幽门螺杆菌感染对消化性溃疡患者胃G,D细胞的影响

目的 探讨幽门螺杆菌(Hp)感染对溃疡患者胃G,D细胞的影响.方法 活动性十二指肠溃疡(DU)患者77例根据Hp情况分为A组(Hp根除组)51例,男37例,女14例,年龄35岁±13岁,成功根除Hp;B组(Hp持续阳性组)12例,男9例,女3例,年龄35岁±10岁,未根除Hp;C组(Hp阴性组)14例,男9例,女5例,年龄38岁±12岁.D组为Hp阳性的功能性消化不良(FD)25例,男15例,女10例,年龄38岁±13岁,成功根除Hp.在治疗之前及疗程结束之后1 mo再复查内镜,了解溃疡愈合和Hp感染情况,并取胃窦粘膜查G,D细胞数量(ABC法免疫组化)、促胃液素(Gas)和生长抑素(SST)基因表达(α-32PdATP掺入RT-PCR).结果 治疗后各DU组溃疡灶均愈合.各组胃窦G细胞数量无统计学差异(P＞0.05).Hp阳性组的D细胞数量(个/nlm2,A组9.3±2.4,B组11.9±5.3,D组12.9±5.9)低于Hp阴性患者(C组19.2±5.6个/mm2,P＜0.05),Hp根除之后D细胞数量增多(A组18.5±5.6,D组20.3±7.1个/mm2,P＜0.01),未根除Hp的B组D细胞数量依然较低(10.6±6.4个/mm2).A,D两组间的D细胞数量、G/D细胞比值均接近.治疗前各DU组Gas基因表达水平(A/gq,A组424±152,B组435±114,C组368±184)高于FD组(D组216±95 A/Bq,P＜0.01),Hp阳性DU组(A,B组)与Hp阴性DU组(C组)的差异无统计学意义(P＞0.05).治疗后不论Hp是否被根除,各DU组(A,B,C组)Gas基因表达有下降趋势,但无统计学差异(P＞0.05),D组在Hp被根除后Gas基因表达水平(113±73 A/Bq)低于根除前(P＜0.05).治疗前FD组SST基因表达水平(D组180±65 A/Bq)高于各溃疡组,Hp阴性的溃疡组(C组120±48 A/Bq)高于Hp阳性溃疡组(A/Bq,A组65±22,B组77±23,P＜0.05);治疗后各组SST基因表达均增加(P＜0.01),但其他组相比Hp持续阳性的B组SST基因表达水平仍然低下(A组324±144,B组147±47,C组541±197,D组369±144 A/Bq,P＜0.05).结论 Hp感染不影响胃G细胞数量,但使D细胞数量减少,SST基因表达下降,Gas基因表达增多;溃疡灶可抑制SST基因表达,刺激促胃液素过度释放.     

根除幽门螺杆菌对消化性溃疡合并胃炎及胃泌素的影响

目的 :评估胃舒散联合呋喃唑酮、阿莫西林对消化性溃疡 (PU)患者Hp根除的效果及其对溃疡合并胃炎、血清胃泌素(Gas)的影响。方法 :77例Hp阳性十二指肠溃疡组 (DU ,52例 )和胃溃疡组 (GU ,2 5例 )患者 ,均服用胃舒散 2 .0g(含铋 0 .1 2g) ,呋喃唑酮0 .1g,阿莫西林 0 .5g ,各 3次 /d ,2周后再继服胃舒散 4周。治疗前及疗程结束 1月后进行内镜检查并对胃窦、胃体胃炎予以内镜下评分。采用放射免疫法于治疗前及结束 1月、6月后检测胃泌素水平。结果 :DU组与GU组溃疡愈合率分别为 1 0 0 %和 92 % ,Hp根除率分别为 90 .3 %和 84.0 % ,二组比较差异均无显著性 (P >0 .0 5)。将根除Hp的 47例DU和 2 1例GU患者分为 2组 ,治疗前 2组胃窦胃炎的评分差异无显著性 (P >0 .0 5) ;GU组胃体胃炎的评分显著高于DU组 (P <0 .0 0 1 ) ;血浆中胃泌素含量 (DU组 39.4± 1 3 .6pg/ml;GU组38.4± 1 2 .3pg/ml)均显著高于正常对照值 (2 8.5± 1 0 .6pg/ml,P <0 .0 5)。Hp根除 1月后 ,2组患者胃窦胃炎与胃体胃炎的评分均显著下降 ,与治疗前自身比较 ,差异有统计学意义 (均P <0 .0 0 1 )。DU组Hp根除治疗 1月后 ,胃泌素水平显著下降到 32 .7± 1 0 .5pg/ml (P <0 .0 5)。GU组Hp根除 1月后 ,胃泌素水平有所下降 ,但与治疗前相比 ,差     

