24小时胃内酸度监测评价多种抑酸剂静脉使用对十二指肠溃疡患者的抑酸效果

目的　对比各种常用抑酸剂对十二指肠溃疡出血患者胃酸的抑制效果。方法　运用随机、开放的方法分析５０ 例十二脂肠溃疡出血患者,分别使用奥美拉唑静脉滴注、法莫替丁静脉注射、雷尼替丁静脉注射、西咪替丁静脉注射或滴注。持续监测患者２４ 小时胃内ｐＨ 动态变化的情况、不同胃内ｐＨ值持续时间的百分率、２４ 小时平均胃内ｐＨ 和中位ｐＨ 值。结果　只有奥美拉唑８０ｍｇ／天组可达到胃内平均ｐＨ 和中位ｐＨ 均＞６ ,法莫替丁８０ｍｇ／天组可达到胃内平均ｐＨ 和中位ｐＨ 均＞ ４,其他治疗组均未达到ｐＨ＞ ４ 。２４ 小时胃内ｐＨ＜ ４ 、ｐＨ＜ ５、ｐＨ＜ ６ 时间所占百分比依次递增为：奥美拉唑８０ｍｇ／天组、法莫替丁８０ｍｇ／ 天组、雷尼替丁２００ｍｇ／天组、西咪替丁８００ｍｇ／天组。各Ｈ２ 受体拮抗剂组与奥美拉唑静脉滴注组比较,差异均有显著性。结论　静脉使用质子泵抑制剂的抑酸效果明显优于Ｈ２ 受体拮抗剂,尤其是奥美拉唑静脉滴注胃内ｐＨ 提高持续的时间较长。     

幽门螺杆菌根除治疗的随机对照研究

根除幽门螺杆菌（Ｈｐ）可促使消化性溃疡的愈合,显著地降低溃疡的复发率,并使慢性活动性胃炎的炎症消退［１］。目前,抗Ｈｐ治疗的方案大致上分为两类：一类以铋剂为基础的二联或三联疗法［２,３］,另一类以质子泵抑制剂为基础的二联或三联疗法［４］,但以Ｈ２受体拮抗剂为基础的二联或三联疗法,研究相对较少。本文将受体拮抗剂（西咪替丁,中美史克制药有限公司生产）为基础的短程三联疗法,同以质子泵抑制剂（洛赛克,阿斯特拉（无锡）制药有限公司生产）为基础的短程三联疗法及以铋剂（德诺,山西迈特兴华药品有限公司生产）为基…     

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。     

质子泵抑制剂及H_2受体拮抗剂联合抗生素治疗上消化道溃疡及清除Hp疗效比较

质子泵抑制剂及Ｈ＿２受体拮抗剂联合抗生素治疗上消化道溃疡及清除Ｈｐ疗效比较周忠杰本文应用兰索拉唑（达克普隆）、奥美拉唑、法莫替丁分别加用阿莫西林治疗上消化道溃疡合并Ｈｐ阳性病人共９０例。以比较溃疡愈合率与Ｈｐ清除率。现报道如下：材料和方法一、病例所选...     

溃疡病的愈合质量与复发

溃疡病的愈合质量与复发李益农目前指导溃疡病治疗的学说，以“无酸无溃疡”和“无幽门螺杆菌（Ｈ．ｐｙｌｏｒｉ，Ｈｐ）无溃疡”最受重视。依照前者用Ｈ＿２受体拮抗剂抑制胃酸分泌取得了显著的疗效。质子泵抑制剂奥美拉唑有更强的抑酸作用，应用于临床以来，更使难治性...     

老年人胃食管反流性疾病的研究现状

胃食管反流性疾病是胃、十二指肠的内容物自发性反流引起食管粘膜损伤，其发病与食道下端括约肌短暂和／或持久的松弛有关。其患病率在一定群体中随年龄而增加。临床表现多样且轻重不一。病史可提示诊断，但需做进一步检查。２４小时食道内ｐＨ检查是诊断胃食管反流性疾病的最敏感的试验。治疗包括调整生活方式，无效后可根据症状和食管炎的严重程度决定选用抗酸剂、Ｈ２受体阻滞剂、质子泵抑制剂等。严重的难治病例可外科手术。     

