儿童幽门螺杆菌感染与HLA-DQB1等位基因遗传多态性研究

目的　研究HLA -DQB1基因位点上是否存在幽门螺杆菌(H .pylori)感染及其相关胃炎的易感基因或抵抗基因,从免疫遗传角度探讨H .pylori感染后临床结局多样性的可能发生机制。方法　对1 999年9月至2 0 0 0年7月上海第二医科大学附属瑞金医院收治的1 3 3例慢性胃炎及80名健康儿童(对照组) ,进行H .pylori检测,应用PCR SSO杂交方法确定其HLA -DQB1等位基因型别。结果　80名对照组儿童中H .pylori阳性3 3名,H .pylori阴性47名;1 3 3例慢性胃炎患儿中,H .pylori阳性85例,H .pylori阴性48例。DQB1 0 3 0 3 2等位基因频率在血清学H .pylori阳性者中低于血清学H .pylori阴性的健康儿童( 1 0 . 61 %vs 2 5. 53 % ,P <0 . 0 5)。DQB1 0 60 2等位基因频率在H .pylori阳性胃炎患儿低于H .pylori阴性胃炎患儿( 4 . 71 %vs 1 2 . 50 % ,P <0 . 0 5)。结论　DQB1 0 3 0 3 2对H .pylori感染可能具有抵抗保护作用,DQB1 0 60 2缺乏可能是H .pylori相关性胃炎发生的宿主遗传因素。     

天津地区汉族Graves病患儿人类白细胞抗原-DQB1基因多态性

目的 检测天津地区汉族儿童Graves病(GD)人群的人类白细胞抗原(HLA)-DQB1基因,分析其易感基因,并观察家族性GD与散发性GD之间HLA-DQB1基因的差异.方法 采用PCR-序列特异性引物方法检测天津地区40例汉族GD患儿及50例健康儿童HLA-DQB1基因型,计算和比较各组间等位基因出现频率,并应用SPSS 11.5软件进行统计学分析.结果 1.GD组HLA-DQB1*0303基因分布频率与健康对照组比较明显增高(χ2=9.097,P=0.003);2.家族性GD组HLA-DQB1*0301基因频率分布与散发性GD组比较明显升高(χ2=9.724,P=0.002);3.DQB1*02、DQB1*0302等位基因频率比较差异均无统计学意义(P=0.953,0.414,0.902).结论 DQB1*0303基因是天津地区汉族儿童GD的易感基因,具有此基因者易患GD,而有GD家族史的儿童具有DQB1*0301基因也易患GD.     

儿童幽门螺杆菌相关性胃炎及十二指肠球部溃疡与血清胃泌素水 …

为探讨幽门螺杆菌（ＨＰ）相关性胃炎及十二指肠溃疡一高胃泌素血症的关系,以及根治疗对血清胃泌素的影响,我们对２５例十二例肠球部溃疡和２４例慢性胃炎患儿进行空腹血清胃泌素及ＨＰ检测,并对１５例ＨＰ阳性十二指肠球部溃疡儿应用三联疗法,停药１月后再检测ＨＰ与血清胃泌素,结果显示,ＨＰ阳性的十二指肠溃疡和慢性胃炎患儿血清胃泌素水平高于ＨＰ阴性的患儿（ｔ值分别为２．９７６,３．４８７,Ｐ均〈０．０１）,也高于     

人类白细胞抗原-Ⅰ基因多态性与急性淋巴细胞白血病的相关性

目的对急性淋巴细胞白血病(ALL)患儿进行人类白细胞抗原(HLA)基因多态性分型,寻找ALL的易感基因。方法采用特异性寡核苷酸探针杂交(PCR/SSO)法,对ALL患儿和健康对照组进行HLA-A、B基因分型。结果ALL患儿HLA-A01基因位点较健康对照组明显升高[χ2=4.947P=0.026,相对危险率(RR)=10.20]、A02基因位点较对照组降低(χ2=4.187P=0.041,RR=3.13)、A33基因位点较对照组降低(χ2=4.403P=0.036,RR=0.21)。结论HLA-A01、A33与小儿ALL有遗传相关性,其中A01为ALL发生的危险因素;而HLA-A33基因对儿童ALL有遗传拮抗作用。     

儿童幽门螺杆菌相关性胃炎及十二指肠球部溃疡与血清胃泌素水平的关系

为探讨幽门螺杆菌(HP)相关性胃炎及十二指肠溃疡与高胃泌素血症的关系。以及根治治疗对血清胃泌素的影响,我们对25例十二指肠球部溃疡和24例慢性胃炎患儿进行空腹血清胃泌素及HP检测,并对15例HP阳性十二指肠球部溃疡患儿应用三联疗法。停药1月后再检测HP与血清胃泌素。结果显示:HP阳性的十二指肠球部溃疡和慢性胃炎患儿血清胃泌素水平高于HP阴性的患儿(t值分别为2.976,3.487,P均<0.01);也高于正常对照组(t值分别为2.686、2.632,P均<0.05)。HP根治后病人血清胃泌素水平较治疗前显著下降(P<0.05)。结论:血清胃泌素水平在HP相关性上消化道疾病中具有重要意义。     

