胃肠相关疾病中幽门螺杆菌感染与胃黏膜白细胞介素-8含量的关系

目的　研究各种胃肠疾病幽门螺杆菌 (Hp)感染情况及其与胃黏膜白细胞介素 8(IL 8)含量的关系。 方法　采用双抗体夹心酶联免疫吸附试验检测 10 2例Hp感染与非感染患者胃黏膜匀浆上清液中的白细胞介素 8含量 ,其中胃镜下黏膜正常者 5例 ,单纯性慢性胃炎 (CG) 2 5例 ,十二指肠球部溃疡 (DU) 36例 ,胃溃疡 (GU) 15例 ,胃癌(Gca) 2 1例。结果　 10 2例中有 6 0例感染了Hp(5 8.8% ) ,其中以十二指肠球部溃疡组Hp感染率最高 (88.9% ) ,明显高于其他组 (均P <0 .0 5 ) ,Hp感染者胃黏膜IL 8含量明显高于非Hp感染者 (P <0 .0 1) ;GU、Gca、DU、CG组胃黏膜IL 8含量均明显高于黏膜正常组 (均P <0 .0 5 ) ,GU、Gca、DU组又明显高于CG组 (均P <0 .0 5 ) ,而GU、Gca、DU组间比较差异无统计学意义 (均P >0 .0 5 ) ;同时发现中度胃炎黏膜IL 8含量明显高于轻度胃炎 ,活动性胃炎又明显高于非活动性胃炎 (均P <0 .0 5 )。结论　Hp感染者与非感染者胃黏膜IL 8含量存在差异 ,疾病组胃黏膜IL 8含量明显高于正常黏膜 ,并与胃炎炎症程度和活动性有一定相关性 ,推测IL 8可能参与了Hp相关性胃炎胃黏膜损伤机制     

胃上皮化生、幽门螺杆菌感染和十二指肠溃疡的关系研究

目的：幽门螺杆菌（Hp）是引起消化性溃疡的重要致病因素，十二指肠溃疡（DU）患者HP感染率约90％。正常情况下HP主要定植于胃型上皮，也有DU患者十二指肠可见胃上皮化生，可供HP定植引起溃疡形成。本研究是经胃镜检查确诊为活动期十二指肠溃疡患者，检测十二指肠胃上皮化生、HP感染的情况，并与胃溃疡（GU）、功能性消化不良（FD）患者资料进行对照。结论：本组资料表明：十二指肠球部HP的检出率在DU、GU、FD三组差异无显著性。DU、GU、FD组的十二指肠胃上皮化生检出率分别为57．9％、11．1％、16．7％，3组患者在十二指肠球部均可出现胃上皮化生，但DU组显著高于其他2组，推测胃上皮化生与DU组的发病有关。     

236例消化性溃疡的发病特点及胃镜特征

本院1986年11月至1996年10月行胃镜检查1053例，其检出消化性溃疡(PU)236例，检出率224％；其中十二指肠溃疡(DU)190例，占805％；胃溃疡(GU)32例，占13．6％；二之比为59：1；复台性溃疡(CU)14例，占5.9％。PU中男164例，占69.5％，女72例，占30.5％；DU中男132例，占69.5％，女58例，占30.5％：男女之比为均为23：1。GU中男20例，占62.5％，女12例，占37.5％，男女之比17：1。CU中男12例，女2例，男女之比为6：1。DU30岁～39岁组最多，占37.4％。CU30岁～39岁组占43.8％，50岁以上占37．5％。CU40岁～59岁组占64.3％。春季、夏季、秋季、冬季PU发病分别为23.3％、17.8％、25.8％和33.1％。DU92．6％发生在十二指肠球部，球后溃疡占7.4％。位于球前壁、大弯、小弯和后壁的溃疡依次为43.5％、21.5％、20.9％和6.7％。GU部位：幽门前区和胃窦46.9％，胃角43.8％,胃体3.1％，胃底6.2％。CU中的胃溃疡数与十二指肠溃疡数之比为1.4：1；其胃部溃疡92.3％发生在胃角、胃窦和幽门前区；其十二指肠溃疡44.4％位于球前壁。DU中霜斑样溃疡占11.1％。PU的伴随疾病中，检出各类慢性胃炎71.6%;DU伴发疣状胃炎都13.7％。     

