不同胃疾患胃内微生态变化的研究

本文对75例不同胃疾患胃液内的菌群及影响胃内微生态环境的因素进行了研究,发现健康胃内基本无菌或只有少量口腔细菌,未发现厌氧菌。而不同胃疾患胃内均分离到细菌(log10~n/ml),慢性萎缩性胃炎:3.89±0.99,残胃炎:4.45±0.16,胃癌:4.23,十二指肠球部溃疡治疗前(2.8±0.62)与抗酸治疗后(4.35±0.61)差别显著,慢性浅表性胃炎:3.39±0.98,胃溃疡:3.42±0.29。所分离到的细菌既有来自于口腔的细菌,也有来自于肠道的细菌。影响胃内细菌增殖的主要因素是胃液的PH值,幽门功能失调及幽门切除亦可使胃内细菌过度生长。本研究提示对胃病的治疗亦应进行生态防治。     

血清胃蛋白酶原联合G-17对萎缩性胃炎及胃癌早期诊断价值

目的:探索检测血清胃蛋白酶原Ⅰ(PGⅠ)、胃蛋白酶原Ⅱ(PGⅡ)、胃泌素-17(G-17)在萎缩性胃炎及胃癌中的诊断价值。方法:收集医院2015年2月至12月门诊及住院的慢性非萎缩性胃炎44例(非萎缩性胃炎组),慢性萎缩性胃炎47例(萎缩性胃炎组),早期胃癌42例(胃癌组)。采用酶联免疫吸附试验(ELISA)测定各组血清PGⅠ、PGⅡ、G-17的水平,同时计算PGⅠ/PGⅡ的比值(PGR),比较各组指标间的差异,同时绘制各指标筛查萎缩性胃炎及胃癌的受试者工作曲线(ROC)曲线,分别评价其诊断价值。结果:胃癌组及萎缩性胃炎组的血清PGⅠ、PGR水平较非萎缩性胃炎组明显下降,且胃癌组下降更明显,差异均具有统计学意义(P0.05),萎缩性胃炎组血清PGⅡ显著低于非萎缩性胃炎组,差异均具有统计学意义(P0.05);胃癌组的血清G-17水平较非萎缩性胃炎组及萎缩性胃炎组均升高,差异有统计学意义(P0.05)。血清PGⅠ筛查萎缩性胃炎的最佳界值为PGⅠ90 ng/m L,其灵敏度和特异度分别为71.5%和51.0%,血清PGR筛查萎缩性胃炎的最佳界值为PGR8,其灵敏度和特异度分别为71.9%和54.0%,血清G-17筛查萎缩性胃炎的最佳界值为G-175 pmol/L,其灵敏度和特异度分别为66.1%和64.0%。血清PGⅠ筛查胃癌的最佳界值为PGⅠ73 ng/m L,其灵敏度和特异度分别为86.0%和74.9%;血清PGR筛查胃癌的最佳界值为PGR3,其灵敏度和特异度分别为90.2%和62.5%;血清G-17筛查胃癌的最佳界值为G-174 pmol/L,其灵敏度和特异度分别为62.5%和61.3%。结论:胃癌及萎缩性胃炎患者血清PGⅠ、PGR水平下降明显,且胃癌患者的血清G-17异常升高,血清PG联合GS-17测定可用于萎缩性胃炎及胃癌的早期筛查。     

大肠癌及大肠息肉患者肠道膜菌群的分析

机体各系统微生态的失衡和某些疾病的发生、发展密切相关。研究它的变化有助于揭示疾病的相关性质及其发生 ,发展的规律 ,如宫颈上皮内瘤样病变的发生与阴道内乳杆菌的明显减少密切相　关 [1] 。胃腔内菌群失调也参与了慢性萎缩性胃炎胃及胃癌的发生与发展[2 ] 。目前对大肠癌及大肠息肉患者肠道菌群的研究较少 ,本文分析了 32例大肠癌及 54例大肠息肉患者肠道膜菌群的变化 ,旨在探讨肠道膜菌群与大肠癌和大肠息肉发生、发展的关系及其临床意义。1材料与方法1 .1　病例选择　大肠癌 32例 ,其中男性 2 1例 ,女性 1 1例 ,年龄介于 39～ 73岁 ,…     