幽门螺杆菌cagⅡ对胃上皮细胞IL-8基因转录的影响及机制

目的探讨HpcagⅡ对胃上皮细胞IL-8基因转录的影响及信号传导机制。方法构建 cagⅡ基因位点缺失Hp突变株及带有IL-8报告基因的人胃癌细胞系L5F11,用液体闪烁计数仪测定荧光素酶(IL8转录)活性,用ELISA法测定IL8蛋白浓度。结果所有Hp突变株诱导荧光素酶活性与IL8蛋白浓度较亲代菌株26695均降低[(0．13±0．01)×cpm比(0．59±0．05)×(P<0．01);(0．73±0．13)ng／ml比(2．22±0．65)ng／ml,(P<0．05)]。PTK抑制剂herbimycinA不仅抑制Hp诱导的荧光素酶活性[(0．71±0．18)×cpm比(1．51±0．23)×cpm,(P<0．05)],而且抑制IL-8蛋白表达[(0．83±0．41)ng／ml比(3．22±0．59)ng／ml,(P<0．05)],但herbimycinA对TNFα诱导的荧光素酶活性及IL8蛋白表达均无影响(P均>0．05);PKA抑制剂H7抑制TNFα诱导的荧光素酶活性[(0．74±0．16)×cpm比(2．62±0．26)×cpm,(P<0．001)]及IL8蛋白表达[(1．45±0．38)ng／ml比(4．12±0．43)ng／ml,(P<0．01)],而对Hp诱导的荧光素酶活性无影响(P>0．05)。结论HpcagⅡ中的多基因能够调节胃上皮细胞IL-8基因转录,且这一作用主要经蛋白酪氨酸激酶途径。     

三联短程疗法治疗幽门螺杆菌相关性十二指肠溃疡

目的探讨奥美拉唑(Omeprazole)、羟氨苄青霉素(Amoxycillinum)和甲硝唑(Metronidazole)1wk短程疗法根除幽门螺杆菌(Hp)的疗效,对Hp相关性活动期十二指肠溃疡(DU)治疗效果和复发的影响,并与2wk疗法相比较.方法将128例Hp阳性的活动期DU患者随机分成两组.A组奥美拉唑20mg、羟氨苄青霉素1000mg、甲硝唑400mg、均为2次/d,治疗1wk.B组奥美拉唑20mg,羟氨苄青霉素1000mg,甲硝唑400mg,均为2次/d,治疗2wk.两组均继续给奥美拉唑20mg,满4wk停药.治疗前和治疗后1mo,1a各做一次电子内镜检查,并取活组织做快速尿素酶检测和组织学Silver-Staining银染色法检测Hp.结果A,B两组Hp根除率分别为92.19%(59/64),95.31%(61/64)(P>0.05);DU治愈率为93.75%(60/64),96.88%(62/64)(P>0.05);副作用发生率为4.69%(3/64),12.50%(8/64)(P<0.01).Hp根除和未根除者1a后DU复发率分别为3.33%(4/120),75.00%(6/8)(P<0.01).结论以奥美拉唑为主,合并羟氨苄青霉素和甲硝唑治疗Hp相关性DU,Hp清除率和DU治愈率高,并能有效预防DU复发.1wk短程疗法即可达到治疗目的,副作用小、顺应性好,可以取代2wk疗法,是目前治疗Hp相关性DU较好的治疗方案.     

