部份中文雷贝拉唑钠处方资料（仅供参考）
药品英文名
Rabeprazole
药品别名
拉贝拉唑钠、雷贝拉唑钠、RabeprazoleSodium、Na Rabeprazol、Pariet
药物剂型
1.胶囊：20mg；
2.肠溶片：10mg，20mg。
药理作用
本药为苯并咪唑类质子泵抑制药，其抑制H ，K -ATP酶作用具有部分可逆性。本药较奥美拉唑抑制H ，K -ATP酶和胃酸分泌的效果更明显。
1.胃酸分泌抑制作用：家兔胃腺体外研究表明，本药可抑制二丁酰环磷酸腺苷(cAMP)引起的胃酸分泌，对留置胃瘘管的犬由组胺、五肽胃泌素引起的胃酸分泌，大鼠的基础胃酸分泌及组胺引起的胃酸分泌均有强大的抑制作用；相对于其他质子泵抑制药(如奥美拉唑)而言，本药能更快、更彻底地与H ，K -ATP酶分离，从而可更快实现胃酸分泌抑制作用的恢复。
2.抗溃疡作用：对各种大鼠实验性溃疡及实验性胃黏膜病变(寒冷束缚应激性反应、水浸束缚应激反应、幽门结扎、巯乙胺及盐酸-乙醇刺激)，本药均显示很强的抗溃疡及改善胃黏膜病变的作用。
3.抗幽门螺旋杆菌作用：体外实验显示本药比奥美拉唑和兰索拉唑有更强的抗幽门螺旋杆菌活性，其可在几个位点直接攻击幽门螺杆菌，并可非竞争性、不可逆地抑制幽门螺旋杆菌的脲酶。
药动学
单次口服本药20mg，最大血浆浓度(Cmax)为每升0.406mg，药峰时间(tmax)为3.1h，血浆半衰(t1/2)为1.02h，清除率(CL)为每天0.504L/kg；每天口服本药40mg连续7天，Cmax为0.418mg/L，tmax为3.8h。t1/2为1.49h，CL为每天0.648L/kg。其中Cmax具有剂量依耐性，但tmax、t1/2和CL不依赖于剂量。本药主要经肝脏代谢，血浆蛋白结合率为94.8%～97.5%。餐后虽然Cmax无改变，但tmax被明显延迟(1.7h)。48h内尿中排出总量以雷贝拉唑钠硫醚羧酸及葡萄糖醛酸化物计算占给药量的34%。
适应证
用于胃溃疡、十二指肠溃疡、吻合口溃疡、反流性食管炎、胃泌素瘤(卓-艾综合征)。
禁忌证
1.有药物过敏史者。
2.肝硬化患者。
3.高龄患者。
4.孕妇。
注意事项
1.应在排除恶性肿瘤前提下给药。
2.根据病情将用量控制在治疗所需的最低限度内。
3.不宜于维持治疗。
不良反应
1.血液系统：可引起红细胞、淋巴细胞减少、白细胞减少或增多、嗜酸粒细胞、中性粒细胞增多。如出现此类异常状况时，应停药并采取适当措施。
2.消化系统：可引起便秘、腹泻、腹胀感、恶心、下腹部痛、消化不良及肝脏酶学指标(如氨基转移酶、碱性磷酸酶等)升高。
3.心血管系统：可有心悸。
4.精神神经系统：可有头痛、眩晕、困倦、四肢乏力、感觉迟钝、握力低下、口齿不清、步态蹒跚等。国外有导致既往有肝性脑病的肝硬化患者精神错乱、识辨力丧失和嗜睡的个案报道。
5.致癌性：在给大鼠按5mg/kg以上用量，连续2年口服给药的毒性试验中，观察到雌鼠中胃部发生类癌病变。
6.其他：可有皮疹、荨麻疹、瘙痒感、水肿、总胆固醇及尿素氮升高、蛋白尿等。如出现此类异常状况时，应停药并采取适当措施。
用法用量
口服给药：胶囊每次20mg，每天1～2次，单用或合用抗生素。肠溶剂每次10mg，每天1次，根据病情(如病情严重及属复发性、顽固性病例)也可增加到每次20mg，每天1次。一般情况下，胃溃疡、吻合口溃疡、反流性食管炎的疗程以8周为限，十二指肠溃疡的疗程以6周为限。
药物相应作用
1.由于本药可升高胃内pH值，与地高辛合用时，可促进地高辛的吸收并导致其血中浓度升高，故合用时应监测地高辛的浓度。
2.据报道，本药与含氢氧化铝、氢氧化镁的制酸剂同时服用，或在服制酸剂1h后再用时，本药的平均血浆浓度和药时曲线下面积分别下降8%和6%。
3.酮康唑不影响本药代谢，但本药可降低酮康唑的Cmax故在应用酮康唑时，应停用本药。
4.对健康志愿者的研究中，尚未发现本药和地西泮、茶碱、华法林、苯妥英钠之间的相互作用。

临床研究
本品治疗胃和十二指肠溃疡，反流性食管炎和HP(与抗菌药联用)疗效确切，与其他PPI药相比，具有耐受性好、起效快，与其他药物相互作用少，老年及肾功能不良者也可应用等特点。

本品英国上市（ Eisai Ltd ）产品，包装规格
10mg：14、28、56、98、112或120片
20mg：14、28、56、98、112或120片
Pariet 10mg & 20mg
1. Name of the medicinal product
PARIET ® 10mg gastro-resistant tablet
PARIET ® 20mg gastro-resistant tablet
2. Qualitative and quantitative composition
10mg rabeprazole sodium, equivalent to 9.42mg rabeprazole
20mg rabeprazole sodium, equivalent to 18.85mg rabeprazole
For a full list of excipients, see section 6.1.
