缺铁性贫血儿童血清幽门螺杆菌抗体的检测及临床意义

幽门螺杆菌（Hp）感染是广泛存在且常见的细菌感染。近年来Hp感染与缺铁性贫血（IDA）铁缺乏（ID）之间的关系越来越受到众多学者的关注。为进一步探讨儿童Hp感染与儿童IDA之间的关系，本文对我院2002年10月至2004年1月632例儿童进行了上述项目的检测。现报告如下。     

幽门螺杆菌的根治与血清幽门螺杆菌抗体滴度间关系的分析

幽门螺杆菌的根治与血清幽门螺杆菌抗体滴度间关系的分析赵颖王维杨丽强欧华西医科大学附属第一医院消化科对于幽门螺杆菌感染，血清学检查抗ＨＰ抗体有助于幽门螺杆菌的诊断及疗效观察，也是目前唯一的简便、快速、经济及非侵入性的一种血清学诊断方法。为了研究其在监测...     

糖尿病患者血清谷氨酸脱羧酶抗体测定结果分析

谷氨酸脱羧酶（GAD）是抑制性神经递质-氨基丁酸的生物合成酶,存在于人和动物的脑、胰岛等组织内。目前认为血清GAD抗体的检测是临床上诊断1型糖尿病,特别是成人隐匿性自身免疫性糖尿病（LADA）的主要指标,并对糖尿病的正确分型及指导治疗有重要价值。笔者对70例糖尿病患者及17例正常对照用ELISA试剂盒进行血清GAD抗体的检测,现就测定结果分析报告如下。 1 对象与方法 1.1 对象:70例病人均来自我院内分泌专科住院及门诊病人,均按WHO标准确诊为糖尿病。根据发病年龄、病史、治疗情况及胰岛素测定及释放试验分为:（1）1型糖尿病组5例     

胃黏膜相关淋巴组织淋巴瘤幽门螺杆菌分离株与胃炎分离株的转录组比较

目的本研究对胃黏膜相关淋巴组织淋巴瘤（MALT淋巴瘤）幽门螺杆菌分离株与胃炎分离株的转录组进行比较,以阐述胃MALT淋巴瘤幽门螺杆菌分离株的转录组特征。方法对2株分离自胃MALT淋巴瘤的菌株与胃炎菌株26695的转录组进行比较。结果胃MALT淋巴瘤幽门螺杆菌分离株之间转录组非常相似,而与胃炎菌株26695之间差异较大。 对差异表达基因进行GO功能富集分析,结果显示富集基因数前5位的为催化活性、代谢进程、细胞进程、结合、单组织进程。 Pathway显著性富集分析表明差异基因的功能主要参与氨基酸和核苷酸糖代谢、卟啉和叶绿素代谢以及乙醛和二羧酸代谢。结论胃MALT淋巴瘤幽门螺杆菌相关菌株可能通过代谢调控菌体生长和侵染宿主,从而在胃MALT淋巴瘤形成过程中发挥着重要作用。     

SARS病房工作的医护人员血清中特异抗体测定分析

目的 检测密切接触SARS患者的医护人员血清中SARS病毒IgM及IgG抗体的水平，对SARS病毒有无隐性感染作初步调查。方法 分别用酶联免疫吸附法和间接免疫荧光法(IIFA)检测200例正常人，200例在SARS病房工作1个月的医护人员血清中SARS病毒IgM及IgG抗体的水平。结果 正常人及医护人员血清中未检测到SARS病毒IgM及IgG抗体。结论 不同于普通的流行性传染性疾病，SARS病毒可能不具有隐性感染性。     

