质子泵抑制剂与H2受体拮抗剂治疗十二指肠球部溃疡抑酸效果的比较

应用各种抗酸剂治疗酸相关性疾病已取得肯定的临床疗效．为比较质于泵抑制剂与H：受体格抗剂抑制胃酸的动态变化，我们使用非卧床24小时pH记录仪，对十二指肠没疡（DU）患者分别给予具美拉哩、兰索拉华、雷尼管丁与西咪替了治疗，并观察服药前后的同内pH变化，现报告如下．对象     

减少胃酸的治疗和难辨梭状杆菌感染风险增高有关

据Medscape．com 12月21日报道（原载JAMA 2005；294：2989-2995），服用胃酸抑制剂的患发生难辨梭状杆菌相关疾病（CDAD）的风险比普通人群升高2-3倍。加拿大魁北克蒙特利尔麦吉尔大学重症医学科的Sandra Dial，MD，MSc称，这些风险与质子泵抑制剂和组胺-2受体拮抗剂（H2受体拮抗剂）都有关系，前使这种风险增加3倍，后使之增加2倍。社区中使用这两种药物的患和没有用这些药的患相比，都更可能被全科医生诊断为CDAD。他们对CDAD病例和对照人群进行了一项多因素分析。     

胃镜检查前抑酸疗法对胃癌诊断影响的回顾性研究

目的通过对临床病例的分析,研究抑酸疗法对胃癌首次胃镜检查诊断的干扰程度及相应对策。方法实验对象均为经胃镜与病理检查最终证实的胃癌患者,包括胃体腺癌与胃窦腺癌。根据首次电子胃镜检查前抑酸剂的使用情况,分为H2受体阻滞剂(H2RA)治疗组、质子泵抑制剂(PPI)治疗组及未经抑酸治疗的对照组,通过组间比较以探讨抑酸剂的使用与胃癌漏诊率之间的关系。按日本Borrmann分型标准,对各组胃癌的分型构成及漏诊病例的分型构成进行分析,试图找出漏诊的规律。结果H2受体阻滞剂治疗组的漏诊率:胃体腺癌为6.66%(5/75),胃窦腺癌为10.7%(9/84)。质子泵抑制剂治疗组相应的漏诊率为9.37%(6/64)和12.7%(13/102)。而未经抑酸治疗的对照组的相应漏诊率为1.36%(1/73)和2.63%(2/76)。胃体腺癌及胃窦腺癌经过抑酸疗法后,其首次内镜检查漏诊率均高于未经抑酸治疗的对照组,组间比较差异有显著性。通过Borrmann分型发现,漏诊患者均为早期胃癌Ⅱb型、Ⅱc型及进展期胃癌Ⅱ型、Ⅲ型。结论抑酸疗法作为消化系统疾病常用的治疗手段,在胃镜检查前的不恰当应用,对某些胃癌的及时诊断产生负面影响,致使部分患者漏诊,甚至延误治疗。     

新型抑酸制剂治疗研究进展

随着人们生活节奏的加快、生活方式的改变以及饮食结构的调整．酸相关性疾病的发病率在全球呈逐年上升趋势，在酸相关性疾病的治疗中，目前应用的药物主要有H2受体拮抗剂和质子泵抑制剂（PPIs）等．而现在应用最为广泛的是PPIs。目前使用的PPIs存在的局限性主要有：①药物达到作用最强时间较长。常用的PPIs在治疗剂量下需要3～5天才能达到最大抑酸作用．有屿患者酸抑制作用不完全，还需使用抗酸剂和H2受体拮抗剂。②夜间酸突破。夜间酸突破在许多使用PPIs治疗的患者中十分常见，     

抑酸药对消化性溃疡并出血的疗效

目的探讨抑酸药H2受体拮抗剂与质子泵抑制剂（PPI）对消化性溃疡并出血的疗效。方法（1）用不同pH值的缓冲液冲洗大白鼠胃内活检伤口，测定其胃粘膜出血时间（GMBT）；（2）连续48小时监测胃内pH值；（3）回颀性分析303例应用雷尼替了与326例应用奥美拉唑的消化性溃疡并出血病人手术率与死亡率。结果（1）体外动物实验结果显示当pH≥6时，其GMBT明显减少，约57．6±18．6秒。（2）胃内pH值监测结果，西咪替丁1600mg静脉注射与奥美拉唑40mg静脉注射，胃内pH值相仿，分别为5．4±1．3和5．8土1．3，逐步降低西咪替丁用量，其pH值亦逐步下降，至常规剂量800mg时，胃内pH值为1．5，基本无作用。（3）临床疗效观察，303例雷尼替丁与326例奥美拉唑组的消化性溃疡并出血者手术率与死亡率，前者分别为7．28％和1．99％，后者分别为4．91％和1．84％。结论质子泵抑制剂奥美拉唑静脉注射的抑酸效果，适用于消化性溃疡并出血病人，其疗效优于H2受体拮抗剂。     