奥美拉唑西沙比利联合治疗反流性食管炎

１９９７年６月起，我们应用奥美拉唑西沙比利联合治疗反流性食管炎取得了显著疗效，现报告如下。一、对象和方法１．对象：经内镜检查证实反流性食管炎患者排除食管狭窄、肿瘤、胃十二指肠溃疡、炎性肠病、肠梗阻、胰腺炎及其他疾病；治疗前１周内未用过H２受体拮抗剂或质子泵抑制剂，均为采取抬高床头和改进食谱等抗反流措施无效者，符合以上条件患者共９７例，且同意定期来院复诊治疗和复查内镜。２．方法：９７例患者随机分为２组，治疗组４９例用奥美拉唑（无锡阿斯特拉制药有限公司产品）２０mg，每日１次，加西沙比利（西安杨森公司…     

法莫替丁单剂量肌肉注射抑制胃酸效应的观察

Ｈ２受体拮抗剂通过抑制胃酸、胃蛋白酶分泌和保护胃黏膜的作用，使其在治疗酸相关疾病中被广泛应用。法莫替丁（商品名：高舒达，沈阳山之内制药有限公司生产）是第三代Ｈ２受体拮抗剂，其针剂多用于治疗由胃黏膜病变和消化性溃疡引起的上消化道出血，其机制是通过提高胃...     

H1和H2组胺受体拮抗剂对中华硬蜱感染宿主的影响

中华硬蜱雌性成虫再次感染家兔后，叮咬局部组织中组胺含量较初次感染显著升高（Ｐ＜０．０１）。为了进一步证实组胺在抗蜱免疫中的作用，本文选用苯海拉明（Ｈ１组胺受体拮抗剂）、盐酸雷尼替丁（Ｈ２组胺受体拮抗剂）给再次感染组家兔灌胃，观察使用组胺拮抗剂对中华硬蜱吸血、生殖能力的影响。结果显示：单独给予Ｈ１或Ｈ２受体拮抗剂不改变家兔获得性抵抗力，但同时给予Ｈ１和Ｈ２受体拮抗剂则可明显降低家兔的抗蜱免疫反应，从而使中华硬蜱吸血量、吸血时间、产卵量等较再次叮咬组家兔有显著变化（Ｐ＜０．０１）。     

不同pH值对消化性溃疡并出血疗效的影响

目的：探讨不同ｐＨ值对消化性溃疡并出血疗效的影响，方法和结果：１临床和动物实验富血小板血浆（ＰＲＰ）中加入不同剂量的ＨＣｌ以改变其ｐＨ环境并测定其血小板聚集率。结果显示，随着ＨＣｌ量的增加，ｐＨ下降，血小板聚集率也降低，当ｐＨ＜６８时，血小板聚集率显著下降，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），结果显示，当ｐＨ≥６０时，ＧＭＢＴ明显减少，约５７６±１８６秒。２胃内ｐＨ值监测连续４８小时监测胃内ｐＨ值，结果显示，甲氰米胍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±１３，逐步降低甲氰米胍用量，其ｐＨ值亦逐步下降，至８００ｍｇ时，胃内ｐＨ值为１５，基本无作用。３临床疗效观察回顾性分析３０３例应用雷尼替丁与３２６例应用奥美拉唑的溃疡出血病人，前者手术率与死亡率为７２８％和１９９％，后者为４９１％和１８４％。结论：ｐＨ值与血小板聚集率及ＧＭＢＴ密切相关，药物治疗溃疡出血成功的关键在于有效提高胃内ｐＨ值。     

Effect of pantoprazole versus other proton pump inhibitors on 24-hour intragastric pH and basal acid output in Zollinger-Ellison syndrome

AIM: In this open prospective study, the efficacy of pantoprazole in reducing gastric acid secretion in Zollinger-Ellison syndrome patients was compared to that obtained previously with other proton pump inhibitors.METHODS: Eleven male patients previously treated with omeprazole (n=7, mean dosage: 63 mg/day; range: 20-100 mg/day) or lansoprazole (n=4, mean dosage: 75 mg/day; range: 30-120 mg/day) were included. These patients underwent a 24-hour intragastric pH-metry, measurement of basal acid output and of serum gastrin first while receiving their usual therapy and second after 7 to 10 days of pantoprazole treatment at a mean dosage of 116 mg/day (range: 40-200 mg/day). Basal acid output was evaluated after each intragastric pH-metry, one hour before the next intake of proton pump inhibitor and a serum gastrin curve was determined according to 9 fixed time points.RESULTS: One patient dropped out before the second intragastric pH-metry due to an adverse event (varicella) unrelated to pantoprazole and was reinvestigated thereafter. The median 24-h intragastric pH with pantoprazole was not significantly different than that with the other proton pump inhibitors (5.3 versus 4.6, respectively; P=0.90). Neither the median basal acid output values nor the median serum gastrin levels were significantly different between pantoprazole and the other proton pump inhibitors.CONCLUSION: In these patients with the Zollinger-Ellison syndrome, pantoprazole was well tolerated and equally effective to the other proton pump inhibitors in terms of antisecretory potency.     