急性心肌梗死患者血清幽门螺杆菌抗体与C反应蛋白的关系

目的：观察急性心肌梗死（AMI）患者血清中幽门螺杆菌（Hp)抗体和C反应蛋白（CRP）的水平，以探讨两者之间的关系。方法：对71例AMI患者同时采用酶联免疫吸附试验（ELISA）检测血清Hp-IgG和Hp-IgM，用散射速率比浊法检测血清CRP的含量。结果：AMI患者CRP，血清Hp-IgG和Hp-IgM的阳性率分别为71．8％，61．9％和67．6％，明显高于对照人群（P＜0．005）；Hp抗体阳性者CRP含量明显高于Hp抗体阴性者及对照人群（P＜0．001），其CRP与Hp抗体阳性的符合率为79％，并对Hp抗体阳性和Hp抗体阴性的AMI病人各10例，分别作CRP和肌酸激酶同工酶MB（CK－MB）24h动态观察，发现随病程延长，其CRP呈峰值变化，与CK－MB出现峰值的时间相同，Hp抗体阳性者CRP水平升高幅度大于Hp抗体阴性者（P＜0．001），结论：Hp感染和CRP含量的变化与AMI的疾病发生过程密切相关，是AMI病情监测和预后估计的重要指标。     

患儿粪便中幽门螺杆菌抗原及血清抗体检测

幽门螺杆菌（Hp）是小儿慢性胃炎、十二指肠炎及消化性溃疡的重要病因之一。临床检测Hp的方法较多，传统多采用侵入性内镜检查法，此法准确性、特异性较高，是诊断Up感染的金标准，但儿童、老人及孕妇难以接受。非侵人性方法有^13C尿素呼气试验（^13C-UBT）、粪便中Hp抗原（HpSA）检测及血清抗体（Hp—IgG）检查等。本研究通过对153例患儿HpSA、Hp-IgG的检测，与金标准进行了对比分析，并对36例Hp阳性患儿根治后进行了^13C-UBT检测，复查了HpSA、Hp-IgG，且进行了对比分析。     

血清HP抗体测定对小儿腹痛的临床意义

小儿腹痛症状多样，无特异性．且小儿对疼痛诉说不清．定位性差，给临床诊断带来很大的困难。临床表现小儿腹痛大部分与慢性胃炎、胃溃疡有关。近年又发现幽门螺杆菌是上述病变的主要致病原因。我们对62例腹痛患儿作血清幽门螺杆菌(HP)抗体测定。现报告如下。     

支气管哮喘并发幽门螺杆菌感染患儿粪便抗原与血清抗体特征分析

目的了解支气管哮喘(哮喘)并发幽门螺杆菌感染患儿幽门 螺杆茵(HP)感染情况、免疫表型及其血清型的分布特征。方法收集 2016年12月～2017年12月支气管哮喘患儿与同龄健康体检儿童的14C-BUT检测结果, 并收集两组人群的粪便与血清样本,分别采用粪便HP抗原和血清HP抗体检测,比较其与 14C-BUT对于儿童HP感染检测结果之间的差异;采用三种HP诊断方法(14C-BUT, 粪便HP抗原,血清HP抗体检测)筛查两组HP感染,比较各组间HP感染的阳性率是否存在差异 ;另外,对血清HP抗体阳性的哮喘和健康体检儿童,进一步采用HP血清抗体谱进行分析,以 了解哮喘并发HP感染儿童HP血清抗体谱的分布,并比较分析两组间抗体谱及血清型分布差异 。结果通过在哮喘和健康体检儿童中三种HP诊断方法比较,三者间 的差异无统计学意义( χ2=1.06,0.77,0.72,均P >0.05),在支气管哮喘与健康 体检儿童中HP感染率分别为:30.4%~32.6%和35.4%~37.4%,两组间差异无统计学意义( P >0.05),HP抗体阳性哮喘患儿和健康体检儿童中各抗体谱阳性率为:抗VacA-95KD(3 1.8%,50.9%),VacA-91KD (31.8%,50.9%),UreA-66KD(65.9%,54.5%),UreB-3 0KD(63.6%,52.7%),其抗体的阳性率在两组之间差异无统计学意义( χ2=3.64,3. 64,1.31,1.19,均P >0.05);仅CagA-116 KD抗体阳性率(36.4%,56.4%)在两组间 差异具有统计学意义( χ2=3.92,P ＜0．05)。另外I型和Ⅱ型HP感染率在两组中的百 分比分别为:哮喘组Ⅰ型36.4%(16/44)和Ⅱ型63.6%(28/44),健康体检组Ⅰ型56.4%(31/ 55)和Ⅱ型43.6%(31/55),两组间差异存在统计学意义( χ2=3.92,P <0.05)。〖HT 5结论哮喘的发病率与HP的感染率无直接联系,但其与抗-CagA抗体的阳 性率存在明显的负相关,且具有特定的血清型和抗体谱分布特征,这为我们进一步研究哮喘 与HP感染的内在联系奠定了理论基础。     