中西医结合治疗消化性溃疡148例

目的观察法莫替丁联合中药对消化性溃疡的疗效.方法在内镜下确诊为胃溃疡(GU)和十二指肠溃疡(DU)患者242例,按入院的先后随机分为法莫替丁组、中药组.法莫替丁组94例,平均年龄42岁±4岁,GU80例,DU9例,复合溃疡5例;法莫替丁20mg,2次/d,用药6wk.中药组法莫替丁20mg,2次/d,用药6wk,中药汤散剂并服2wk.结果两组治愈率比较无明显差异(P>0.05),复发率比较,中药组与法莫替丁组比较差异非常显著(P<0.05).Hp转阴率比较,中药组与法莫替丁组比较差异非常显著(P<0.05).结论法莫替丁联合该中药治疗PU,疗效佳,复发率低,且价格低廉,副作用小,在临床上值得推广应用.     

不同血压心力衰竭患者肾素-血管紧张素-醛固酮系统的活性

目的为探讨不同血压的充血性心力衰竭(CHF)患者肾素-血管紧张素-醛固酮系统(RAAS)的活性。方法运用放免法测定收缩压(SBP)<100mmHg(1mmHg=0．133kPa)的CHF患者(LPCHF组,22例),SBP>100mmHg的CHF患者(HPCHF组,25例)及健康人(对照组,18例)血浆肾素活性(PRA)、血管紧张素Ⅱ(AngⅡ)及醛固酮(ALD)水平。结果LPCHF组及HPCHF组血浆PRA、AngⅡ和ALD均明显高于对照组(P<0．05～0．01),LPCHF组血清钠、SBP及脉压SBP显著低于对照组(P<0．05～0．01);LPCHF组血浆PRA、AngⅡ和ALD高于HPCHF组(P<0．05～0．01),LPCHF组血清钠、SBP及脉压SBP显著低于HPCHF组(P<0．05～0．01);CHF患者脉压SBP与血浆AngⅡ及ALD呈显著负相关(r=－0．501,P<0．01,r=－0．439,P<0．01)。结论CHF患者体内RAAS活性增高,且SBP<100mmHg者较SBP>100mmHg更高。     

幽门螺杆菌感染与细胞凋亡及一氧化氮

目的研究Hp感染对胃粘膜上皮细胞凋亡的影响.探讨细胞凋亡与胃粘膜一氧化氮(NO)之间的关系.方法分别用切口末端标记法和硝酸还原酶法对Hp阳性的十二指肠球部溃疡、胃溃疡、癌前病变、胃癌以及组织学上正常的Hp阴性者各10例的胃粘膜活检组织进行细胞凋亡和一氧化氮检测.结果Hp阴性者细胞凋亡仅见于胃粘膜的浅层,Hp阳性者细胞凋亡不仅见于胃粘膜的浅层,而且在深层甚至固有层也可见到.从Hp阳性的十二指肠溃疡→胃溃疡→癌前病变→胃癌→Hp阴性的正常组织细胞凋亡逐渐减少,凋亡指数分别为17.5%,15.1%,9.2%,5.1%,2.5%.凋亡指数在胃溃疡组与球部溃疡组之间无统计意义(P>0.05),而在其他各组间相互比较差别均有统计学意义(P<0.01).NO含量在Hp阳性的各实验组比Hp阴性的正常对照组显著增高(P<0.01),但在各实验组之间差别均无显著性(P>0.05).Hp根除以后细胞凋亡及NO含量均有显著下降,在Hp阳性的十二指肠溃疡、胃溃疡细胞凋亡与NO呈显著正相关(P<0.05),而在癌前病变组和胃癌组细胞凋亡与NO之间无显著相关性(P>0.05).结论上述结果提示①Hp感染可能诱导胃上皮细胞凋亡,这可能是Hp致胃癌的机制之一;②Hp感染可能引起胃粘膜一氧化氮含量的增高;③在Hp感染的早期大量产生的NO可能有助于胃上皮细胞凋亡.根除Hp,以减少细胞凋亡有助于预防胃癌的发生.     

