基质金属蛋白酶-7基因在幽门螺杆菌相关性胃十二指肠疾病儿童胃黏膜中的表达

目的探讨基质金属蛋白酶-7(MMP-7)基因在幽门螺杆菌(Hp)相关性胃十二指肠疾病儿童胃黏膜中的表达。方法具有上消化道不适主诉症状的患儿96例(包括慢性胃炎66例及十二指肠溃疡30例),经上消化道内镜检查获取其胃窦黏膜活检标本。根据Sydney胃炎标准对HE染色的活检组织进行胃窦黏膜慢性炎症程度评价。以血清Hp-IgG抗体检测、胃黏膜PCR、尿素酶试验及组织学检查结果作为确定Hp感染状态的依据。患儿均采用RT-PCR法及免疫组织化学法检测其胃窦黏膜MMP-7的表达。结果96例患儿的Hp感染率为51.0%。免疫组织化学染色结果显示MMP-7主要在胃上皮细胞中表达。Hp感染者的胃窦黏膜MMP-7mRNA及蛋白的阳性表达率(87.8%及89.8%)与无Hp感染者的阳性表达率(70.2%及63.8%)比较差异均有统计学意义(Pa<0.05)。Hp感染者胃窦黏膜MMP-7mRNA表达水平较无Hp感染者高(P<0.05),其表达水平与胃窦黏膜的慢性炎症程度呈正相关(r=0.312,P<0.05)。结论Hp感染诱发儿童胃十二指肠疾病胃窦黏膜中MMP-7基因的表达,推测基因表达的增高是Hp感染的早期事件,其主要作用可能是促...     

基质金属蛋白酶-9基因多态性与儿童幽门螺杆菌相关性胃十二指肠疾病的关系

目的：研究基质金属蛋白酶-9（MMP-9）基因启动子多态性与儿童幽门螺杆菌（Hp）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：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,对100例慢性胃炎及32例十二指肠溃疡儿童和102例健康对照组儿童的MMP-9 基因-1562C/T多态性进行检测。采用反转录 聚合酶链反应(RT-PCR)方法检测胃黏膜MMP-9 mRNA的表达。结果：MMP-9基因-1562 C/T多态性位点的基因型和等位基因频率在病例组和对照组儿童中的分布无明显差别。在慢性胃炎组中,C/C基因型携带者发生Hp感染的风险是T等位基因（C/T+T/T）携带者的3.1倍。MMP-9 基因-1562C/T多态性不影响MMP-9 mRNA在胃黏膜中的表达水平。结论：MMP-9 基因-1562C/T多态性与儿童慢性胃炎和十二指肠溃疡的发生无相关性,该基因位点的C/C基因型携带者可能与Hp易感性相关。［中国当代儿科杂志,2010,12（4）：262-266］     

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     

胃幽门螺杆菌感染患儿细胞毒素相关基因A和细胞空泡毒素A与十二指肠疾病

目的　了解幽门螺杆菌（Ｈｐ） 阳性患儿感染的Ｈｐ 菌株类型,探讨细胞毒素相关基因Ａ（ＣａｇＡ） 、细胞空泡毒素Ａ（ＶａｃＡ）与小儿慢性胃炎、消化性溃疡病发生之间的关系。方法　采用免疫印迹法对３３ 例十二指肠溃疡、３１ 例慢性胃炎患儿做血清Ｈｐ 的１１６ ０００（ＣａｇＡ） 、８９ ０００ （ＶａｃＡ） 、３５ ０００ 、３０ ０００ 、２６ ５００ 和１９ ５００ 蛋白抗体的检测。结果　在十二指肠溃疡患儿８９ ０００ 检出率达７２％ ,而慢性胃炎仅为２３％ ,但ＣａｇＡ在溃疡与胃炎患儿中差异不显著。以ＣａｇＡ、ＶａｃＡ结合分型发现,在十二指肠溃疡患儿６９％ 的Ｈｐ 为ＣａｇＡ＋ 、ＶａｃＡ＋ 菌,而在慢性胃炎中６８％ 的Ｈｐ 为ＣａｇＡ＋ 、ＶａｃＡ－ 菌,两者比较差异有显著性（ Ｐ＜ ０．０５）。结论　小儿十二指肠溃疡及中、重度胃炎的发生与感染Ｈｐ 的毒力菌株相关,ＶａｃＡ很可能是致溃疡的毒力因素。     