血清胰岛素抗体对胰岛素测定的干扰及纠正方法

目的　测定正常人及糖尿病患者血清游离胰岛素 (freeimmunoreactive insulin ,F IRI)与免疫活性胰岛素 (immunoreactive insulin ,IRI)水平 ,探讨血中胰岛素抗体 (insulinantibodies,IA)对胰岛素测定的干扰及纠正方法。方法　采集正常人和糖尿病人血样 ,聚乙二醇 (PEG)预沉淀除去血清中IA和结合胰岛素 ,用12 5I 胰岛素和胰岛素分别行热、冷回收鉴定 ;采用RIA法分别测定样品IA、IRI和F IRI。结果　IA阳性血样的F IRI热回收率 (5 .87% )显著低于IA阴性者 (98.35 % ) (P <0 .0 1) ,而F IRI冷回收率在IA阴、阳性组间无差异 (P >0 .0 5 ) ;正常人及IA阴性的糖尿病患者 ,血清IRI与F IRI测定值无差异 (P >0 .0 5 ) ;IA阳性的糖尿病患者血清IRI高于F IRI测值 (P <0 .0 5 ) ,而且与餐后相比 ,空腹时IRI与F IRI二者的差异程度更明显 (P <0 .0 5 )。结论　血清内源性IA可干扰IRI放免测定 ,使测定值出现偏差。采用PEG对标本预沉淀后测定F IRI,可排除IA的干扰 ,对了解病情和指导用药有实际意义     

Analysis of long-term serological and histological changes after eradication of Helicobacter pylori

Stratification of gastric cancer risk by measuring serological biomarkers is useful for screening of gastric cancer. However, this method has problem such as overlooking past infected patients. We aimed to evaluate the association between Helicobacter pylori infection status and serological biomarkers. We divided 5,268 patients according to Helicobacter pylori infection status and past infected patients were divided into 12 groups according to time elapsed since eradication. We analyzed mean serum H. pylori immunoglobulin G antibody, pepsinogen titers, histological and endoscopic atrophy score of each group. Mean H. pylori immunoglobulin G antibody showed a decreasing tendency, there was no significant difference from the uninfected group at 11 years after eradication (p = 0.19). PGI, PGII decreased in short term after eradication. However, both PGI and PGII gradually increased as long-term changes after eradication, became comparable to those in the uninfected group (p = 0.41, p = 0.37, respectively). Histological atrophy improved gradually, became equivalent to uninfected group. Endoscopic atrophy score did not improve for long term after eradication. In conclusion, patients with long term after eradication reach the uninfected condition serologically, histologically. Endoscopic assessment of gastric mucosal atrophy may be useful for accurate assessment of gastric cancer risk.     

应激状态下幽门螺杆菌感染与胃黏膜损伤的关系探讨

目的研究应激时胃黏膜的损伤程度与幽门螺杆菌(Hp)感染的变化情况及其相关性。方法选取新兵60名,在其军训前后进行血清皮质醇(COR)、儿茶酚胺(CA)、14 C-尿素呼气试验、Hp抗体检测,以及《症状自评量表》(SCL-90)评估,部分受试者行胃镜检查和胃黏膜病理分析。结果心理调查问卷分析中,军训后较军训前SCL-90总分、躯体化、抑郁、偏执分明显升高,与军训前比较,差异有统计学意义(P0.05)。军训后新兵的血清COR和CA水平分别为(276.64±156.89)μg/dL、(320.76±123.75)pg/mL,明显高于军训前的(8.28±2.43)μg/dL、(18.69±5.98)pg/mL,差异有统计学意义(P0.05)。胃黏膜病理检查显示军训后胃黏膜炎症积分和14 C-尿素呼气试验检测结果明显升高。结论应激可导致胃黏膜损伤加重,且加重了机体Hp的感染。     