3. Pharmaceutical form
Gastro-resistant tablet.
10mg: Pink, film coated biconvex tablet with 'E 241' printed on one side.
20mg: Yellow, film coated biconvex tablet with 'E 243' printed on one side.
4. Clinical particulars
4.1 Therapeutic indications
PARIET tablets are indicated for the treatment of:
• Active duodenal ulcer
• Active benign gastric ulcer
• Symptomatic erosive or ulcerative gastro-oesophageal reflux disease (GORD).
• Gastro-Oesophageal Reflux Disease Long-term Management (GORD Maintenance)
• Symptomatic treatment of moderate to very severe gastrooesophageal reflux disease (symptomatic GORD)
• Zollinger-Ellison Syndrome
• In combination with appropriate antibacterial therapeutic regimens for the eradication of Helicobacter pylori in patients with peptic ulcer disease. See section 4.2
4.2 Posology and method of administration
Adults/elderly:
Active Duodenal Ulcer and Active Benign Gastric Ulcer: The recommended oral dose for both active duodenal ulcer and active benign gastric ulcer is 20mg to be taken once daily in the morning.
Most patients with active duodenal ulcer heal within four weeks. However a few patients may require an additional four weeks of therapy to achieve healing. Most patients with active benign gastric ulcer heal within six weeks. However again a few patients may require an additional six weeks of therapy to achieve healing.
Erosive or Ulcerative Gastro-Oesophageal Reflux Disease (GORD): The recommended oral dose for this condition is 20mg to be taken once daily for four to eight weeks.
Gastro-Oesophageal Reflux Disease Long-term Management (GORD Maintenance): For long-term management, a maintenance dose of PARIET 20mg or 10mg once daily can be used depending upon patient response.
Symptomatic treatment of moderate to very severe gastro-oesophageal reflux disease (symptomatic GORD): 10mg once daily in patients without oesophagitis. If symptom control has not been achieved during four weeks, the patient should be further investigated. Once symptoms have resolved, subsequent symptom control can be achieved using an on-demand regimen taking 10mg once daily when needed.