静脉注射抑酸药物对胃内PH控制的对照研究

本文采用24小时胃内PH监测仪对确诊十二指肠溃疡的病人进行前瞻交叉对照研究,观察胃壁细胞H_2受体拮抗剂泰胃美(Tagamet,Cimetidine)和质子泵抑制剂洛赛克(Losec,Omeprazole)的抑酸效果。结果显示泰胃美1600mg静注抑酸时间为12.2±2.2小时,此期胃内PH为5.6±1.2;而洛赛克40mg分别为13.2±2.6小时和PH5.6±1.4。两药均有明显抑酸作用,使用上述剂量效果无显著性差异(P>0.05)。     

法莫替丁可抑制夜间胃酸分泌和酸突破

夜间酸突破 (NAB)指服用质子泵抑制剂 (PPI)后夜间pH <4持续 1h以上。国外有研究表明 ,正常人和胃食管反流病患者每日口服 2次PPI不足以完全控制夜间胃酸分泌 ,其中 3/4可发生NAB ,而H2 受体拮抗剂可有效地抑制NAB[1,2 ] 。为研究十二指肠溃疡 (DU)患者服用法莫替丁后NAB情况 ,我们比较服用奥美拉唑后 ,睡前加服法莫替丁和加服奥美拉唑对DU夜间胃酸分泌和NAB的影响。一、对象和方法1.研究对象 :2 0例患者 ,男 11例 ,女 9例 ,年龄 19～ 5 3岁 ,平均 38.6岁。胃镜诊断为活动性DU 1～ 2个 ,溃疡直径>3mm ,<2 0mm。近 4周未用抗溃疡…     

壁细胞对H2受体拮抗剂和质子泵抑制剂耐受性研究

目的研究鼠胃黏膜壁细胞对H2受体拮抗剂和质子泵抑制剂的耐受性(脱敏)。方法用酶消化法分离壁细胞后,分为西咪替丁、法莫替丁、奥美拉唑和潘托拉唑4组,每组均包括三部分实验。其一是给予药物100mg/L干预细胞不同时间;其二是给予药物100mg/L干预细胞不同时间,然后洗涤细胞,再给予100mg/L作用1h;其三是给予不同浓度药物干预细胞2h后,洗涤细胞,再加入100mg/L作用2h。最后测定各组壁细胞H K ATP酶活力。结果H2受体拮抗剂和质子泵抑制剂均对H K ATP酶具有抑制作用;在不同干预时间下,西咪替丁1、2h组酶活性均显著高于对照组(4.96±0.247,4.63±0.054vs4.18±0.324),法莫替丁、2、4h组酶活性均显著高于对照组(3.71±0.017,5.11±0.053,4.01±0.029vs0.63±0.019);在不同干预浓度下,西咪替丁、法莫替丁0、100、1000mg/L组酶活性均显著高于对照组(分别为4.56±0.159,4.62±0.275,4.05±0.026vs3.69±0.145和3.42±0.391,4.32±0.315,4.48±0.120vs1.92±0.144);质子泵抑制剂各组无显著性差别。结论H2受体拮抗剂能够诱导壁细胞H2受体出现脱敏,质子泵抑制剂未出现耐受现象。     

Effect of Chewing Gum on Gastric Acid Secretion

In 15 patients, of whom 10 had a duodenal ulcer, aspirations were made of the gastric contents for one hour before and one hour after they had been chewing gum for 30 minutes. The volume and acidity was measured in each 15-min sample and the acid output was calculated. Differences between the secretion in the 3 periods were tested for significance with the Wilcoxon rank sum test for paired differences. During the chewing period the volume of gastric contents increased from 23 to 39 ml/15 min, p < 0.01, the acidity decreased from 29 to 25 meq/l, p < 0.05, and the acid output increased insignificantly (from 0.75 to 1.23 meq/15 min). The bicarbonate concentration of the saliva during chewing was on average 9 meq/l. The salivary flow during chewing was calculated to 13 ml/15 min. When the neutralization of gastric acid with salivary bicarbonate was taken into account, a significant increase in acid secretion was found during chewing. This stimulation continued during the one-hour period after chewing, causing a secretion rate of 29 ml/15 min, with an acidity of 42 meq/l and an acid output of 1.32 meq/15 min. It is concluded that although chewing gum causes a stimulation of the gastric acid secretion, this increase is so small that it does not justify an advice against the use of chewing gum in patients with duodenal ulcer or x-ray negative dyspepsia.     