消化道疾病患者胃微生态环境的改变

本文对５９例具有消化不良症状的患者做了内镜检查。取胃粘膜组织进行细菌的分离培养,镜检,测定胃液中的ｓＩｇＡ的含量及ｐＨ。结果表明,不同消化道疾病,胃的微生态环境会发生不同的改变。其中胃癌患者改变最明显,胃内微生物检出率高,ｐＨ均大于４,ｓＩｇＡ含量１４０．５７±３７．４５μｇ／ｍｌ,幽门螺杆菌（ＨＰ）的检出率为６６．７％;溃疡组,ＨＰ的检出率为７９．２％,其它微生物检出率较胃癌组低,ｓＩｇＡ含量１３３．８０±６５．８４μｇ／ｍｌ;胃炎组,微生物的检出率较低,ｓＩｇＡ含量７１．００±６０．３８μｇ／ｍｌ,ｐＨ大部分在２一４。     

树突状细胞对胃癌前病变的免疫保护分析

摘要 目的：探究树突状细胞(Dendritic cells,DC)对胃癌的免疫保护作用。方法：选择2016年1月至2018年1月于我院接受治疗的145例胃癌、39例慢性萎缩性胃炎、21例不典型增生、27例肠上皮化生以及20例正常对照组患者为研究对象,分别采集其胃粘膜标本进行染色,记录和比较其胃粘膜中S100⁺、CD4⁺和CD8⁺细胞的数量、平均面积以及平均吸光度,并将胃癌患者分为中分化腺癌(49例)、低分化腺癌(53例)和未分化癌(43例)进行对比。结果：(1)胃癌组、慢性萎缩性胃炎组、不典型增生、肠上皮化生组的胃粘膜S100⁺阳性细胞计数明显高于正常对照组（P<0.05）,胃癌组平均吸光度低于对照组,其他3组平均吸光度显著高于对照组,(P<0.05);胃癌组平均面积与正常对照组相比无差异(P>0.05),其他三组平均面积显著高于对照组（P<0.05）;(2)慢性萎缩性胃炎组、肠上皮化生组、不典型增生组患者CD4⁺细胞数均低于对照组(P<0.05);胃癌组、慢性萎缩性胃炎组、肠上皮化生组患者平均面积均低于对照组(P<0.05);胃癌组、慢性萎缩性胃炎组、不典型增生、肠上皮化生组平均吸光度均低于对照组(P<0.05);(3)慢性萎缩性胃炎组、肠上皮化生组、不典型增生组患者CD8⁺细胞数明显高于对照组(P<0.05),胃癌组稍低于对照组(P>0.05);胃癌组患者平均面积低于对照组(P<0.05);胃癌组患者平均吸光值低于对照组,慢性萎缩性胃炎组、肠上皮化生组患者高于对照组(P均<0.05);(4)随着胃癌分化程度的降低,胃癌患者DC细胞数有降低趋势。结论：胃癌前病变患者胃粘膜中DC数量会显著增多,免疫功能加强,DC细胞数量会随胃癌分化程度的降低而减少,分析其原因与DC细胞能够抑制癌前病变有关。     

RUNX3与CHFR基因甲基化提示胃癌癌前病变的研究

本研究通过比较胃癌与萎缩性胃炎的RUNX3及CHFR基因表达情况探讨其中的相关性。选取2014年1月至2016年7月前来浙江舟山群岛新区旅游与健康职业学院进行胃镜检查的137例慢性萎缩性胃炎患者作为研究对象,分为胃炎轻度组、胃炎中度组与胃炎重度组,并选取同期胃癌患者42例作为胃癌组。取胃炎患者的胃体与胃窦处的黏膜,胃癌患者的癌灶组织、癌旁组织与远端正常处组织进行DNA的提取,并进行比较。经比较后,胃炎重度组患者的RUNX3与CHFR基因甲基化阳性率分别为29.63%、37.04%,与胃癌组患者的正常组织处比较,有显著的统计学差异,与胃癌组癌灶组织处比较无差异;而胃炎重度组患者的蛋白表达有缺失情况发生,经Elisa检测后,蛋白表达量与胃癌组癌灶组织处比较无差异。严重萎缩性胃炎患者的RUNX3与CHFR基因甲基化可抑制抑癌基因的表达,而异常升高的阳性率会影响患者的病程进展,可认为RUNX3与CHFR基因甲基化对癌前病变进程具有临床诊断意义。     