幽门螺杆菌所致胃肠道疾病血清学相关性研究

目的 :探讨幽门螺杆菌 (Helicobaterpylori,Hp)所致胃肠道不同部位的病变与其机体免疫反应的相互关系。方法 :采用免疫印迹法和间接ELISA法分别检测患者血清中Hp -CagAIgG抗体和Hp -IgE抗体含量。结果 :在 350例Hp感染患者血清中Hp -CagA抗体阳性率为 80 .2 8%明显高于Hp -IgE58.57% ,P <0 .0 1 ;不同病变部位的阳性率 ,Hp -CagAIgG含量 :慢性活动性胃炎 (ACG)和十二指肠球部溃疡 (DU)明显高于慢性非活动性胃炎 (NACG)、胃溃疡 (GU)、胃癌 (GCa)及溃疡性结肠炎 (UC) ,P <0 .0 1 ;Hp -IgE含量 :ACG明显高于其它被测的任何一组。结论 :在Hp感染过程中 ,Hp -CagAIgG抗体和IgE抗体参与了炎症反应 ,在十二指肠球部溃疡和慢性活动性胃炎的过程中起了极其重要作用     

2006～2009年胃溃疡及十二指肠球部溃疡内镜检查结果调查

目的 分析胃溃疡(GU)和十二指肠球部溃疡(DU)的内镜检查结果,总结患者发病特点.方法 回顾性分析该院2006～2009年胃溃疡及十二指肠球部溃疡患者342例的临床资料.结果 疡发病与季节无关,十二指肠球部溃疡患者中,冬春季发病的患者占到52.9%,明显高于夏秋季的47.1%(P＜0.05);胃溃疡和十二指肠球部溃疡患者中的男性患者分别占到72.2%、81.7%,均明显高于女性的27.8%、18.3%(P＜0.05);胃溃疡和十二指肠球部溃疡患者中,不良饮食习惯者明显多于饮食习惯良好者(P＜0.05).结论 指肠球部溃疡的发病与季节气候有关,冬春季较夏秋季更易发病;胃溃疡发病与季节无关;十二指肠球部溃疡和胃溃疡均以男性多发;不良饮食习惯者两病均易发.     

幽门螺杆菌cagA、vacA抗体与胃十二指肠疾病的相关性研究

目的：探讨幽门螺杆菌（Hp)毒力基因cagA,vacA抗体与胃十二指肠疾病之间的关系。方法：采用免疫印迹法检测440例胃十二指肠疾病患者血清中的cagA,vacA抗体。结果：cagA,vacA抗体在440例患者中的检出率分别为73%，37.0%。在慢性胃炎（CG），十二指肠肠球部溃疡（DU），胃癌（GC）患者专利号，cagA,vacA抗体摄影性率分别为62.9%,76.1%,96.9%与33.0%,31.0%,62.5%；经u检验显示；慢性胃炎组与十二指肠球部溃疡组比较，无明显差异。胃癌组与慢性胃炎组，十二指肠球部溃疡组比较，有显著性差异。结论：本文通过患者血清中Hp抗体（cagA和vacA)的检测。推知其cagA和vacA抗体的表达状况，可为胃十二指肠疾病的诊断提供血清中Hp抗体（cagA和vacA)的检测，推知其cagA和vacA抗体的表达状况，可为胃十二指肠疾病的诊断提供依据。但不能作为区分Hp感染所致胃十二指肠疾病的单一指标。     

幽门螺杆菌多部位检测与临床及组织学表现的关系

目的 观察幽门螺杆菌（Hp）与胃及十二指肠粘膜病理组织学表现之间的关系。方法 对60例慢性胃炎和22例十二指肠溃疡患者经胃镜分别从胃窦、胃体、十二肠球部取活检,进行组织学检测。结果 在活动性胃炎中无论是胃窦部或胃体部Hp检出率近100％,显著地活动性十二指肠球炎的球部Hp的检出率,胃窦部Hp总检出率及活动性上的发生率均显著高于胃体部及十二指肠球部。22例十二指肠球部溃疡Hp在球部的检出率为54％,显著低于其在胃窦部组织中Hp100％的检出率。结论 Hp感染是胃粘膜活动性炎症的重要原因,并以此为基础发展为重度粘膜炎及溃疡病,因此,对某些慢性胃炎患者应及早进行Hp根除治疗。     