Zollinger-Ellison Syndrome: The recommended adult starting dose is 60 mg once a day. The dose may be titrated upwards to 120mg/day based on individual patient needs. Single daily doses up to 100mg/day may be given. 120mg dose may require divided doses, 60mg twice daily. Treatment should continue for as long as clinically indicated.
Eradication of H. pylori: Patients with H. pylori infection should be treated with eradication therapy. The following combination given for 7 days is recommended.
PARIET 20mg twice daily + clarithromycin 500mg twice daily and amoxicillin 1g twice daily.
For indications requiring once daily treatment PARIET tablets should be taken in the morning, before eating; and although neither the time of day nor food intake was shown to have any effect on rabeprazole sodium activity, this regimen will facilitate treatment compliance.
Patients should be cautioned that the PARIET tablets should not be chewed or crushed, but should be swallowed whole.
Renal and hepatic impairment: No dosage adjustment is necessary for patients with renal or hepatic impairment.
See section 4.4 Special Warnings and Precautions for Use of PARIET in the treatment of patients with severe hepatic impairment.
Children:
PARIET is not recommended for use in children, as there is no experience of its use in this group.
4.3 Contraindications
PARIET is contra-indicated in patients with known hypersensitivity to rabeprazole sodium, or to any excipient used in the formulation. PARIET is contra-indicated in pregnancy and during breast feeding
4.4 Special warnings and precautions for use
Symptomatic response to therapy with rabeprazole sodium does not preclude the presence of gastric or oesophageal malignancy, therefore the possibility of malignancy should be excluded prior to commencing treatment with PARIET.
Patients on long-term treatment (particularly those treated for more than a year) should be kept under regular surveillance.
A risk of cross-hypersensitivity reactions with other proton pump inhibitor or substituted benzimidazoles cannot be excluded.
Patients should be cautioned that PARIET tablets should not be chewed or crushed, but should be swallowed whole.
PARIET is not recommended for use in children, as there is no experience of its use in this group.
There have been post marketing reports of blood dyscrasias (thrombocytopenia and neutropenia). In the majority of cases where an alternative aetiology cannot be identified, the events were uncomplicated and resolved on discontinuation of rabeprazole.
Hepatic enzyme abnormalities have been seen in clinical trials and have also been reported since market authorisation. In the majority of cases where an alternative aetiology cannot be identified, the events were uncomplicated and resolved on discontinuation of rabeprazole.
No evidence of significant drug related safety problems was seen in a study of patients with mild to moderate hepatic impairment versus normal age and sex matched controls. However because there are no clinical data on the use of PARIET in the treatment of patients with severe hepatic dysfunction the prescriber is advised to exercise caution when treatment with PARIET is first initiated in such patients.
Co-administration of atazanavir with PARIET is not recommended (see section 4.5).
Treatment with proton pump inhibitors, including PARIET, may possibly increase the risk of gastrointestinal infections such as Salmonella, Campylobacter and Clostridium difficile (see section 5.1).
Proton pump inhibitors, especially if used in high doses and over long durations (>1 year), may modestly increase the risk of hip, wrist and spine fracture, predominantly in the elderly or in presence of other recognised risk factors. Observational studies suggest that proton pump inhibitors may increase the overall risk of fracture by 10–40%. Some of this increase may be due to other risk factors. Patients at risk of osteoporosis should receive care according to current clinical guidelines and they should have an adequate intake of vitamin D and calcium.
Severe hypomagnesaemia has been reported in patients treated with proton pump inhibitors like PARIET for at least three months, and in most cases for a year. Serious manifestations of hypomagnesaemia such as fatigue, tetany, delirium, convulsions, dizziness and ventricular arrhythmia can occur but they may begin insidiously and be overlooked. In most affected patients, hypomagnesaemia improved after magnesium replacement and discontinuation of the proton pump inhibitor.
For patients expected to be on prolonged treatment or who take proton pump inhibitors with digoxin or drugs that may cause hypomagnesaemia (e.g., diuretics), health care professionals should consider measuring magnesium levels before starting proton pump inhibitor treatment and periodically during treatment.