The Value of Ambulatory 24 hr Esophageal pH Monitoring in Clinical Practice in Patients Who Were Referred with Persistent Gastroesophageal Reflux Disease (GERD)-Related Symptoms While on Standard Dose Anti-Reflux Medications

To determine the value of pH testing in clinical practice in gastroesophageal reflux disease patients who failed anti-reflux treatment. Patients resistant to standard dose proton pump inhibitor or an H₂-blocker underwent pH testing. Randomly selected patients from the proton pump inhibitor failure group underwent the modified acid perfusion test as compared to patients with non-erosive reflux disease. In the proton pump inhibitor failure group (n = 70), 63.8% had a normal pH test as compared to 29% in the H₂-blocker group (n = 31) (P = 0.007). Sensory intensity rating and acid perfusion sensitivity score were significantly higher in the non-erosive reflux disease control group than the proton pump inhibitor failure group (P < 0.05). Most patients who continued to be symptomatic on proton pump inhibitor once daily demonstrated a normal pH test and overall lack of increased chemoreceptor sensitivity to acid.     

Stronger inhibition of gastric acid secretion by lafutidine, a novel H2 receptor antagonist, than by the proton pump inhibitor lansoprazole

AIM： To compare the antisecretory activity and plasma drug concentrations of a single oral dose of 10 mg lafutidine, a novel H2 receptor antagonist, with those of the proton pump inhibitor lansoprazole （LPZ） 30 mg. METHODS： Ten volunteers without H pylori infection participated in this crossover study comparing lafutidine 10 mg with LPZ 30 mg. Intragastric pH was monitored for 6 h in all participants, and blood samples were collected from four randomly selected individuals after single-dose administration of each drug. RESULTS： The median intragastric pH was significantly higher in individuals who received lafutidine 10 mg than in those who received LPZ 30 mg 2, 3, 4, 5, and 6 h after administration. Maximal plasma drug concentration was reached more promptly with lafutidine 10 mg than with LPZ 30 mg. CONCLUSION： In H pylori-negative individuals, gastric acid secretion is more markedly inhibited by lafutidinethan by LPZ.     

Nocturnal acid breakthrough: pH, drugs and bugs

Nocturnal acid breakthrough (NAB) was defined by Peghini et al. in 1998 as the presence of at least 60 continuous minutes of intragastric pH < 4 during the overnight period (22:00-06:00 h) in patients taking a proton pump inhibitor (PPI) twice-daily before meals. NAB was shown to occur in more than 70% of patients on PPI therapy but can be decreased or eliminated by adding a histamine-2 receptor antagonist (H2RA) at bedtime. Helicobacter pylori status influences intragastric acid control on PPI therapy: H. pylori-positive patients having better gastric acid control compared with their H. pylori-negative counterparts. Recent data indicate that NAB might not occur in H. pylori-positive subjects on twice-daily PPI, suggesting there is no need for combined PPI twice-daily and H2RA therapy to control night-time gastric acid secretion in these individuals. The clinical importance of NAB has been debated ever since this concept was introduced. The importance of NAB in healthy subjects and asymptomatic, uncomplicated gastro-oesophageal reflux disease patients on PPI therapy may be low, but ignoring it in patients with poor oesophageal motility and Barrett's oesophagus may result in suboptimal treatment. Further studies are warranted to investigate whether leaving H. pylori to 'assist'acid suppression obtained by PPI twice-daily, adding bedtime H2RAs after successful H. pylori eradication or other approaches to eliminate NAB results in better clinical outcomes.     