儿童幽门螺杆菌感染与白细胞介素-8含量的关系

目的：白细胞介素-8(IL-8)作为趋化因子,可引起粒细胞在局部组织聚集,介导炎症反应。该文探讨小儿幽门螺杆菌(Hp)感染与胃粘膜及血清IL-8含量的关系。方法：53例患儿进行胃镜检查,采集胃粘膜标本用快速尿素酶试验及病理组织学方法检测胃粘膜Hp,同时用双抗体夹心酶联免疫吸附试验法(ELISA)测定其胃粘膜及血清中IL-8的含量。结果：53例患儿中29例Hp阳性,24例阴性;Hp感染患儿胃粘膜中IL-8含量显著高于非Hp感染患儿,差异有显著性(P<0.01),而血清IL-8含量在Hp感染组与非Hp感染组无显著差异(P>0.05),经根治Hp治疗后,Hp感染患儿胃粘膜中IL-8含量下降,差异有显著性(P<0.01),而血清IL-8含量无显著变化(P>0.05)。结论：Hp感染可以诱导胃粘膜炎症细胞合成IL-8,IL-8在Hp相关性胃十二指肠疾病的发病机制中起着重要作用。     

儿童消化性溃疡与幽门螺杆菌感染临床治疗探讨

为探讨儿童消化性溃疡(PU)与幽门螺杆菌(H.pylori)感染的关系,观察274例(4～14岁)有上消化道症状的儿童,男174例,女100例,电子胃镜证实PU。病理及H.pylori检测后,随机分为7组根除H.pylori。A、B组应用枸橼酸铋钾(CBS)和克拉霉素(CLA),A组加甲硝唑(MET)、B组加呋喃唑酮(FUR),疗程7d。D组标准三联疗程14d。A、D两组再加泰胃美6周。质子泵抑制剂(PPI)组洛赛克和CLA,加另一抗生素AMO(C组)、MET(E组)、FUR(F组)疗程7d。G组Smecta、AMO和MET疗程14d。停药4周以上复查胃镜和/或~(13)C-尿素呼气试验(~(13)C-UBT)。结果:①274例患儿H.pylori检出率79.93％,胃镜见十二指肠溃疡95.26％,慢性浅表性胃炎(CSG)89.42％,胃粘膜炎症和溃疡活动度与H.pylori感染有显著相关(P<0.01)。②治疗后1周内PPI组和铋剂A、B两组腹痛缓解均≥90％,各组腹痛消退时问比较差异有显著性(P<0.01);停药4周以上复胃镜53例,溃疡愈合和消失88.68％。③随访210例,H.pylori转阴81.43％、耐药14.29％,复燃2.86％,再感染1.43％,各组转归之间差异无显著性(P>0.05)。用胃镜复查H.pylori转阴75.76％;用~(13)C-UBT检测H.pylori转阴82.17％;胃镜联合~(13)C-UBT检查20例,H.pylori转阴90％,随访方式与转归之间有显著相关(P<0.01)。表明H.pylori是小儿PU的     

Helicobacter pylori duodenal colonization in children

To investigate the prevalence and the significance of Helicobacter pylori duodenal colonization, endoscopic duodenal biopsies were performed in 168 children with chronic abdominal pain, gastroesophageal reflux, gastrointestinal bleeding, and malabsorption syndrome. Helicobacter pylori infection was detected in 68 children (40.4%): in 31 of them H. pylori was present in the gastric antrum, and in 37 in the duodenum also. Duodenitis was observed in 25 children with duodenal H. pylori ; gastric metaplasia in 3. Scanning electron microscopy revealed the presence of the micro-organism in 3/13 cases; the bacteria were located in the intercellular spaces and alterations of the epithelial surface were found. In conclusion, H. pylori gastritis in children is often associated with duodenal colonization which can cause duodenitis, and also without gastric metaplasia, which indicates a possible role of the micro-organism in the pathogenesis of the lesions.     

Helicobacter pylori infection in children

Helicobacter pylori colonizes the human stomach, especially during childhood. However, a variety of H. pylori strains exists, with major differences in virulence characteristics which probably account for different clinical symptoms, and the majority of infected subjects remains asymptomatic. Helicobacter pylori infection is correlated with socioeconomic conditions and hygienic circumstances, resulting in an extremely high prevalence in children in developing countries. Commercial screening tests are not capable of separating the more virulent strains (type I with vacuolating toxin VacA and CagA protein) from the less virulent strains (type II, VacA and CagA negative). Type I strains, but not type II, are associated with an increased risk for duodenal ulcer and gastric cancer. Therefore, future screening tests and vaccinations should focus on the type I strains.     