具有cagA、vacA基因的幽门螺杆菌感染及其与胃十二指肠疾病的关系

目的 研究上海地区儿童慢性胃炎及消化性溃疡患者中具有cagA、vacA基因幽门螺杆菌感染（HP）的感染状况以及cagA、cacA基因的存在与不同种类胃十二指肠疾病发生的关系。方法 对124例有消化道症状，年龄在4－13岁的儿童行胃镜检查，并在胃窦部取活检粘膜作HP的分离培养。利用聚合酶链反应技术（PCR）测定分离培养出的HP菌株的cagA、vacA基因进行分型。扩增所用引物：cagA1：5′－CCGGAGAATTCGATAACAGGCAAGCTTTTGAGG－3′，cag2：5′－GCCTGCAGTTATCGAAAA－GATTGTTTGGCAG－3′，vacA1：5′－GTCAGCATCACACCGCAAC－3′，vacA2：5′－CTGCTTGASATGCGCCAAAC－3′。结果 124例患儿中，分离培养出的HP菌株61株，平均检出率为50％，其中慢性胃炎培养阳性率为48．45％（47／97例），十二指肠球部溃疡为62．30％（14／26例），基因测定结果显示，61株HP中62．30％含有cagA基因，42．62％含有vascA基因。慢性胃炎和二十指肠球部溃疡cagA基因检出率相似（分别为61．70％和62．28％），而vacA基因检出率十二指肠球部溃疡明显高于慢性胃炎组（71．43％和34．04％，χ^2＝6．166，P＜0．05）。进一步分型发现感染Hp菌株的十二指肠球部胃炎组（71．43％和34．04％，χ^2＝6．166，P＜0．05）。进一步分型发现Hp菌株的十二肠球部溃疡患儿中，50％（7／14）为cagA^ 、vacA^ 型，慢性胃炎患儿中330％（18／47）为cagA^ 、vacA^-型Hp菌株，统计学检查差异有显著意义（χ^2＝13．48，P＜0．05），提示vacA与十二指肠球部溃疡的发生密切相关。结论 十二指肠球部溃疡患儿感染的HP多为cagA^ 、vacA^ 的I型菌，vacA是致小儿十二指肠溃疡的重要因素，vagA与慢性胃炎、十二指肠溃疡的发生有关，但不能作为区分HP感染致不同胃肠道疾病的单一指标。     

克拉霉素治疗幽门螺杆菌相关性胃十二指肠疾病

目的　观察克拉霉素治疗幽门螺杆菌相关性胃十二指肠疾病的疗效。方法　 6 4例经胃镜活检或13 C UBT检查 ,确诊为幽门螺杆菌 (HP)相关性胃十二指肠疾病 ,随机分为A、B组 ,A组奥美拉唑 0 .8mg/ (kg·d) ,甲硝唑 2 0mg/ (kg·d)、阿莫西林 4 0mg/ (kg·d)。B组予奥美拉唑、甲硝唑、克拉霉素 15mg/ (kg·d)治疗 2周 ,奥美拉唑、甲硝唑用量同A组 ,停药 4周以后作胃镜或用13 C UBT检查。结果　HP根除率A组 6 2 .7% ,B组94 .1% ,B组明显高于A组 (χ2 =31.80　P <0 .0 1)。治疗后 1、2周疼痛缓解率B组明显高于A组 (χ2 =19.30　P <0 .0 5 )。结论　克拉霉素作为三联疗法中抗HP感染 ,疗效明显优于阿莫西林。     