Pharmacological and pharmacodynamic essentials of H(2)-receptor antagonists and proton pump inhibitors for the practising physician

The suppression of gastric acid secretion with anti-secretory agents has been the mainstay of medical treatment for patients with acid-related disorders. Although the majority of Helicobacter pylori -related peptic ulcers can be healed with antibiotics, ulcer healing and symptom control can be significantly improved when antibiotics are given with anti-secretory agents, especially with a proton pump inhibitor. There is a dynamic relationship between the suppression of intragastric acidity and the healing of peptic ulcer and erosive oesophagitis and control of acid-related symptoms. The suppression of gastric acid secretion achieved with H(2)-receptor antagonists has, however, proved to be suboptimal for effectively controlling acid-related disorders, especially for healing erosive oesophagitis and for the relief of reflux symptoms. H(2)-receptor antagonists are also not effective in inhibiting meal-stimulated acid secretion, which is required for managing patients with erosive oesophagitis. Furthermore, the rapid development of tolerance to H(2)-receptor antagonists and the rebound acid hypersecretion after the withdrawal of an H(2)-receptor antagonist further limit their clinical use. Although low-dose H(2)-receptor antagonists are currently available as over-the-counter medications for self-controlling acid-related symptoms, their pharmacology and pharmacodynamics have not been well studied, especially in the self-medicating population. Proton pump inhibitors have been proved to be very effective for suppressing intragastric acidity to all known stimuli, although variations exist in the rapidity of onset of action and the potency of acid inhibition after oral administration at the approved therapeutic doses, which may have important clinical implications for the treatment of gastro-oesophageal reflux disease and perhaps for eradicating H. pylori infection when a proton pump inhibitor is given with antibiotics. Once-daily dosing in the morning is more effective than dosing in the evening for all proton pump inhibitors with respect to the suppression of intragastric acidity and daytime gastric acid secretion in particular, which may result from a better bio-availability being achieved with the morning dose. When higher doses are needed, these drugs must be given twice daily to achieve the optimal suppression of 24 hour intragastric acidity. Preliminary results have shown that esomeprazole, the optical isomer of omeprazole, given at 40 mg, is significantly more effective than omeprazole 40 mg, lansoprazole 30 mg or pantoprazole 40 mg for suppressing gastric acid secretion. However, more studies in different patient populations are needed to compare esomeprazole with the existing proton pump inhibitors with regard to their efficacy, cost-effectiveness and long-term safety for the management of acid-related disorders.     

Effects of NC-1300-B,A new benzimidazole derivative,on hog gastric H+, K+-ATPase,gastric acid secretion and HCl-ethanol-induced gastric lesions in rats

This study was designed to determine the effect of a newly synthesized benzimidazole derivative NC-1300-B on H⁺,K⁺ -ATPase (proton pump) in the hog gastric mucosa and on the basal gastric acid secretion and necrotizing agent-induced gastric lesions in rats. NC-1300-B inhibited the proton pump in a concentration-dependent manner and concentrations which inhibited the enzyme activity by 50% were 4.4×10^–6 M at pH 6.0 and 3.1 ×10^–5 M at pH 7.4. NC-1300-B administered orally or intraperitoneally 0.5 hr before ligating the pylorus inhibited the gastric acid secretion in a dose-dependent manner. The ED₅₀ values (doses which inhibit acid output or lesion formation by 50%) for acid secretion were 11.5 and 11.0 mg/kg with oral and intraperitoneal administration, respectively. The antisecretory effect in a dose of 100 mg/kg persisted for up to 72 hr. NC-1300-B administered orally or intraperitoneally 0.5 hr before HCl-ethanol administration protected against damage of the gastric mucosa in a dose-dependent manner. The ED₅₀ values for lesion formation were 13.3 and 23.0 mg/kg with oral and intraperitoneal administration, respectively. This protection with an oral dose of 100 mg/kg persisted for up to 72 hr. While pretreatment with 5 mg/kg of indomethacin given subcutaneously did not appreciably reverse the NC-1300-B protection, the pretreatment with 10 mg/kg of N-ethylmaleimide given subcutaneously potently reversed the NC-1300-B protection. NC-1300-B administered intragastrically at 30 mg/kg significantly inhibited the amplitude of gastric contraction for 50 min after intragastric administration. These effects of NC-1300-B on gastric secretion and lesion formation are much the same as those of the established proton pump inhibitor omeprazole, except for the short duration of the action of omeprazole (<24 hr).     