消化性溃疡出血季节发病的观察

目的　观察消化性溃疡 (PU)出血与季节的关系。方法　选取 10年胃镜结果 ,观察PU发生及出血与月份、季节及季节变换的关系。结果　十二指肠溃疡 (DU)并出血以秋、冬、春季及冬春季节变换时发生率较高 (P <0 .0 1) ;胃溃疡 (GU)并出血冬季及冬春季节变换时发生率较高 (但P >0 .0 5 ) ;复合型溃疡 (CU)并出血秋季发生率最高 (P <0 .0 1)。结论　PU并出血与季节相关。     

幽门螺杆菌CagA+株感染对胃液EGF的影响

【目的】了解幽门螺杆菌（Hp）产毒株（CagA）感染对胃液表皮生长因子（EGF）浓度的影响及其与十二指肠球部溃疡（DU）发生的关系。【方法】158例DU与非溃疡消化不良（NUD）患者，用ELISA方法检测其血清CagA抗体（CagA-IgG）滴度并用目测法定性，并测定胃液EGF浓度。【结果】CagA^＋者胃液EGF浓度显著低于CagA^-者，且差异有显著性（P〈0．01）。【结论】CagA^＋株Hp感染使胃液EGF水平降低。     

重庆市巴南地区消化性溃疡的流行病学分析

目的了解巴南地区消化性溃疡病的发病特点,以便有效预防其发生。方法回顾性分析2001年1月至2010年12月临床和胃镜检查确诊为消化性溃疡的患者资料。结果 13 518例患者中共检出消化性溃疡1 726例,十二指肠球部溃疡(DU)1 129例,胃溃疡(GU)473例,复合性溃疡(CU)35例,消化性溃疡患者男女比例为1.96∶1,平均年龄为(43.5±6.4)岁,十二指肠球部溃疡以50岁以下居多;胃溃疡和复合性溃疡以50岁以上居多。检出率以秋冬季和春季最高,夏季最低。结论巴南地区消化性溃疡病以十二指肠球部溃疡最多,胃溃疡次之,复合性溃疡最少,男性高于女性,发病有明显的季节性,男性患者仍是消化性溃疡的主要患病人群,与不良嗜好、生活无规律及精神因素有关。     

Molecular forms of gastrin in peptic ulcer: comparison of serum and tissue concentrations of G17 and G34 in gastric and duodenal ulcer subjects

We have studied the relationships between the main molecular forms of gastrin (G17 and G34) in the serum, antral and duodenal mucosa of duodenal (DU) and gastric (GU) ulcer patients. Fasting serum G17 was similar in both DU and GU (about 6 pmol/l) and in both groups increased about three-fold with feeding. In contrast, basal serum G34 was significantly higher in GU (29 pmol/l) than in DU (12 pmol/l) and the peak post prandial increase over basal of G34 was also higher in GU (57 pmol/l) compared with DU (10 pmol/l). In sharp contrast, in the same groups of DU and GU patients mean total antral gastrin concentrations were similar (about 12 nmol/g), and in both groups 95% of antral gastrin was G17, most of the remainder being G34. In both groups total duodenal gastrin concentrations were about 20% those in antral mucosa and about 70% of duodenal gastrin was attributable to G34. The higher serum G34 in GU could therefore be explained by increased secretion of duodenal gastrin, but further work is needed to examine whether there might also be preferential secretion of antral G34 in GU, or a difference in the metabolism (or volume of distribution) of gastrin variants in GU and DU.     