幽门螺杆菌毒素因子与儿童胃十二指肠疾病的相关性研究

目的　研究贵阳地区儿童幽门螺杆菌感染的CagA蛋白及VacA蛋白的感染状况 ,以及不同Hp菌株类型与胃肠黏膜病理组织学改变的关系。方法　采用免疫印迹法 (WesternBlot)对 6 7例Hp阳性及 32例Hp阴性患儿血清进行Hp毒素因子的测定及血清学菌株分型 ,参照悉尼胃炎分类标准 ,对不同Hp菌株类型进行病理组织学对比研究。结果　本地区Ⅰ型高毒力Hp菌株检出率 6 8.6 % ,中间型Hp菌株为 2 6 8% ,Ⅱ型Hp低毒力菌株为 4 4 %。Ⅰ型Hp菌株 1 0 0 %存在胃肠黏膜组织学改变 ,胃窦黏膜以中度炎症为主 ,占 73 9% ,重度炎症占 1 1 % ,活动性占 73 9%。十二指肠球部黏膜以中 重度炎症为主 ,占77 3% ,活动性占 6 6 4 %。中间型Hp菌株 72 %存在黏膜组织学改变 ,胃窦黏膜以轻度炎症为主 ,占 5 5 6 % ,活动性占 5 5 % ,十二指肠球部黏膜以轻 中度炎症为主 ,占 5 5 1 % ,活动性占 1 1 1 %。Ⅰ型Hp菌株与中间型Hp菌株在致黏膜炎症改变程度及活动性方面有差异性 (P <0 0 5 )。在淋巴滤泡形成方面 ,Ⅰ型Hp菌株较中间型Hp菌株有显著性差异 (P <0 0 1 )。结论　本地区Hp感染菌株类型以Ⅰ型为主 ,占 6 8 6 % ,同时存在 2 6 8%的中间型菌株及 4 4 %的Ⅱ型菌株的感染。Ⅰ型Hp菌株及中间型菌株在黏膜炎症程度及活动性上有差异性     

幽门螺杆菌致胃,十二指肠疾病机制的研究

幽门螺杆菌是慢性胃炎，消化性溃疡的主要病因，近年的研究发现，ＨＰ的致病机制有赖于毒力因素和致病因素，ＨＰ的螺旋形和能动性。     

Symptomatology of Helicobacter pylori infection in children

In a retrospective evaluation we reviewed the symptomatology of 143 children (age 2–15 years, mean 8.9 years) who were referred to us for upper gastrointestinal endoscopy because of recurrent abdominal pain with a duration of 6 weeks or longer. Helicobacter pylori infection was diagnosed in 36 out of 143 patients (25.2%). No statistically significant differences could be detected between the symptoms experienced by the 36 H. pylori-infected children and those experienced by the remaining 107 H.pylori-negative pediatric patients (p = 0.18–0.60). We conclude that no specific symptoms are associated with H. pylori gastritis in children. Our observations suggest that the recurrent abdominal complaints found in children with H. pylori infection seem to be caused by the secondary gastroduodenal pathology, rather than by H. pylori infection itself.     

人类白细胞抗原-DQB1与儿童十二指肠溃疡和幽门螺杆菌感染的相关性研究

目的探讨人类白细胞抗原(HLA)-DQB1等位基因与儿童十二指肠溃疡(DU)和幽门螺杆菌(H.pylori)感染的遗传关联性。方法采用非同位素标记的聚合酶链反应-序列特异性寡核苷酸探针(PCR-SSO)杂交的方法,对上海地区汉族健康儿童80例、DU患儿58例的HLA-DQB1等位基因进行分型;并同时检测DU患儿H.pylori感染情况。结果在DU患儿中,HLA-DQB1×05031等位基因频率明显高于正常健康儿童(分别为:6.02%、0.63%,P<0.05,RR=9),而在H.pylori阳性和H.pylori阴性DU组之间差异无显著性。结论HLA-DQB1×05031与DU呈正相关,DU患儿与正常对照组儿童之间存在着遗传学的差异;虽然H.pylori感染是DU的重要致病因素,但HLA-DQB1×05031并不是通过H.pylori感染而影响DU的遗传易感性。     

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 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.     