丽珠胃三联治疗Hp相关性胃炎的研究

目的丽珠胃三联对Hp相关性胃炎的Hp根除效果的研究.方法选择门诊因消化道症状而就诊的患者,均行必要检查,排除相关症状疾病.经内镜检查,进行Hp尿素酶检查为阳性者52例,选入研究对象,其中男38例,女14例,年龄为20岁～70岁,进行随机分组,A组为丽珠三联(枸橼酸铋钾)0.22g,2次/d,克拉霉素0.25g,2次/d,替硝唑2次/d);B组奥美拉唑组(奥美拉唑20mg,2次/d;甲硝唑400mg,2次/d,阿莫西林1g,2次/d).疗程均为1wk.分别对Hp根除率及治疗后3d、1wk,2wk内上腹痛缓解率治疗期间副反应进行统计,其中疼痛消失按0～3级分类,治疗后属0级或偶1级为疼痛缓解.结果Hp根除率A组为96.2%(25/26),B组为92.3%(24/26),二组间的Hp根除率相比,无显著差异(P>0.05),疼痛缓解率3dA组7/22(31.8%),B组18/23(78.1%)P<0.05.wk1A组11/22(50%),B组22/23(98.3%),P<0.01.wk2A组19/22(86.3%),B组23/23(100%)P>0.05.药物副反应二组中仅一例服药后诉轻度恶心、未发现其他副反应.结论丽珠胃三联具有药物剂量小、疗程短、疗效高、副反应轻等优点,是较为理想的根除Hp的治疗方案.     

黄连素与钙剂伍用治疗病态窦房结综合征初步观察

目的探讨黄连素与钙剂伍用对病态窦房结综合征的治疗作用。方法对符合病态窦房结综合征患者21例,口服黄连素片0．5～0.8g,每天3次,1周后同时加用10％葡萄糖酸钙10ml加5％葡萄糖或0．9％氯化钠液稀释静脉滴注8～10d。治疗前后分别作动态心电图检查,观察窦性最长R-R间期、窦性最短R-R间期、24h平均心率、24h总心搏数、长R-R间期(≥2s)、长R-R间期发生次数。结果治疗后最长窦性R-R间期、最短窦性R-R间期分别由(1．86±0．42)s、(0．76±0．15)s缩短至(1.67±0．63)s(P<0．05)、(0．66±0．10)s(P<0．01)。24h平均心率、24h总心搏数分别由(53．20±5．63)次／min、(73974．60±8234．85)次增至(55．73±5．05)次／min(P<0．05)、(78934．00±7194．21)次(P<0．01)。≥2s的长R-R间期由(2．79±1．54)s缩短至(2．22±1.17)s(P<0．05)、长R-R间期发作次数由(16．60±12．70)次减少至(5．10±5．38)次(P<0．01)。11例有持续较长时间的交界区逸搏心律者,其中7例交界区逸搏心律消失。结论黄连素与钙剂伍用对窦房结功能改善有一定作用,且无明显副作用。     

奥美拉唑三联疗法根除幽门螺杆菌的疗效观察

目的探讨奥美拉唑三联疗法根除幽门螺杆菌(Hp)的疗效.方法Hp阳性的活动性十二指肠溃疡患者61例,男50例,女11例,年龄18岁～62岁.将患者随机分为三联疗法组30例,口服奥美拉唑20mg,1次/d,阿莫西林500mg,呋喃唑酮100mg,3次/d;二联疗法组31例,口服奥美拉唑20mg,1次/d,阿莫西林500mg,3次/d.疗程均为2wk,疗程结束1mo后内镜检查溃疡愈合情况及Hp检测.结果三联疗法Hp根除率及溃疡愈合率分别为93.3%(28/30)及90%(27/30),高于二联疗法组的77.4%(24/31)及80.6%(25/31),经x2检验,差异无显著性(P>0.05).结论奥美拉唑三联疗法有很理想的Hp根除率及溃疡愈合率,不良反应少     

Gastrin and antral G cells in course of Helicobacter pylori eradication： Six months follow up study