Helicobacter pylori eradication and associated changes in the gastric mucosa

Persistent Helicobacter pylori infection contributes towards the development of chronic gastritis. To clarify the changes in chronic gastritis as a precursor of gastric cancer secondary to H. pylori eradication is an important issue, as it has significant implications for reducing the risk of gastric cancer. Studies published to date, however, are far from consistent with regard to the morphologic changes reported following H. pylori eradication. Of these, some papers reported improvement in gastric atrophy or intestinal metaplasia, versus others reporting no improvement, with the majority of papers published after 2000 reporting improvement in these end points. The inconsistent results concerning the impact of H. pylori eradication on gastric atrophy could be due to the inconsistency of the diagnostic criteria employed for evaluation of the morphology, confounded by the difficulties involved in evaluating atrophic changes in the gastric mucosa. While adherence to the Updated Sydney System available for evaluation of gastritis is primarily required worldwide to ensure consistency in evaluating gastritis, long-term research into the morphologic changes associated with H. pylori eradication is also required to explore strategies for the prevention of gastric cancer with H. pylori eradication.     

幽门螺杆菌根除后胃黏膜的病理变迁

目的探讨根除幽门螺杆菌(Hp)对胃黏膜萎缩、肠上皮化生等癌前病变的转归,以及胃黏膜上皮细胞增殖指标ki-67表达的影响。方法67例Hp感染且有胃黏膜萎缩和(或)肠上皮化生的慢性胃炎患者,随机分为实验组(37例)和对照组(30例),分别给予Hp根除和对症治疗,1年后复查,比较Hp根除与否对胃黏膜萎缩、肠上皮化生等癌前病变的影响;用免疫组化方法检测治疗前后胃黏膜上皮细胞增殖指标ki-67的表达,比较Hp根除与否对它的影响。结果实验组炎症程度减轻(34/37,91.9%,P<0.01),活动性炎症者减少(P<0.01),萎缩、肠上皮化生等癌前病变减轻或逆转(21/32,65.6%vs15/26,57.7%,均P<0.05);ki-67表达降低(46.5±27.7vs15.4±18.7,P<0.01)。结论根除Hp可使胃黏膜炎症程度减轻,活动性炎症消失,萎缩、肠化等癌前病变减轻或逆转,胃黏膜上皮细胞增殖指标ki-67表达减少,从而有利于预防胃癌的发生。     

胆汁反流、胃酸、幽门螺杆菌感染对胃黏膜损伤的影响

目的　探讨胆汁反流、胃酸、幽门螺杆菌 (Hp)感染对胃黏膜损伤的影响。方法　 30例具有胆汁反流症状并经胃镜检查证实有胆汁反流的患者 ,同步行动态 2 4小时胃内胆汁及 pH值监测 ,胃镜下取胃窦胃小弯处黏膜 4块 ,1块做快速尿素酶试验 ,3块做病理检查 ;常规固定、包埋、切片和苏木精和伊红 (HE)、Giemsa染色 ,后者用于Hp检测 ;根据胃窦黏膜有无活动性炎症、萎缩、肠化和不典型增生分别记 2分或 1分 ;根据上腹痛、腹胀、吐苦水、恶心、嗳气和食欲不振的程度给予症状评分 ;得出胆红素吸收值 (Abs)≥ 0 .14的时间百分比、pH值 <4的时间百分比 ,以及胃内Abs与pH值对应表。结果　 30例患者中Hp的感染率是 2 3.3% ,胃内Abs≥ 0 .14的时间百分比是 (30 .6 4±14 .6 7) % ;胃内Abs≥ 0 .14的时间百分比Hp阳性组 (2 0 .6 4± 7.13) % ,Hp阴性组 (4 0 .38± 13.35 ) % ,两者相比差异有统计学意义 (P <0 .0 5 ) ;胃窦部黏膜糜烂、肠化的程度积分与胆汁反流程度呈正相关 (r =0 .74 9,P =0 .0 0 5 )。结论　胆汁反流可以抑制Hp在胃内的定植 ,胆汁反流是胃黏膜损伤的危险因素     