Helicobacter pylori infection, histopathological gastritis and gastric epithelial cell apoptosis in children

AIM: Features of gastritis and gastric epithelial cell apoptosis in children infected with Helicobacter pylori genotypes are seldom studied. Therefore, we investigated the relationship between vacA genotypes and the severity of gastritis, and gastric epithelial cell apoptosis in H. pylori-infected children. METHODS: Antral biopsies from 52 children infected with H. pylorivacA genotypes (s1a/m1 = 17, s1a/m2 = 21 and s2/m2 = 14) were analysed for severity of gastritis on histopathology. Fifteen biopsies infected with different vacA genotypes were studied for gastric epithelial cell apoptosis by terminal uridine deoxynucleotidyl nick-end labelling. RESULTS: Children infected with the s1a/m1 and s1a/m2 vacA genotypes had higher severity of chronic inflammation than the s2/m2 genotype (s1a/m1 vs s2/m2, p=0.05; s1a/m2 vs s2/m2, p=0.01). The vacA s1a allele was more independently associated with severe chronic inflammation than the s2 allele (p=0.02). Children infected with the s1a/m1 and s1a/m2 strains had higher gastric epithelial cell apoptosis than the s2/m2 strain (s1a/m1 or s1a/m2 vs s2/m2, p<0.0001). CONCLUSION: The s1a/m1 and s1a/m2 H. pylorivacA genotypes have significantly higher association with severe chronic gastritis and gastric epithelial cell apoptosis than the s2/m2 genotype in children. The role of H. pylorivacA genotypes and their allelic subtypes in relation to pathogenicity and disease potential in children needs further studies.     

有上消化道症状患儿幽门螺杆菌感染调查

目的了解门诊有上消化道症状患儿幽门螺杆菌感染率。方法对1997年7月至2009年9月,2 161例有上消化道症状的门诊患儿行空腹13C-尿素呼气试验(UBT)。结果 2 161例有上消化道症状患儿中男1 138例,女1 023例,年龄4～16岁,平均(9.2±5.1)岁。H.pylori阳性608例,占28.14%,其中男361例(31.72%),女247例(24.14%),差异有统计学意义(χ2=15.299,P<0.001)。1997年7月—2000年共检测821例,H.pylori阳性256例(31.18%),2001年—2004年检测713例,H.pylori阳性202例(28.33%),2005年—2009年9月检测627例,H.pylori阳性154例,(24.56%),感染率有逐年下降趋势,差异有统计学意义(χ2=7.675,P=0.022)。结论门诊中有上消化道症状儿童H.pylori感染率有逐年下降趋势。     

CagA seropositivity and the severity of Helicobacter pylori infection in dyspeptic children

AIM: To assess the incidence of cagA (cytotoxin-associated protein) and to evaluate its correlation with endoscopic-histologic findings and with eradication rate in a series of children affected by Helicobacter pylori (H. pylori) gastritis. METHODS: Fifty consecutive H. pylori gastritis children (27M; median age 10 y and 11 mo) were tested for IgG cagA protein (Western Blot technique). Pretreatment H. pylori infection was assessed on the grounds of endoscopic antral biopsy specimens by means of rapid urease test and histologic examination (Giemsa staining). All the children were treated with omeprazole (1 mg/kg/d), clarithromycin (15 mg/kg/d) and amoxycillin (50 mg/kg/d) for 2 wk. According to universally accepted clinical practice, outcome of treatment was assessed by 13C urea breath test at least 6 wk after the end of therapy. RESULTS: Thirty-five children (70%) were seropositive to cagA+ protein (median age 11 y and 1 mo). Endoscopic findings of cagA+ patients were similar to those of cagA- patients. In cagA seropositive patients the severity of histologic gastritis was higher (p < 0.05) and the granulocytic infiltration more marked (p < 0.01) than in seronegative ones. In cagA+ children, H. pylori eradication rate was significantly lower (p < 0.02). CONCLUSIONS: cagA testing may be of useful clinical interest because its positivity can imply a more severe gastritis and a lower susceptibility to eradication treatment.     

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.