ABM: To assess long-term effects of Helicobacter pylori (H pylori) eradication on antral G cell morphology and function in patients with and without duodenal ulcer (DU). METHODS: Consecutive dyspeptic patients referred to the endoscopy entered the study. Out of 39 H pylori positive patients, 8 had DU (Hpylori+DU) and 31 gastritis (Hpylori +G). Control groups consisted of 11 uninfected dyspeptic patients (CG1) and 7 healthy volunteers (CG2). Basal plasma gastrin (PGL), antral tissue gastrin concentrations (ATGC), immunohistochemical and electron microscopic characteristics of G cells were determined, prior to and 6 mo after therapy. RESULTS: We demonstrated elevated PGL in infected patients compared to uninfected controls prior to therapy. Elevated PGL were registered in all H pylori+patients (H pylori +DU: 106.78±22.72 pg/mL, H pylori+G: 74.95±15.63, CG1: 68.59±17.97, CG2: 39.24±5.59 pg/mL, P<0.01). Successful eradication (e) therapy in H pylori+patients lead to significant decrease in PGL (H pylori+DU:59.93±9.40 and H pylori+Ge: 42.36±10.28 pg/mL, P<0.001). ATGC at the beginning of the study were similar in infected and uninfected patients and eradication therapy lead to significant decrease in ATGC in H pylori+gastritis, but not in DU patients. In the H pylori+DU patients, the mean number of antral G cells was significantly lower in comparison with all other groups (P<0.01), but after successful eradication was close to normal values found in controls. By contrast, G cell number and volume density were significantly decreased (P<0.01) in H pylori+Ge group after successful eradication therapy (294±32 and 0.31±0.02, respectively), in comparison to values before eradication (416±40 and 0.48±0.09). No significant change of the G cell/total endocrine cell ratio was observed during the 6 mo of follow up in any of the groups. A reversible increase in G cell secretory function was seen in all infected individuals, demonstrated by a more prominent secretory apparatus. However, differences between DU and gastritis group were identified. CONCLUSION: H pylori infection induces antral G cell hyperfunction resulting in increased gastrin synthesis and secretion. After eradication therapy complete morphological and functional recovery is observed in patients with gastritis. In the DU patients some other factors unrelated to the H pylori infection influence antral G cell morphology and function.     

不同幽门螺杆菌根除方案对功能性消化不良影响的临床研究

背景:功能性消化不良(FD)是常见的功能性胃肠病,幽门螺杆菌(H.pylori)是FD的重要致病因素之一。目的:探讨不同H.pylori根除方案对FD患者临床症状的疗效。方法:160例H.pylori(+)FD患者随机分为10d序贯治疗组(60例)、7d三联治疗组(60例)和对照组(40例)。所有患者于停药4周后复查~(14)C-尿素呼气试验以评估H.pylori根除率。患者于治疗前、治疗后第3、6、12个月评估FD症状。结果:10d序贯治疗组、7d三联治疗组和对照组的H.pylori根除率分别为93.2%、74.1%和48.6%(符合方案分析)以及91.7%、71.7%和42.5%(意向治疗分析),各组相比差异有统计学意义(P0.05)。治疗后第6、12个月,10d序贯治疗组和7d三联治疗组中H.pylori根除者的FD症状改善率显著高于对照组(P0.05),但两治疗组之间无明显差异。结论:10d序贯治疗和7d三联治疗的FD症状改善率无明显差异,但前者H.pylori根除率高于后者,临床可推荐10d序贯疗法治疗H.pylori(+)FD患者。     

Helicobacter pylori and Duodenal Ulcer Recurrence

Preliminary evidence suggests that eradication of Helicobacter pylori (H. pylori) may lead to prolonged remission of duodenal ulcer (DU). The aim of this study was to assess the long-term effect of eradication of H. pylori on the natural history of DU. Fifty-one patients with endoscopically proven duodenal ulcers, who were found to have H. pylori infection on histology and culture, and who were successfully eradicated of H. pylori with combination treatment of colloidal bismuth subcitrate and antibiotics, were studied. All patients were endoscoped at entry, 4 wk after cessation of treatment and again at 1 yr or sooner, if symptoms recurred. At each endoscopy, two antral biopsies were taken and assessed histologically and microbiologically for evidence of H. pylori infection. Recurrence of H. pylori infection occurred in 18/51 patients (35.3%) and, of these, 12 patients had evidence of recurrent peptic disease (five DU, seven duodenitis). In contrast, of the 33 who remained negative for H. pylori at 1 yr, none developed evidence of recurrent DU. Overall, DU recurrence occurred in 5/51 patients (11.7%), and occurred only in patients reinfected with H. pylori. This relapse rate compares favorably with patients on maintenance H2-receptor antagonist treatment. These results lend further support to the hypothesis that antral reinfection with H. pylori is associated with relapse of DU.     