胃癌患者胃液可溶性白细胞介素2受体的改变

白细胞介素2受体（interleukin－2re－ceptor,IL-2R）,因其在IL－2介导免疫反应中的重要作用,SIL－2R作为免疫功能的标志物与调节物已迅速应用于临床多种疾病的研究[1,2]。但有关胃癌患者胃液SIL－2R改变的文献报道甚少。本文通过对胃癌患者胃液SIL—2R定量分析旨在探讨其病变局部免疫功能状态及其可能相关因素,并为临床诊断胃癌提供了有用资料。1材料与方法1．1材料1．1．1研究对象共91例患者,其中胃癌组（实验组）34例,其他消化道疾病力例（对照组）,后者包括胃溃疡25例、萎缩性胃炎13例、浅表性胃炎19例,上述患者均经电子…     

P53、PCNA、CA724、胃泌素17 及幽门螺杆菌抗体联合检测在萎缩性胃炎与早期胃癌鉴别中的应用价值

目的探讨P53、增殖细胞核抗原(PCNA)、糖类抗原724(CA724)、胃泌素17(G-17)及幽门螺杆菌(HP-IgG)抗体联合检测在萎缩性胃炎与早期胃癌鉴别中的应用价值。方法选取2017年11月至2018年11月在湖南省人民医院(湖南师范大学第一附属医院)消化科行胃镜检查的186例患者作为研究对象,根据病理诊断结果分为正常对照组(50例),萎缩性胃炎组(76例),胃癌组(60例)。采用免疫组化检测P53、PCNA的表达情况;采用电化学发光免疫分析法检测血清CA724水平;采用酶联免疫法检测血清G-17水平;采用胶体金法定性检测HP-IgG抗体表达。分析各指标对萎缩性胃炎与早期胃癌鉴别的价值。结果胃癌组患者P53、PCNA阳性率高于萎缩性胃炎组和对照组(均P0.05)。胃癌组、萎缩性胃炎组患者HP-IgG阳性率明显高于对照组(均P0.05),同时胃癌组HP-IgG阳性率高于萎缩性胃炎组(均P0.05)。胃癌组患者血清CA724水平明显高于对照组和萎缩性胃炎组(P0.05)。胃癌组患者血清G-17水平高于萎缩性胃炎组和对照组(均P0.05),同时萎缩性胃炎组血清G-17水平明显低于对照组(P0.05)。HP-IgG抗体阳性患者P53、PCNA阳性率以及血清CA724、G-17水平均高于HP-IgG抗体阴性患者(均P0.05)。CA724预测胃癌的AUC为0.815,截断值为33.57 U/mL,灵敏度为70.00%,特异性为83.33%。G-17预测胃癌的AUC为0.847,截断值为15.36 U/mL,灵敏度为80.00%,特异性为85.71%。各指标联合检测胃癌的灵敏度、特异性、阳性预测值、阴性预测值及准确度均高于单指标检测。结论胃癌患者P53、PCNA、HP-IgG抗体阳性率较高,血清CA724、G-17水平升高,而萎缩性胃炎患者血清G-17水平降低,可作为萎缩性胃炎与早期胃癌的鉴别指标。各指标联合检测可提高对胃癌的诊断价值。     

抗胃酸分泌药物对胃内菌群的影响

收集４０例内镜确诊为胃十二指肠溃疡病人,随机分成两组,分别予泰胃美、奥美拉唑口服;干服药前后分别行胃镜检查,并抽吸胃液行需氧菌、厌氧菌及真菌培养。结果示：胃液细菌量及硝酸盐还原菌量与胃液ｐＨ值呈正相关（ｒ＝０．８０２和０．７,ｐ＜０．０１）,抗胃酸分泌药物尤以奥美拉唑引起胃内菌量增加明显。临床治疗消化性溃疡时,应注意胃内微生态防治。     