Molecular forms of gastrin in peptic ulcer: comparison of serum and tissue concentrations of G17 and G34 in gastric and duodenal ulcer subjects

Abstract We have studied the relationships between the main molecular forms of gastrin (G17 and G34) in the serum, antral and duodenal mucosa of duodenal (DU) and gastric (GU) ulcer patients. Fasting serum G17 was similar in both DU and GU (about 6 pmol/1) and in both groups increased about three-fold with feeding. In contrast, basal serum G34 was significantly higher in GU (29 pmol/1) than in DU (12 pmol/1) and the peak post prandial increase over basal of G34 was also higher in GU (57 pmol/1) compared with DU (10 pmol/1). In sharp contrast, in the same groups of DU and GU patients mean total antral gastrin concentrations were similar (about 12 nmol/g), and in both groups 95% of antral gastrin was G17, most of the remainder being G34. In both groups total duodenal gastrin concentrations were about 20% those in antral mucosa and about 70% of duodenal gastrin was attributable to G34. The higher serum G34 in GU could therefore be explained by increased secretion of duodenal gastrin, but further work is needed to examine whether there might also be preferential secretion of antral G34 in GU, or a difference in the metabolism (or volume of distribution) of gastrin variants in GU and DU.     

老年人消化性溃疡与慢性萎缩性胃炎的相关性研究

目的研究老年人消化性溃疡与慢性萎缩性胃炎的相关性。方法对十二指肠溃疡（DU）、胃溃疡（GU）和复合性溃疡（CU）的老年患者胃窦、胃窦胃体交界处和胃体黏膜以及慢性胃炎（CG）患者胃窦黏膜活检标本进行组织学检查,统计各自胃黏膜的萎缩、肠化生、慢性炎症、活动性和幽门螺杆菌（Hp）感染的发生率。结果 DU患者胃窦、胃窦胃体交界处和胃体黏膜的萎缩发生率分别为54.0%、8.0%和16.0%,肠化生发生率分别为19.0%、6.0%和4.0%。其胃窦黏膜肠化生的发生率明显低于相应的GU、CU或CG者。3种消化性溃疡和CG患者均存在胃窦部慢性炎症,且老年消化性溃疡患者胃体部炎症的发生率较高,其胃炎活动性以胃窦部为主,且均较CG者高。结论老年人消化性溃疡均可有胃窦部灶性萎缩和肠化生发生,但DU胃窦黏膜肠化发生率最低,这可能是老年DU患者罹患胃癌危险性较低的原因之一。     

湖南地区幽门螺杆菌CagA基因3’端多态性与胃小二指肠疾病的关系

目的 探讨湖南地区幽门螺杆菌（Helifcobacter Hpylori）细胞毒素相关基因（CagA基因）3＇端可变区序列特征及其与胃十二指肠疾病的关系.方法 本地区有明显上消化道症状患者235例,其中慢性胃炎（CG）57例,胃溃疡（GU）62例,十二指肠溃疡（DU）70例,胃癌（GC）46例.于胃镜检查时用灭菌活检钳取胃窦组织1块,分离培养出H.pylori 89株,用PCR法对上述菌株的CagA基因扩增及测序,并通过生物信息学软件进行多重序列比对和相似性分析.结果 H.pylori培养阳性率为37.9%（89/235）,其中H.pylori CagA阳性者占91.7%（77/84）,GU组、DU组和GC组CagA阳性率高于CG组,其差异有统计学意义（P〈0.05）.77株H.pylori CagA基因3＇端均具有3个EPIYA重复序列,其中第2个EPIYA序列存在3种突变型,占18.2%（14/77）.H.pylori CagA基因3＇端序列特征以东亚型为主,占88.3%（68/77）,东亚型的CagA阳性菌株在GU组、DU组及GC组高于CG组（P〈0.05）.所有东亚型CagA阳性菌株CagA序列特征类似于Yamaoka报道的A型.结论 湖南地区H.pylori CagA阳性菌株以东亚型为主,均具有3个EPIYA重复序列,其中第2个序列存在3种突变型,其与消化性溃疡和胃癌发生有关.     

Reactions of humoral and cellular immunity in peptic ulcer in relation to the condition of the gastric mucosa

A total of 160 persons including 50 patients with duodenal ulcer (DU) and 38 with gastric ulcer (GU) were examined for antibodies to the parietal cells of the stomach (PCA) and cell cellular immunity responses to autologous antigen from the gastric mucosa. It was shown that both PCA of the stomach and cell immunity responses in patients with GU and DU occurred in an insignificant number of cases. No differences were revealed in the humoral and cellular immunity in GU and DU persons with and without concomitant gastritis or in the stage of exacerbation and ulcer cicatrization.     