Eradication of Helicobacter pylori restores the inhibitory effect of cholecystokinin on postprandial gastrin release in duodenal ulcer patients.

Helicobacter pylori infection may be associated with duodenal ulcer (DU) and accompanied by enhanced gastrin release but the mechanism of this H pylori related hypergastrinaemia in DU patients is unclear. Cholecystokinin (CCK) has been implicated in the feedback control of gastrin release and gastric acid secretion in healthy subjects. This study therefore investigated if CCK participates in the impairment of postprandial gastrin release and gastric secretion in six DU patients. Tests were undertaken with and without elimination of endogenous CCK by loxiglumide, a selective CCK-A receptors antagonist, before and after eradication of H pylori with triple therapy (omeprazole, amoxicyllin, bismuth). In H pylori positive DU patients, the post-prandial decline in pH (with median pH 3.5) was accompanied by a pronounced increment in plasma gastrin but the administration of loxiglumide did not affect significantly this postprandial rise in plasma gastrin and gastric pH profile. After eradication of H pylori, the plasma gastrin concentration was reduced while the median postprandial pH was significantly increased (median pH 4.3). The administration of loxiglumide resulted in significantly greater increase in postprandial plasma gastrin and greater decrease in pH (median pH 3.1) in these patients. This study shows that (a) infection with H pylori is accompanied by an enhanced gastrin release and gastric acidity in DU patients, (b) the failure of loxiglumide to affect plasma gastrin or gastric acid secretion in H pylori infected DU patients could be attributed, at least in part, to the failure of endogenous CCK to control gastrin release and gastric secretion by releasing somatostatin, and (c) the test with loxiglumide may be useful in the identification of patients with impaired feedback control of gastrin release and gastric secretion resulting from infection with H pylori.     

Helicobacter pylori-related hypergastrinaemia is not due to elevated antral surface pH. Studies with antral alkalinisation.

It has been postulated that Helicobacter pylori-related hypergastrinaemia is due to bacterial ammonia raising antral surface pH and thus preventing acid inhibition of gastrin release. If true, the infection should not alter gastrin release at neutral intragastric pH. To test this, we have studied basal and meal-stimulated gastrin at uncontrolled pH and at pH greater than 6 in duodenal ulcer patients before and after eradication of H. pylori. The median integrated gastrin response to the meal alone was 2525 ng/l.min (range, 550-8725) before and 725 ng/l.min (range, 250-2925) after eradication of H. pylori (p less than 0.01). The corresponding values when intragastric pH was maintained above 6 were 3700 ng/l.min (range, 1900-14,100) and 1400 ng/l.min (range, 400-3400) (p less than 0.01). The median reduction in gastrin after eradication of H. pylori was thus similar when the meal was taken at uncontrolled pH (61%; range, 0-97%) and at pH greater than 6 (69%; range, 36-89%). Likewise, 5 h of gastric alkalinisation did not cause the basal gastrin values when H. pylori was eradicated to increase to those observed when H. pylori was present. These findings indicate that the hypergastrinaemia is not due to elevated antral surface pH.     

根除Hp前后胃窦粘膜COX-2表达的变化

目的检测胃窦粘膜在根除Hp前后环氧化酶-2(Cyclooxygenase-2,COX-2)表达水平的变化,探讨COX-2表达与急、慢性炎症的关系.方法对我院1999.6-2000.3胃镜诊断为慢性胃炎、胃粘膜活组织尿素酶试验和14C尿素呼气试验均证实Hp阳性的14例住院病人,在根除Hp前后取胃粘膜活检组织,HE染色显示组织结构和炎性细胞浸润情况,用免疫组织化学方法(SP法)显示COX-2表达情况.结果感染区域的胃窦上皮细胞和相应的壁细胞、单核细胞均可检测到COX-2的阳性表达,与根除Hp后比较,COX-2的表达明显减少而不完全消失(P＜0.005),COX-2阳性表达率与胃粘膜的急性炎症程度无关,而与慢性炎性细胞浸润密切相关(r=0.74 P＜0.05).结论COX-2的高表达可能是Hp相关性胃炎发生的重要机制.     