幽门螺杆菌感染对舌苔菌群的影响

探讨慢性萎缩性胃炎患者和慢性浅表性胃炎患者胃内幽门螺杆菌(Helicobacter pylori, H.pylori)感染与舌苔菌群的关系。

根据61名患者内镜、病理和H.pylori检测结果, 将其分成慢性萎缩性胃炎H.pylori阳性组(12名)、慢性萎缩性胃炎H.pylori阴性组(16名)、慢性浅表性胃炎H.pylori阳性组(8名)和慢性浅表性胃炎H.pylori阴性组(25名)。采集舌苔样本进行16S rRNA基因测序, 分析各组患者舌苔菌群结构。

16S rRNA基因测序结果显示, 此次测序样本数据量足够, 样本所含物种的丰富程度和均匀程度合理。4组舌苔菌群样本中Observed species指数差异有统计学意义(H=10.023 3, P < 0.05)。门水平上, 舌苔菌群由拟杆菌门、厚壁菌门、变形菌门3大优势菌门组成。属水平上, 4组间共有11种菌属的丰度差异有统计学意义(均P < 0.05)。在慢性萎缩性胃炎患者中, H.pylori阳性的患者拟普雷沃菌属相对丰度显著低于H.pylori阴性患者, 而罗氏菌属的相对丰度则显著升高。此外, 61例舌苔菌群样本中, 仅1例检测到H.pylori。

H.pylori感染与舌苔菌群结构存在相关性, 然而胃内与口腔中H.pylori的具体关联还需要进一步研究。

     

Endoscopic review of patients who have had gastric surgery.

Seventy one patients who had had operations on their stomachs over 15 years previously were examined by endoscopy and multiple mucosal biopsy sampling. Sixty six had histologically proved gastritis (56 chronic atrophic gastritis, 10 superficial gastritis), 38 intestinal metaplasia, and 11 epithelial dysplasia. In three cases the epithelial dysplasia was severe (carcinoma in situ). One patient had an infiltrating carcinoma and another, whose biopsy appearances were reported as severe dysplasia, developed a carcinoma of the stomach eight months later. All patients having undergone gastric surgery more than five years previously should be screened endoscopically and any found to have moderate dysplasia subjected to regular endoscopic screening thereafter. Patients with severe dysplasia (carcinoma in situ) should be considered for radical surgery.     

Gastritis of the Herniated Stomach in Patients with Esophageal Hiatus Hernia

Seven illustrative cases of gastritis of the herniated stomach in patients with sliding esophageal hiatus hernia are reported. Five had superficial gastritis (three mild, one moderate and one severe); two had atrophic gastritis. Gastritis was present in two patients whose mucosa appeared normal at esophagoscopy. Interstitial hemorrhage into the lamina propria was present in four of the seven biopsy specimens. The possibility that interstitial hemorrhage may be related to the development of gastric erosions is considered. The pathogenesis of this form of gastritis is discussed.     

Difference in chromatin sensitivity to heparin of chronic atrophic gastritis, of carcinoma-free and carcinoma-bearing stomach in comparison with normal gastric mucosa and gastric carcinoma as revealed by flow cytometry

DNA distribution patterns from gastric mucosal cells corresponding to four groups defined by histological examination were measured by flow cytometry before and after treatment with heparin, a polyanion. Group I comprised normal gastric mucosal cells; group II, chronic atrophic gastric mucosal cells originating from a carcinoma free stomach; group III, chronic atrophic gastric mucosal cells originating from a carcinoma bearing stomach; and group IV, malignant gastric mucosal cells. The heparin concentrations used were 1.25, 1.5, and 5 U/ml cell suspension. Heparin caused increases in fluorescence intensity and in coefficients of variation, which are interpreted as a reflection of alterations in chromatin structure. For the four groups investigated, the heparin-initiated changes were dependent, in varying degree, on concentration and time. Group I showed a much more extensive sensitivity to heparin than group IV. Group II and III reacted similarly to group I or group IV, depending on the source, i.e., either a carcinoma-free stomach or a carcinoma-bearing stomach. Further extension of this method might yield information concerning the real premalignant potential of a specific case of chronic atrophic gastritis.     