Tumour necrosis factor alpha stimulates gastrin release from canine and human antral G cells: possible mechanism of the Helicobacter pylori–gastrin link

There is evidence that gastric Helicobacter pylori ( Hp ) infection promotes duodenal ulceration by releasing gastrin. We therefore asked how Hp releases gastrin. Tumour necrosis factor alpha (TNF-α) is up-regulated in Hp gastritis and stimulates hormone release from pituitary cells, so we tested its effect on primary cultures of canine antral G cells and human antral fragments. TNF-α pretreatment (100ngmL^–1) of canine G cells significantly increased both basal (by 89%: P <0.01) and bombesin-stimulated (by 39% P <0.05) gastrin release. A similar pattern of increase was seen following TNF-α (20ngmL⁻¹) pretreatment of human antral fragments: basal gastrin release was increased by 38% ( P  < 0.05) and bombesin-stimulated by 26% ( P  < 0.05). This effect persisted during immunoblockade with anti-somatostatin antibody S6. We propose that TNF-α provides the link between Hp infection and gastrin release and thus contributes to duodenal ulceration.     

霜斑样病变与胃上皮化生及Hp感染关系的研究

目的 :了解霜斑样病变与幽门螺杆菌感染及十二指肠溃疡的关系。方法 :比较胃镜下十二指肠溃疡、霜斑样病变、十二指肠炎、正常球粘膜的炎症、胃化生程度及其胃窦幽门螺杆菌密度 ;把接受胃镜复查的霜斑样病变随机分为抗幽门螺杆菌治疗与抑酸治疗两组 ,观察治疗结果。结果 :十二指肠球部不同病变的组织学炎症程度各不相同 (P <0 0 5 ) ,以霜斑样病变最重 ;胃化生程度及胃窦Hp密度均以十二指肠溃疡与霜斑样病变为高 ,但后二者间无显著差别 (P >0 0 5 ) ;4 2例霜斑样病变患者中 4周治疗后内镜复查 2 6例 ,抗Hp治疗组 1 2例均恢复正常 ,单纯抑酸治疗组 1 4例仍有 5例霜斑样病变且 1例伴发溃疡 (P <0 0 4 2 5 )。结论 :幽门螺杆菌感染的重度活动性十二指肠炎是十二指肠溃疡的病理基础 ,霜斑样病变可能是十二指肠溃疡的前驱病变     

Serum IL-8 as a possible marker for determining the status of<Emphasis Type="Italic">Helicobacter pylori</Emphasis> infection in patients with untreated and treated peptic ulcer

Failure to eradicateHelicobacter pylori can lead to peptic ulcer recurrence and gastric malignancy. Therefore, the objective of this study was to develop a noninvasive method for determining whetherH pylori infection was eradicated with antibiotic-based triple therapy. A total of 17 patients with duodenal ulcer (DU) and 17 with gastric ulcer (GU) were evaluated both before and after treatment. Outcomes included serum levels of interleukin-8 (IL-8), pepsinogen I, and gastrin, and the Wilcoxon signed rank test was used to test significance. Changes in these parameters were also correlated with disease status. In those patients where both GU and DU healing occurred as a result of treatment, most showed an increase in serum IL-8 and a decrease in serum pepsinogen. Serum gastrin levels were not significantly changed in either group. Posttreatment increases in serum IL-8 were seen in 15 of 17 (88%) recovered DU patients and 14 of 17 (82%) recovered GU patients (P < .05 for each). Posttreatment decreases in pepsinogen I were found in 15 of 17 DU and 15 of 17 GU patients (P < .05 for each). These preliminary findings suggest that an increase in serum IL-8 and possibly a decrease in pepsinogen I may be useful in identifying the successful eradication ofH pylori infection in patients with peptic ulcer treated with antibiotics. A more systematic analysis of these putative diagnostic markers is now warranted.