Effect of Nicotinic Acid on Gastric Secretion of Acid in Human Subjects and in Dogs

The effect of nicotinic acid on gastric secretion was studied in 19 fasting patients who had coronary heart disease and hyperlipoproteinemia. Among 10 patients with basal secretion of acid, 9 had increased acid output following oral administration of 0.5 g of nicotinic acid — the increase ranged from 13 to 232 per cent. Also in Pavlov pouch dogs, i.v. infusion of nicotinic acid gave rise to a significant increase in gastric acid output. The mechanism behind gastric stimulatory action of nicotinic acid is unknown.     

血浆降钙素基因相关肽、内皮素及胃酸在颅脑手术患者中的变化观察

目的 观察颅脑手术患者胃酸、内皮素(ET)及降钙素基因相关肽(CGRP)在应激性胃黏膜损伤中的变化规律,探讨在应激状态下胃黏膜损害的可能机制.方法 监测15例颅脑手术患者术前4 h至术后72 h的胃酸变化,并应用放射免疫法分点测定术前及术后ET与CGRP含量.结果 15例颅脑手术病人手术结束时胃内pH均明显升高(P<0...     

Sensitivity of Gastric Acid Secretion in Patients with Chronic Renal Failure

By means of a dose-response secretion test the sensitivity of gastric acid secretion was investigated in 85 patients with chronic renal failure and in 85 age- and sex-matched controls. The renal patients were also gastroscoped, with biopsy specimens taken from the gastric body. The examinations were repeated on 18 patients undergoing regular dialysis and 8 patients after successful transplantation. The acid secretion sensitivity of the stomach among the non-dialyzed patients was decreased when compared with the controls (p < 0.01) but tended to normalize during the intermittent dialysis treatment (p < 0.05) and particularly after transplantation (p < 0.01). The low secretion responses were independent of gastric body histology and were also seen in patients with normal body mucosa. The maximum theoretic acid output did not differ significantly from that of the controls. It is concluded that there is an inhibition of gastric acid secretion in chronic renal failure. This inhibition depends on the decreased sensitivity to stimulation and is diminished by treatment of renal failure by dialysis or transplantation.     

Effect of Serotonin on Bethanechol-Stimulated Gastric Acid Secretion and Gastric Antral Motility in Dogs

The purpose of the present study was to evaluate the effect of serotonin on bethanechol-stimulated gastric acid secretion and antral motility in conscious dogs with gastric fistula. Bethanechol stimulated the acid secretion dose-dependently and maintained the frequency and strength of the antral contractions at a high level. Serotonin inhibited the acid secretion dose-dependently, whereas the antral motility was stimulated. The acid inhibition was blocked by propranolol, and dose-response analysis showed inhibition of a non-competitive type. This study thereby shows that serotonin inhibits bethanechol-stimulated gastric acid secretion similarly to salmefamol (β₂-adrenergic agonist)-that is, dose-dependently and non-competitively. Serotonin has been proposed to be a mediator of the β-adrenergic influence on gastric function in vivo, but the counteracting effect of propranolol and the stimulatory effect of serotonin on motility contradict this hypothesis.     

Gastric Acid Secretion,Oesophageal Acid Reflux,and Oesophagitis in Patients with Symptomatic Gastro-Oesophageal Reflux

Forty-seven patients with symptomatic gastro-oesophageal reflux were evaluated on the basis of symptoms, endoscopy, extended 18-h pH-monitoring of the lower oesophagus, and the pentagastrin test. The patients' acid secretion capacity did not correlate with symptoms or duration of acid reflux, but men with endoscopic oesophagitis had significantly higher BAO and MAO values than men without oesophagitis. In women this correlation was not found. The higher MAO values (in meq/h) in men than in women were abolished when the MAO was expressed as meq/h/FFB (fat-free body mass). The MAO values in all the men or all the women were not higher than the values obtained from a normal Finnish population. Both men and women with endoscopic oesophagitis had a significantly longer duration of oesophageal acid reflux than men and women with normal mucosa.     