Plasma obestatin levels in men with chronic atrophic gastritis

Obestatin is a recently discovered active peptide isolated from the stomach. The purpose of the present study was to investigate the modification of plasma obestatin levels in men with chronic atrophic gastritis. Men older than 65 years undergoing upper gastrointestinal endoscopy were included. All patients with chronic atrophic gastritis underwent multiple biopsies. Fasting plasma obestatin and ghrelin levels were examined in 50 men with chronic atrophic gastritis and 50 healthy men. Plasma obestatin levels were significantly lower in patients with chronic atrophic gastritis than in healthy subjects. Plasma ghrelin levels and ghrelin to obestatin ratio was decreased in men with chronic atrophic gastritis. There was a significant relationship between atrophy and decreased obestatin. A negative correlation was found between circulating obestatin levels and body mass index (BMI) in healthy subjects, but not in patients with chronic atrophic gastritis. The data indicated that chronic atrophic gastritis influenced plasma obestatin levels as well as ghrelin to obestatin ratio in elderly men.     

PGI、PGⅡ在胃癌组织中的表达及意义

目的：研究胃蛋白酶原I(PGI)、胃蛋白酶原Ⅱ(PGⅡ)在胃癌组织中的表达及意义。方法：将我院2011 年5 月至2013年10月 收治的上消化道疾病患者243 例纳入研究,根据胃镜及病理组织学结果,按照胃癌、慢性萎缩性胃炎、慢性非萎缩性胃炎、不典型 增生以及胃溃疡分为5 组,对照组为57 名来我院检查的健康的人群。应用酶联免疫法测定各组血清PGI、PGⅡ的含量并计算胃 蛋白酶原比值(PGR),比较胃癌患者手术前后血清PGI、PGⅡ的含量以及PGR,并通过ROC曲线下面积评价血清PGI、PGⅡ以及 PGR 诊断胃癌的效能。结果：与对照组比较,胃溃疡组PG I、PG II均明显升高,PGR 降低(P<0.05),慢性萎缩性胃炎组、不典型增生 组及胃癌组PGI、PGR均明显降低(P<0.05);与慢性萎缩性胃炎组比较,不典型增生组和胃癌组PGR 显著降低(P<0.05)。手术治疗 后,胃癌患者血清PGⅠ、PGⅡ含量较手术前明显下降(P＜0.05)。血清PGⅠ、PGⅡ以及PGR含量诊断胃癌的ROC 曲线下面积依 次为0.779、0.920 以及0.991。结论：胃癌患者血清PGI、PGR均明显降低,二者可用于初步筛查胃癌。     

人慢性胃炎与神经内分泌G、D细胞关系的研究

探讨神经内分泌G、D细胞与慢性胃炎的关系,用免疫细胞化学方法对52例慢性胃炎及9例对照者进行胃窦粘膜内G、D细胞密度计数。结果显示慢性胃炎病人的G、D细胞数均低于对照组,特别是萎缩性胃炎G、D细胞显著减少,同时还发现不同组别、不同程度的萎缩性胃炎,其G细胞的数量均大于D细胞,G／D细胞的比值在中、重度性胃炎与其它组相比有显著性差异（P＜0.01）。资料还显示G、D细胞的计数不仅可以判断胃窦粘膜的萎缩程度,而且可作为观察临床疗效的一项重要指标。     

Is There a Possible Relation Between Atrophic Gastritis and Premature Atherosclerosis?