The effect of H2-receptor antagonist and proton pump inhibitor on microbial proliferation in the stomach

BACKGROUND/AIMS: Intra-gastric bacterial proliferation is frequent in patients with hypochlohydria. However, status of gastric bacterial infection in patients receiving proton pump inhibitor or H2-receptor antagonist remains controversial. The purpose of this study was to investigate the microbial condition of the stomach in patients who received H2-receptor antagonist or proton pump inhibitor. METHODOLOGY: Between November 2000 and January 2002, 102 patients were enrolled in this study. Of these, 52 did not receive any treatment (group I), 26 received H2-receptor antagonist (group II), and 24 received proton pump inhibitor (group III). Ten mL of gastric juice were aspirated for culture during endoscopic examination. The aerobic and anaerobic bacterial and fungal cultures were performed immediately. A glass pH meter measured the pH of the gastric juice. RESULTS: The intra-gastric pH was 2.91+/-2.06 (mean +/- SD), 4.12+/-2.83, and 5.11+/-2.47 for groups I, II, and III, respectively (p=0.001 between groups I and III, p>0.05 between groups I and II, and groups II and III). The positive bacterial culture rates were 66.7% (16/24) in group III, 46.2% (12/26) in group II, and 28.8% (15/52) in group I (p=0.007 between groups III and I,p>0.05 between groups I and II, and groups II and III). The positive candidal culture rates were 12.5% (3/24) in group III, 11.5% (3/26) in group II, and 17.3% (9/52) in group I (p>0.05). CONCLUSIONS: Patients who received proton pump inhibitor had more acid suppression and intra-gastric bacterial infection than those of the control group. The intra-gastric candidal infection was not related to intra-gastric pH or anti-secretory medication in this study.     

The effect of rabeprazole alone or in combination with H2 receptor blocker on intragastric pH: a pilot study.

BACKGROUND/AIMS: Proton pump inhibitors have been widely used in recent years. However, there are studies suggesting that proton pump inhibitors may not control the gastric acidity effectively during the night, especially in gastroesophageal reflux disease. It has therefore been suggested that H2 receptor blockers should be added to the therapy. The aim of our study was to evaluate the effects of proton pump inhibitors alone or in combination with H2 receptor blockers on gastric acidity with 24-hour gastric pH monitoring. METHODS: Esophagogastroscopy and 24-hour gastric pH monitoring were performed on 10 patients with dyspeptic symptoms. No patient had antacidity. All patients had erosive antral gastritis. Patients were randomized to two groups as either proton pump inhibitor therapy group (rabeprazole 20 mg/day, p.o.) or proton pump inhibitor + H2 receptor blocker therapy group (rabeprazole 20 mg/day, p.o. + famotidine 40 mg/day, p.o). After one month of treatment, 24-hour gastric pH monitoring was re-performed. RESULTS: Seven female and three male patients were enrolled into the study. The mean age was 51.1+/-11.56 years. All patients had antral erosive gastritis. Gastric pH was measured as less than 4 in 81.4% of the 24-hour period prior to rabeprazole treatment. With rabeprazole treatment this ratio decreased to 27.6% (p<0.05). These ratios were 86.3% and 4.55%, respectively, in the group that received combination therapy (p<0.05). CONCLUSIONS: Combination therapy with H2 receptor blockers and proton pump inhibitors seemed to control intra-gastric pH better than proton pump inhibitors alone. Use of H2 receptor blockers and proton pump inhibitors in combination to control intra-gastric pH is more beneficial.     

Low yield of endoscopy in patients with persistent dyspepsia taking proton pump inhibitors

BACKGROUND: Options for the evaluation of dyspepsia include a Helicobacter pylori test-and-treat strategy, empiric acid suppression, and initial endoscopy. The aim of this study was to determine the yield of endoscopy in patients in whom empiric therapy is unsuccessful compared with patients who received no empiric therapy and to identify factors associated with endoscopic findings. METHODS: A total of 100 patients with dyspepsia referred for endoscopy completed a questionnaire that included a query concerning response to therapy. EGD findings were compared in patients taking an H2-receptor antagonist, patients taking a proton pump inhibitor, and those not receiving empiric therapy. RESULTS: There were fewer endoscopic findings in patients being treated with a proton pump inhibitor compared with those taking an H2-receptor antagonist or those not receiving therapy (p < 0.01). Fewer proton pump inhibitor recipients had esophagitis or ulcer compared with patients in the no therapy group. Lack of symptom relief (<20%) by acid suppression was highly associated with a normal endoscopy (17/17). CONCLUSIONS: Patients with persistent dyspepsia being treated with a proton pump inhibitor have fewer endoscopic abnormalities compared with patients with dyspepsia taking an H2-receptor antagonist and those receiving no therapy. For patients with partial symptom relief, proton pump inhibitor therapy may mask endoscopic findings, particularly esophagitis. Interruption of proton pump inhibitors before endoscopy may increase diagnostic yield. Endoscopy is unlikely to yield a positive finding in patients who experience no symptom relief while taking a proton pump inhibitor or H2-receptor antagonist.