幽门螺杆菌感染对功能性消化不良患者胃酸分泌的影响

目的:探讨幽门螺杆菌(Hp)感染对功能性消化不良(FD)患者胃酸和胃泌素分泌的影响。方法:54例符合FD诊断标准的患者中,Hp阳性23例,Hp阴性31例,所有患者都进行空腹血清胃泌素、基础胃酸排出量(BAO)、五肽胃泌素刺激后的最大胃酸排出量(MAO)和高峰胃酸排出量(PAO)的测定。对照组为Hp阳性的十二指肠溃疡病(DU)患者55例。结果:FD患者中,Hp阳性者与Hp阴性者比较,空腹血清胃泌素(103.1±33.7pg/ml vs 113.3±34.1pg/ml)和BAO(5.21±3.86mmol/h vs 4.80±6.08mmol/h)无明显差异(P>0.05);而Hp阳性者的MAO和PAO分别为16.3±9.30mmol/h和23.6±14.2mmol/h,与Hp阴性者(分别为10.1±8.88mmol/h和14.2±11.3mmol/h)比较,差异有显著性(P<0.05)。Hp阳性的FD患者,其BAO、MAO、PAO及空腹血清胃泌素与Hp阳性的十二指肠溃疡病患者(后者分别为10.4±0.81mmol/h、24.2±1.08mmol/h、31.2±13.1mmol/h和148.5±13.1pg/ml)比较,差异有显著性(P<0.05)。结论:Hp阳性的FD患者,其胃粘膜壁细胞对五肽胃泌素刺激的敏感性增加,刺激后胃酸分泌增高,但增高的程度低于Hp阳性的十二指肠溃疡病患者,提示Hp感染在FD患者的胃酸分泌中可能起一定作用。     

Effect of Somatostatin on Pentagastrin-Stimulated Gastric Acid Secretion and Gastric Antral Motility in Dogs with Gastric Fistula

The purpose of the present study was to evaluate the effect of somatostatin on gastric acid secretion and gastric antral motility in conscious dogs with gastric fistula. Infusion of pentagastrin induced motility with a digestive pattern. Somatostatin inhibited dose-dependently the stimulated acid secretion, whereas the effect on antral motility was more complex, acting especially on the amplitude of the contractions. The effects of somatostatin were not altered by using α-and β-adrenergic, dopaminergic, and serotonergic blocking drugs. The dose-response kinetics with seven doses of pentagastrin with and without somatostatin showed inhibition of a competitive type for gastric acid secretion and of a non-competitive type for antral motility with regard to amplitude.     

Gastric juice for the diagnosis of H pylori infection in patients on proton pump inhibitors

AIM： To determine the efficacy of gastric juice polymerase chain reaction （PCR） for the detection of H pylori infection in comparison with histology and gastric antral biopsy PCR in patients on a proton pump inhibitor （PPI）. METHODS： Eighty-five consecutive patients with dyspeptic symptoms were enrolled. Gastric biopsies for histology, PCR and gastric juice were collected at endoscopy for PCR of the H pylori urease C gene （ure C）. Sensitivity, specificity, positive predictive value （PPV）, negative predictive value （NPV）, accuracy, positive and negative likelihood ratio for PCR of gastric juice for the H pylori ure C gene was compared to histology and gastric antral biopsy H pylori ure C PCR in patients with and without PPI. RESULTS： Gastric juice PCR was positive in 66 （78%） patients. Histology showed H pylori associated gastritis in 57 （67%）. Gastric biopsy PCR was positive in 72 （85%）. In patients not taking PPI, the sensitivity, specificity, PPV, NPV, accuracy and positive and negative likelihood ratio for gastric juice PCR were 89%, 72%, 91%, 67%, 90%, 85%, 3.1 and 0.1 respectively. In patients on PPI these values were 86%, 100%%, 100%, 29%, 86%, 9.5 and 1.4, respectively. CONCLUSION： Gastric juice PCR for the diagnosis of H pylori infection has increased sensitivity compared to histology with PPI. The use of gastric juice PCR is recommended to confirm H pylori status in patients taking PPIs.     

Inhibition of Pentagastrin-Stimulated Gastric Acid Secretion by Pantoprazole and Omeprazole in Healthy Adults

Our objective was to compare the onset and duration of a single dose of pantoprazole or omeprazole on maximally stimulated gastric acid secretion. This double-blind, randomized, placebo-controlled study involved 36 healthy adults and utilized continuous pentagastrin infusion to stimulate acid secretion after administration of pantoprazole, 40 mg, omeprazole, 20 mg, or placebo. Gastric aspirates were collected over 24 hr and analyzed for volume, pH, and hydrogen ion concentration, and gastric acid outputs (GAO) were calculated. Comparison between GAO and intragastric pH was performed. Pantoprazole resulted in significantly greater inhibition of GAO than omeprazole. Mean cumulative 24-hr GAO was 164 ± 130 mEq for pantoprazole versus 283 ± 159 mEq for omeprazole (P = 0.031). Pantoprazole patients reached and maintained GAO levels below the 10-mEq/hr threshold at 5.7 hr, whereas omeprazole patients never reached this threshold. We conclude that pantoprazole significantly suppressed gastric acid secretion compared to omeprazole. Comparisons between pH and GAO showed that GAO was a more appropriate measure of gastric acid secretion than intragastric pH. This work received financial support from Wyeth Pharmaceuticals.