Analysis of serum gastrin-17 and Helicobacter pylori antibody in healthy Chinese population

BackgroundGastrin‐17 (G‐17) and Helicobacter pylori (H pylori) antibody are widely used in the screening of gastric diseases, especially in gastric cancer. In this study, we aimed to evaluate the value of G‐17 and H pylori antibody in gastric disease screening.MethodsHealthy males and females (1368 and 1212, respectively) aged between 21‐80 years were recruited for the study. Serum G‐17 value was measured using ELISA, and H pylori antibodies were measured using Western blotting. Statistical analyses were performed using the chi‐square, Mann‐Whitney U, and Kruskal‐Wallis H tests.ResultsSerum G‐17 level was higher in the H pylori‐positive group than in the negative group. Serum G‐17 level was higher in the type 1 H pylori‐positive group than in the type 2 H pylori‐positive group. Further, serum G‐17 level was higher in females than in males and showed significant differences among different age‐groups, with changes in trend proportional to the age. The positive rate of H pylori infection in all the subjects was 58.29% and did not show a significant difference between males and females. However, it showed significant differences among different age‐groups, with the changing trend proportional to the age.ConclusionAnalysis of serum G‐17 level and H pylori antibody typing is valuable in gastric disease screening. Every laboratory should establish its own reference interval for G‐17 level.     

Helicobacter pylori and non-Helicobacter pylori bacterial flora in gastric mucosal and tumour specimens of patients with primary gastric lymphoma

There is an association between Helicobacter pylori (H. pylori) and gastric mucosa-associated lymphoid tissue (MALT) and MALT lymphoma. Histologically, mainly non-specific stains are used to detect H. pylori, such as haematoxylin–eosin (HE) or modified Giemsa (MG). In this study, both a MG and a specific immunohistochemical stain (IMM) for H. pylori (Dako B471) were performed on sequential slides of resected material containing tumour and non-tumorous gastric mucosa from patients with primary gastric lymphoma (n = 52). Special attention was paid to the presence of non-H. pylori bacterial flora diagnosed by a positive MG (according to form and localization) and a subsequently negative IMM. On all slides, bacterial density was scored semiquantitatively (grades 0, 1, 2, 3). In total, 32 (61.5%) patients were H. pylori positive using IMM and 34 (65.4%) were non-H. pylori positive using MG. In 24 out of the 34 patients, the non-H. pylori flora consisted mainly of cocci in combination with rods in 15 patients, mostly in minor quantities; in another 10 patients, high numbers of both cocci and different types of rods were present. Most non-H. pylori bacteria were localized superficially, although in 22 patients minor quantities of non-H. pylori were also seen in the glandular lumina. After all of the patients had been analysed, no differences in the density of H. pylori and of non-H. pylori flora were found. Only when comparing patients who had a small-cell lymphoma with those who had a large-cell lymphoma was a significantly higher density of H. pylori found in the corpus mucosa of large-cell lymphomas and a higher prevalence of non-H. pylori was found in tumours, in antrum or corpus, of patients with large-cell lymphomas. In conclusion, with joint evaluation using MG and a H. pylori-specific immunohistochemical stains, the proportion of H. pylori-positive gastric lymphoma patients was lower than in most previous studies but other bacteria were found in a relatively high proportion. The role of the non-H. pylori intragastric bacterial flora identified in this study has to be further elucidated in the aetiopathogenesis of primary gastric lymphoma.     