Gastroduodenal ulcers in the Helicobacter pylori era

The aim of the study was to evaluate the current spectrum of gastroduodenal ulcers in children referred to a regional paediatric unit in the United Kingdom. During a 5-y period (1994-98), all children with a visibly discrete gastric and/or duodenal ulcer diagnosed at endoscopy were prospectively identified. Patients with ulcers associated with Helicobacter pylori gastritis underwent repeat endoscopy 2-3 mo after medical treatment. Thirty-seven children, 21 boys and 16 girls of median age 11 y (range 7 mo to 16 y), had gastric and/or duodenal ulceration. Specific aetiological factors were identified in 21 of 22 with H. pylori negative ulcers, including Crohn's disease (n = 6), coeliac disease (n = 4) and treatment with ulcerogenic drugs (n = 4). Fifteen children (41%) had ulcers associated with H. pylori gastritis, including all 10 children with a chronic ulcer. Endoscopically confirmed ulcer healing was achieved in 14 of these using a 1 wk triple therapy regimen (omeprazole and a combination of two antibiotics). In conclusion, the recognized spectrum and the management of gastroduodenal ulceration have changed during the last decade. Although H. pylori gastritis is an important aetiological factor, a wide range of other conditions needs to be considered. Surgical intervention is only rarely necessary.     

幽门螺杆菌感染与过敏性紫癜相关性的研究

目的　研究幽门螺杆感染与过敏性紫癜的关系并指导治疗。方法　对1 0 2例过敏性紫癜患儿全部进行幽门螺杆菌的检测,阳性者在常规治疗的基础上进行抗幽门螺杆菌治疗。结果过敏性紫癜患儿中4 3 1 4 %感染幽门螺杆菌,给与对抗HP正规治疗,过敏性紫癜症状控制快,复发少。结论　幽门螺杆菌感染是过敏性紫癜的诱因之一     

幽门螺杆菌与小儿慢性胃炎的研究

为探讨幽门螺杆菌（ｈｅｌｉｃｏｂａｃｔｅｒｐｙｌｏｒｉ，Ｈｐ）与小儿慢性胃炎关系，应用细菌培养及组织病理学技术，对７３例具有消化道症状行胃镜检查患儿胃粘膜标本进行研究，并测定患儿血清抗幽门螺杆菌抗体ＨｐＩｇＧ、ＨｐＩｇＡ。结果显示，７３例患儿中Ｈｐ总检出率为３７％（２７／７３），在慢性胃炎者中检出率为４４％（２７／６１），与组织学检查正常者比较差异有非常显著意义（精确概率Ｐ＝０．００２１）；Ｈｐ的检出与胃粘膜炎症程度相关，表明Ｈｐ可能是慢性胃炎的一种致病因素。细菌学Ｈｐ阳性组和阴性组ＨｐＩｇＧ、ＨｐＩｇＡ抗体水平比较，阳性组高于阴性组，差异有非常显著意义（ｔ＝６．９３６，Ｐ＜０．０１）。提示与胃粘膜Ｈｐ检查相对照，ＨｐＩｇＧ有较好的敏感性、特异性，有助于Ｈｐ感染的诊断，ＨｐＩｇＡ抗体水平在两组间重叠较多。     

幽门螺杆菌相关性胃十二指肠疾病患儿MMP-7基因多态性研究

目的 研究基质金属蛋白酶-7(MMP-7)基因启动子多态性与儿童幽门螺杆菌(H-pylori)相关性慢性胃炎、十二指肠溃疡的易感性和临床特征的关系.方法 提取100例慢性胃炎、32例十二指肠溃疡和102例健康对照组儿童的外周血或胃黏膜基因组DNA,采用聚合酶链反应-限制性片段长度多态性技术(PCR-RFLP)和测序方法检测其MMP-7基因-181A/G多态性位点的基因型,分析该基因的基因型和等位基因频率在病例组和对照组人群中的分布及基因型分布与临床病理特征的关系,采用反转录-聚合酶链反应(RT-PCR)方法检测各组胃黏膜MMP-7 mRNA的表达.结果 MMP-7基因-181A/G多态性位点的基因型和等位基因频率在病例组和对照组人群中的分布差别无统计学意义,亦与H.pylori易感性无关.MMP-7基因-181A/G多态性不影响MMP-7 mRNA在胃黏膜中的表达,且与胃窦黏膜慢性炎症程度无相关性.结论 MMP-7基因-181A/G多态性与儿童慢性胃炎和十二指肠溃疡发生的易感性无关.