4.5 Interaction with other medicinal products and other forms of interaction
Rabeprazole sodium produces a profound and long lasting inhibition of gastric acid secretion. An interaction with compounds whose absorption is pH dependent may occur. Co-administration of rabeprazole sodium with ketoconazole or itraconazole may result in a significant decrease in antifungal plasma levels. Therefore individual patients may need to be monitored to determine if a dosage adjustment is necessary when ketoconazole or itraconazole are taken concomitantly with PARIET.
In clinical trials, antacids were used concomitantly with the administration of PARIET and, in a specific drug-drug interaction study, no interaction with liquid antacids was observed.
Co-administration of atazanavir 300mg/ritonavir 10mg with omeprazole (40 mg once daily) or atazanavir 400mg with lansoprazole (60mg once daily) to healthy volunteers resulted in a substantial reduction in atazanavir exposure. The absorption of atazanavir is pH dependent. Although not studied, similar results are expected with other proton pump inhibitors. Therefore PPIs, including rabeprazole, should not be co-administered with atazanavir (see Section 4.4).
4.6 Pregnancy and lactation
Pregnancy:
There are no data on the safety of rabeprazole in human pregnancy. Reproduction studies performed in rats and rabbits have revealed no evidence of impaired fertility or harm to the foetus due to rabeprazole sodium, although low foeto-placental transfer occurs in rats. PARIET is contraindicated during pregnancy.
Lactation:
It is not known whether rabeprazole sodium is excreted in human breast milk. No studies in lactating women have been performed. Rabeprazole sodium is however excreted in rat mammary secretions. Therefore PARIET should not be used during breast feeding.
4.7 Effects on ability to drive and use machines
Based on the pharmacodynamic properties and the adverse events profile, it is unlikely that PARIET would cause an impairment of driving performance or compromise the ability to use machinery. If however, alertness is impaired due to somnolence, it is recommended that driving and operating complex machinery be avoided.
4.8 Undesirable effects
The most commonly reported adverse drug reactions, during controlled clinical trials with rabeprazole were headache, diarrhoea, abdominal pain, asthenia, flatulence, rash and dry mouth. The majority of adverse events experienced during clinical studies were mild or moderate in severity, and transient in nature.
The following adverse events have been reported from clinical trial and post-marketed experience.
Frequencies are defined as: common ( >1/100, <1/10), uncommon ( > 1/1,000, <1/100), rare ( >1/10,000, <1/1000) and very rare ( <1/10,000).

1 Includes facial swelling, hypotension and dyspnoea
2 Erythema, bullous reactions and hypersensitivity reactions have usually resolved after discontinuation of therapy.
3 Rare reports of hepatic encephalopathy have been received in patients with underlying cirrhosis. In treatment of patients with severe hepatic dysfunction the prescriber is advised to exercise caution when treatment with PARIET is first initiated in such patients (see section 4.4)
4 See Special warnings and precautions for use (4.4)
4.9 Overdose
Experience to date with deliberate or accidental overdose is limited. The maximum established exposure has not exceeded 60mg twice daily, or 160mg once daily. Effects are generally minimal, representative of the known adverse event profile and reversible without further medical intervention. No specific antidote is known. Rabeprazole sodium is extensively protein bound and is, therefore, not dialysable. As in any case of overdose, treatment should be symptomatic and general supportive measures should be utilised.
5. Pharmacological properties
5.1 Pharmacodynamic properties
Pharmacotherapeutic group: Alimentary tract and metabolism, Drugs for peptic ulcer and gastro-oesophageal reflux disease (GORD), proton pump inhibitors,
ATC code: A02B C04
Mechanism of Action: Rabeprazole sodium belongs to the class of anti-secretory compounds, the substituted benzimidazoles, that do not exhibit anticholinergic or H2 histamine antagonist properties, but suppress gastric acid secretion by the specific inhibition of the H+/K+-ATPase enzyme (the acid or proton pump) The effect is dose-related and leads to inhibition of both basal and stimulated acid secretion irrespective of the stimulus. Animal studies indicate that after administration, rabeprazole sodium rapidly disappears from both the plasma and gastric mucosa. As a weak base, rabeprazole is rapidly absorbed following all doses and is concentrated in the acid environment of the parietal cells. Rabeprazole is converted to the active sulphenamide form through protonation and it subsequently reacts with the available cysteines on the proton pump.