东亚型幽门螺旋杆菌感染与胃癌发生的关系

目的 通过检测各部位慢性胃炎、胃溃疡、胃上皮内瘤变、胃癌幽门螺旋杆菌(Hp)感染情况,探讨河北省消化道肿瘤高发地区Hp感染,特别是东亚型幽门螺旋杆菌(EAS)感染与胃癌发生的关系.方法 依据国际最新悉尼系统分级标准和直观模拟评分法对慢性胃炎进行分级;分别应用Giemsa染色和免疫组织化学法检测贲门、胃体、胃窦3个部位Hp和EAS感染情况,分析Hp感染率、部位分布以及与胃癌发生的关系.结果 总体结果表明,慢性胃炎和胃溃疡中EAS阳性检出率分别为67.0%(138/206)、100.0%(12/12)明显高于上皮内瘤变43.8%(32/73)和胃癌21.7%(13/60)(P<0.05).进一步按病变部位分析贲门、胃体、胃窦和EAS阳性检出率,结果发现同一部位中慢性胃炎、胃溃疡、低级别上皮内瘤变、高级别上皮内瘤变、胃癌Hp和EAS阳性率差异无统计学意义(P>0.05).从慢性胃炎严重程度方面分析,中性粒细胞浸润程度、单核细胞浸润程度、萎缩程度、肠化生程度最严重部位均位于贲门,差异均有统计学意义(P<0.05).Hp密度最高部位位于胃体(P>0.05),但差异无统计学意义.Spearman相关性分析显示,在贲门、胃体、胃窦,Hp密度分别与中性粒细胞浸润程度、单核细胞浸润程度、萎缩程度、肠化生程度呈正相关(P均<0.05).结论 河北省消化道肿瘤高发地区ESA阳性检出率较高,其感染分别与中性粒细胞浸润深度、单核细胞浸润深度、萎缩程度、肠化生程度呈正相关,且在贲门处较易引起严重病变,贲门癌的发生与ESA感染密切相关.     

Follow-up analysis and histopathological study of gastric mucosa in patients with Helicobacter pylori infection

ObjectiveTo investigate the histomorphological characteristics of the gastric mucosa and the prognosis in patients with Helicobacter pylori infection.MethodsProgressive damage to the gastric mucosa was examined by immunohistochemistry in 2294 patients with H. pylori infection and follow-up information was analyzed.ResultsH. pylori initially colonized the mucus layer covered by the gastric mucosa epithelium, then selectively adhered to and destroyed the surface mucus cells causing intra-gastric and extra-gastric lesions. Gastric mucosal damage induced by H. pylori was divided into five stages according to the depth of H. pylori invasion and degree of lesion deterioration: mucilaginous, surface mucocellular, lamina propria lesion, mucosal atrophy, and intraepithelial neoplasia stages. Morphological follow-up analysis revealed no significant difference in 6-month curative effects between stage I and stage II, but significant differences were found between stages II and III, stages III and IV, and between stages IV and stage V, respectively.ConclusionsThis novel staging strategy may be a valuable tool for diagnosing and predicting the results of gastric mucosal damage induced by H. pylori infection.     

transgelin基因在幽门螺杆菌感染胃癌细胞及人胃癌组织中的表达

目的研究幽门螺杆菌(Helicobacter pylori,HP)感染胃癌细胞及人胃癌、淋巴结组织中转凝蛋白基因(transgelin)的表达水平,探讨HP感染、transgelin基因与胃癌发生、发展的相关机制。方法用HP感染胃癌细胞系AGS和SGC-7901,同时收集胃癌患者手术切除的胃癌组织、切缘组织和淋巴结组织,提取及纯化总RNA。实时荧光定量PCR检测transgelin mRNA的表达水平,分析其与临床病理参数的关系。结果 transgelin mRNA在HP感染的AGS、SGC-7901细胞中的表达量增加,分别为对照细胞的11.39倍(t=30.025,P=0.000)、3.41倍(t=5.677,P=0.005);transgelin mRNA在胃癌组织、淋巴结组织中的表达增加,分别是切缘组织的6.48倍(t=2.290,P=0.026)、2.64倍(t=2.043,P=0.046);Ⅳ期胃癌组织transgelin mRNA表达量增加,是Ⅰ~Ⅱ期的2.32倍(t=2.111,P=0.049);淋巴结转移组是无淋巴结转移组的2.93倍(t=2.123,P=0.043)。结论HP可上调transgelin基因的表达,transgelin基因可能参与胃癌的发生、发展,且与p TNM分期及淋巴结转移相关。