Improvement of gastrointestinal quality of life scores in cases of Helicobacter pylori-positive functional dyspepsia after successful eradication therapy

Functional dyspepsia (FD) refers to a broad range of chronic upper abdominal symptoms associated with food intake. A definitive treatment for FD has not yet been established, and the effect of Helicobacter pylori (H. pylori) eradication still remains under debate. The Gastrointestinal Symptom Rating Scale (GSRS) is a specific questionnaire for patients with gastrointestinal symptoms. The present study examined the quality of life (QOL) of patients with H. pylori-positive FD following H. pylori eradication. Methods: Sixty-eight patients with FD who gave informed consent were recruited for the study. H. pylori infection was diagnosed by the culture and histological methods, and the H. pylori eradication consisted of a 7-day course of lansoprazole, amoxicillin and clarithromycin. The overall success of the treatment was confirmed by a 13C urea breath test (UBT) conducted 3 months after the eradication. The GSRS questionnaire was administered to the patient just before the start of the eradication therapy and at 3 months after the therapy, just before the UBT was performed. Results: In successfully eradicated patients, the total GSRS and the abdominal pain score significantly decreased. In particular, the abdominal pain score and indigestion score were significantly decreased after successful eradication in patients with ulcer-like FD or dysmotility-like FD. Conversely, in patients in whom the eradication was unsuccessful, neither the total GSRS nor any of the individual symptom scores showed any significant change. Conclusion: Successful H. pylori eradication improved the QOL of patients with FD, in particular H. pylori-positive patients with ulcer-like FD or dysmotility-like FD.     

Effect of Helicobacter pylori eradication or of ranitidine plus metoclopramide on Helicobacter pylori-positive functional dyspepsia. A randomized,controlled follow-up study

BACKGROUND: A definitive treatment for functional dyspepsia (FD), and the role of Helicobacter pylori eradication on the course of this disease are controversial. AIM: To investigate the effect of a combination of acid-suppressing and prokinetic drugs or eradication therapy on the course of H. pylori-positive FD. METHOD: A total of 157 patients with endoscopically-proven H. pylori-positive FD and no response to 4 weeks of antacid therapy were randomly divided into 2 groups. 84 were placed on bismuth subnitrate plus metronidazole and amoxicillin (group A) and 73 received ranitidine and metoclopramide for 4 weeks (group B). The severity of symptoms (7 items) were assessed on a 6-point categorical scale. Group B patients who failed to respond to their medication underwent eradication therapy after 3 months. All patients were followed and assessed for 9 months after the end of therapy by the same clinicians who initiated the therapy. RESULTS: At the end of the medication period, symptom's score decreased significantly, and to the same extent. At 3-month follow-up moderate or complete response was achieved in 27.4% (group A) and 19.2% (group B) by intention-to-treat analysis. 34 patients of group B, not responding to treatment, underwent eradication therapy and followed as group A. Eradication of H. pylori was successful in 60 of 110 controlled patients (54%). After 9-month follow-up, complete or moderate response was observed in only 30% of 60 patients in whom H. pylori had been eradicated (intention-to-treat analysis), compared to 38% in 50 noneradicated cases (p > 0.05, 95% CI: 19-43 vs. 24-52). CONCLUSION: Eradication therapy with bismuth compound is effective as ranitidine plus metoclopramide in a subgroup of patients with FD not responding to antacid therapy. There is no difference in improvement between patients cured or not cured from H. pylori infection. This suggests that bismuth compounds were effective in FD when used in the eradication regimen. Combination therapy with acid-suppressing drugs plus prokinetic and bismuth seems to hold promise for FD.     