BACKGROUND: In this study, we have aimed to show the possible relation between atrophic gastritis and premature atherosclerosis via hyperhomocysteinemia. MATERIALS AND METHODS: Thirty-four patients with atrophic gastritis were enrolled to the study. The control group consisted of 35 patients with non-atrophic gastritis. Classical cardiovascular disease risk factors did not significantly differ between atrophic gastritis and control subjects. The presence and degree of atrophic gastritis were assessed histologically and Helicobacter pylori infection was determined by both histologic and serologic methods. Body mass index was measured by standard technique blood fasting glucose, serum creatinine, total cholesterol, triglyceride, low-density lipoprotein cholesterol, high-density lipoprotein cholesterol, vitamin B12, folic acid, and homocysteine levels were measured by biochemical methods. Carotid intima-media thickness was measured by B-mode ultrasonography to examine the premature atherosclerosis. RESULTS: Plasma vitamin B12 levels were significantly lower (p = .00) and homocysteine levels were significantly higher (p = .01) in the atrophic gastritis group. There was no statistically significant difference in plasma folic acid levels between the two groups (p = .728). Carotid intima-media thickness was higher in the atrophic gastritis group than in the control group (0.516 mm versus 0.465 mm), but this difference did not show any statistical significance (p = .062). CONCLUSION: Our results showed that atrophic gastritis may cause hyperhomocysteinemia, which is an independent risk factor for atherosclerosis and cardiovascular diseases. However, when compared with controls, carotid intima-media thickness of the atrophic gastritis patients was found to be higher but did not reach statistically significant levels.     

健胃消痞汤联合雷贝拉唑治疗慢性萎缩性胃炎的临床疗效及对血清G-17、ET-1、胃蛋白酶原、EGF及NO水平的影响

目的:探讨健胃消痞汤联合雷贝拉唑治疗慢性萎缩性胃炎(chronic atrophic gastritis,CAG)的临床疗效及对血清胃泌素-17(G-17)、内皮素-1(endothelin-1,ET-1)、胃蛋白酶原、表皮生长因子(EGF)及一氧化氮(NO)水平的影响。方法:选择2015年6月到2017年3月我院收治的100例CAG患者,随机分为对照组和治疗组,每组各50例。对照组患者给予雷贝拉唑治疗,治疗组患者在对照组治疗的基础上联合健胃消痞汤治疗,两组患者均治疗8周。评价并比较两组患者的临床疗效、治疗前后血清G-17、ET-1、胃蛋白酶原I(PG I)、胃蛋白酶原II(PG II)、EGF及NO水平的变化及治疗期间不良反应的发生情况。结果:治疗后,治疗组患者的总有效率为94.00%,明显高于对照组(78.00%)(P=0.021);两组患者血清G-17、PG I、PG II及NO水平均较治疗前明显升高,血清ET-1和EGF水平均明显下降,且治疗组以上指标的改善情况均显著优于对照组(P0.05)。两组患者治疗期间不良反应的发生率比较差异无统计学意义(P=0.461)。结论:健胃消痞汤联合雷贝拉唑治疗CAG的临床疗效显著,且安全性较高,可能与其明显改善患者血清G-17、ET-1、PG I、PG II、EGF及NO水平有关。     

胃癌病理特征改变与幽门螺旋杆菌感染的相关性分析

目的:探究HP感染与胃癌患者病理特征性改变的相关性。方法:选取我院消化内科收治并确诊为胃癌的患者50例,作为胃癌组;确诊为慢性浅表性胃炎的患者50例,作为胃炎组;选取同期进行健康体检未发现胃部异常的患者50例,作为对照组。对三组患者进行快速尿素氮试验、13C尿素呼气试验以及血清抗HPCag A等检查,比较患者HP感染等情况。结果:胃癌组及胃炎组患者HP感染阳性率及抗HPCag A阳性率显著高于对照组,且胃癌组较胃炎组明显增高,差异有统计学意义(P0.05)。胃癌早期及进展期患者HP感染率高于对照组,差异有统计学意义(P0.05)。胃癌组患者非贲门部HP感染率显著高于贲门部及对照组,差异有统计学意义(P0.05)。结论:HP感染是导致胃癌的主要因素,明确HP感染与胃癌病理分期及病变部位的相关性对胃癌的治疗及预防有重要的临床意义。