响

目的:观察阿米洛利(amiloride)预处理对浸水束缚应激大鼠胃黏膜损伤的影响.方法:30只雄性Wistar大鼠随机分为正常对照组(NC组,n=10)、WIRS对照组(ws组,n=10)和amiloride预处理组(AM组,n=10).在(20±1)℃水温下,浸水束缚应激法复制大鼠急性胃黏膜病变模型.6 h后处死取胃组织标本,10倍解剖显微镜下观察各组胃黏膜溃疡指数(UI),光学显微镜下观察各组标本组织学改变,并用比色法测定各组胃组织中丙二醛(MDA)与超氧化物歧化酶(SOD)的含量变化.结果:WS组大鼠胃黏膜呈暗红色,有大量点状出血、线状出血或片状糜烂,黏膜下血管和皮区血管充血,光镜下上皮细胞黏液层变薄、缺失,细胞间隙变大,有不同程度的坏死;而AM组大鼠浸水束缚应激6 h后大鼠黏膜出血或糜烂程度较WS组明显好转,光镜下虽可见大量毛细血管充血扩张,上皮细胞黏液层有少许缺损,但基本完整.与NC组比较,WS组大鼠浸水束缚应激6 h后,胃黏膜UI显著增高(P＜0.01).胃组织SOD活性降低,MDA含量显著增高(P＜0.01);Amiloride预处理能显著降低浸水束缚应激大鼠UI(P＜0.01),提高SOD活性,降低MDA水平(P＜0.01).结论:Amiloride可有效地保护氧自由基介导性浸水束缚应激大鼠急性胃黏膜损伤或病变,提示酸敏感离子通道可能参与了浸水束缚应激大鼠急性胃黏膜病变的发生机制.     

Noninvasive grading of the severity of portal hypertension in cirrhotic patients by echo-color-Doppler

The possibility of estimating portal hypertension combining splenic Doppler pulsatility index (PI), which has been shown strictly to be related to portal resistance, and portal blood flow (PBF) was evaluated. Hepatic venous pressure gradient, and splanchnic Doppler parameters were measured in 40 cirrhotic patients. A formula to assess the severity of portal hypertension from Doppler parameters was calculated in a training group of 19 patients, and then this formula was tested to prospectively predict the degree of portal pressure in 21 further patients. In the training group, the regression of portal resistance over splenic PI was calculated and individual values of estimated portal resistance were obtained for every patient of the test group. From them and from observed values of PBF, an estimated value of portal pressure was calculated. The following formula was obtained [(0.066*splenic PI -0.044)*PBF]. In the second group, predicted and observed portal pressure were well correlated (r = 0.71, p = .0003). A good accuracy for the prediction of mild or severe portal hypertension was obtained.     

IL-6、CRP和血清过敏原检测对急性荨麻疹的临床价值

目的 探讨血清过敏原检测、血清总免疫球蛋白E(IgE)抗体、过敏原特异性(sIgE)抗体、白细胞介素(IL)-6、C反应蛋白(CRP)水平对于急性荨麻疹的临床价值.方法 选取2018年6月—2019年12月上海市浦东新区浦南医院75例荨麻疹患者作为研究组,另选取同期75名健康体检者作为对照组,比较2组血清总IgE抗体、...     

生态营养对重型颅脑创伤继发急性胃黏膜损伤大鼠血清肿瘤坏死因子的影响

[目的]观察生态营养对重型颅脑创伤继发急性胃黏膜损伤大鼠血清肿瘤坏死因子(TNF-α)的影响.[方法]建立大鼠重型颅脑创伤模型,将Sprague-Dawley大鼠随机分为正常对照组(C组)和实验组,实验组又分为创伤对照组(Ⅰ组)、肠内营养组(EN组)和生态营养组(EC组),创伤喂养1 d、3 d、5 d取标本,采用液相竞争法检测血清TNF-α含量.[结果]EC组、EN组和Ⅰ组3个时相点的血清TNF-α含量较C组明显升高(P＜0.01);EN组与Ⅰ组相比血清TNF-α在3个时相点虽有下降趋势,但差异无统计学意义(P＞0.05);EC组创伤喂养3 d、5 d血清TNF-α含量低于Ⅰ组(P＜0.01或P＜0.05);EC组在不同时相点血清TNF-α含量与EN组比较差异无统计学意义(P＞0.05).[结论]大鼠重型颅脑伤后给予生态营养可以降低促炎性细胞因子TNF-α的含量,从而降低重型颅脑创伤后继发急性胃黏膜损伤的发生率.