Basal and stimulated gastrin and pepsinogen levels after eradication of Helicobacter pylori: a 1-year follow-up study

AIM: A decrease in gastrin and pepsinogen (PG) levels 1 month after Helicobacter pylori eradication has been described repeatedly, but the long-term progression of such a decrease has been scarcely studied. We therefore studied the effect of H. pylori eradication on basal and stimulated gastrin and PG levels for 1 year. Initially, the usefulness of measuring these parameters for the noninvasive diagnosis of H. pylori eradication was validated. Furthermore, an assessment was made of the association between H. pylori reinfection and a re-increase in gastrin and PG values. Finally, an evaluation was made of the variables influencing gastrin and PG concentration, with particular attention to H. pylori infection and histological lesions of gastric mucosa. METHODS: Two-hundred and twenty-two patients with duodenal ulcer were studied prospectively. Exclusion criteria were the administration of antibiotics, H2 antagonists, omeprazole or bismuth prior to endoscopy. In all patients serum basal levels of gastrin, PGI, and PGII were measured before and 1 month after completing eradication therapy. In the successfully eradicated patients, gastrin, PGI, and PGII were also measured at 6 and 12 months. In 80 patients stimulated measurements of gastrin (after ingestion of two beef cubes) and PGI (after injection of pentagastrin) were also performed. H. pylori-negative patients after therapy underwent a urea breath test at 6 and 12 months, and patients who had stimulated gastrin and PG concentration measured had also an endoscopy performed at 6 months. RESULTS: H. pylori was eradicated in 73% of patients. A histological improvement was observed 1 month after completing H. pylori eradication therapy, both at gastric antrum and body (P < 0.001), while a further improvement at antrum was demonstrated at 6 months (P < 0.01). With regard to the different cut-off points for decreased basal and stimulated measurements for diagnosing H. pylori eradication, the best results were obtained, respectively, with PGII (sensitivity of 90% and specificity of 76%) and PGI 30 min after stimulation (sensitivity and specificity of 82%), with an area under the ROC curve of 0.87 in both cases. In the multiple regressions analysis H. pylori status correlated with gastrin, PGI and PGII after therapy (P < 0.001), while histological lesions correlated only with gastrin levels (P < 0.05). A decrease in basal and stimulated serum parameters was demonstrated immediately after eradication (Wilcoxon test, P < 0.001), and an additional decrease (at 6 months) was observed just in PGI (Friedman test, P < 0.01). However, gastrin and PGII values remained unchanged after the first month post-eradication. Seven patients were reinfected with H. pylori during follow-up. Quantitation of basal and stimulated gastrin and PGI levels was not reliable as a reinfection marker. Regarding basal PGII, the parallelism was strong at 6 months (re-increase in all four reinfected patients), although only in one out of three with reinfection at 1 year did PGII rise at that stage. CONCLUSIONS: (1) Measurement of gastrin and PG levels (especially basal PGII values) is a useful non-invasive method to confirm H. pylori eradication after therapy. (2) H. pylori eradication is associated with a significant decrease in basal and stimulated gastrin levels and in basal PGII levels that is detected immediately (1 month) after finishing treatment, and remains unchanged for 1 year. However, the decrease in basal and stimulated PGI levels occurs progressively for 6 months, although such levels remain also unchanged afterwards. (3) Measurement of gastrin and PGI concentrations has a limited usefulness in the diagnosis of H. pylori reinfections after successful eradication, although PGII determination could be more useful in this situation.     

根除幽门螺杆菌对功能性消化不良疗效的研究

背景:功能性消化不良(FD)的患病率始终居高不下,目前就幽门螺杆菌(H.pylori)阳性的FD患者是否需根除H.pylori尚存在争议。目的:探讨根除H.pylori对H.pylori阳性FD患者的疗效。方法:200例H.pylori阳性FD患者随机分为治疗组(100例.予以枸橼酸铋雷尼替丁400mg+阿莫西林1000mg+克拉霉素250mg,2次/d,疗程1周)和对照组(100例,予以铝碳酸镁1000mg,3次/d,疗程1周)。随访结束后评估H.pylori根除率和FD症状改善情况。结果:治疗组的H.pylori根除率分别为87.5%(PP分析)和84.0%(ITT分析),对照组H.pylori根除率为0%。H.pylori根除亚组FD症状改善的总有效率显著高于H.pylori未根除亚组和对照组(90.5%对41.7%和45.9%,P0.01)。结论:部分H.pylori阳性FD患者根除H.pylori后,其症状可长期缓解,因此对部分H.pylori阳性FD患者根除H.pylori是一种值得推广的有效治疗手段。