Anti-secretory Activity: After oral administration of a 20mg dose of rabeprazole sodium the onset of the anti-secretory effect occurs within one hour, with the maximum effect occurring within two to four hours. Inhibition of basal and food stimulated acid secretion 23 hours after the first dose of rabeprazole sodium are 69% and 82% respectively and the duration of inhibition lasts up to 48 hours. The inhibitory effect of rabeprazole sodium on acid secretion increases slightly with repeated once-daily dosing, achieving steady state inhibition after three days. When the drug is discontinued, secretory activity normalises over 2 to 3 days.
Decreased gastric acidity due to any means, including proton pump inhibitors such as rabeprazole, increases counts of bacteria normally present in the gastrointestinal tract. Treatment with proton pump inhibitors may possibly increase the risk of gastrointestinal infections such as Salmonella, Campylobacter and Clostridium difficile.
Serum Gastrin Effects: In clinical studies patients were treated once daily with 10 or 20mg rabeprazole sodium, for up to 43 months duration. Serum gastrin levels increased during the first 2 to 8 weeks reflecting the inhibitory effects on acid secretion and remained stable while treatment was continued. Gastrin values returned to pre-treatment levels, usually within 1 to 2 weeks after discontinuation of therapy.
Human gastric biopsy specimens from the antrum and the fundus from over 500 patients receiving rabeprazole or comparator treatment for up to 8 weeks have not detected changes in ECL cell histology, degree of gastritis, incidence of atrophic gastritis, intestinal metaplasia or distribution of H. pylori infection. In over 250 patients followed for 36 months of continuous therapy, no significant change in findings present at baseline was observed.
Other Effects: Systemic effects of rabeprazole sodium in the CNS, cardiovascular and respiratory systems have not been found to date. Rabeprazole sodium, given in oral doses of 20mg for 2 weeks, had no effect on thyroid function, carbohydrate metabolism, or circulating levels of parathyroid hormone, cortisol, oestrogen, testosterone, prolactin, cholecystokinin, secretin, glucagon, follicle stimulating hormone (FSH), luteinising hormone (LH), renin, aldosterone or somatotrophic hormone.
Studies in healthy subjects have shown that rabeprazole sodium does not have clinically significant interactions with amoxicillin. Rabeprazole does not adversely influence plasma concentrations of amoxicillin or clarithromycin when co-administered for the purpose of eradicating upper gastrointestinal H. pylori infection.
5.2 Pharmacokinetic properties
Absorption: PARIET is an enteric-coated (gastro-resistant) tablet formulation of rabeprazole sodium. This presentation is necessary because rabeprazole is acid-labile. Absorption of rabeprazole therefore begins only after the tablet leaves the stomach. Absorption is rapid, with peak plasma levels of rabeprazole occurring approximately 3.5 hours after a 20mg dose. Peak plasma concentrations (Cmax) of rabeprazole and AUC are linear over the dose range of 10mg to 40mg. Absolute bioavailability of an oral 20mg dose (compared to intravenous administration) is about 52% due in large part to pre-systemic metabolism. Additionally the bioavailability does not appear to increase with repeat administration. In healthy subjects the plasma half-life is approximately one hour (range 0.7 to 1.5 hours), and the total body clearance is estimated to be 283 ± 98 ml/min. There was no clinically relevant interaction with food. Neither food nor the time of day of administration of the treatment affect the absorption of rabeprazole sodium.
Distribution: Rabeprazole is approximately 97% bound to human plasma proteins.
Metabolism and excretion: Rabeprazole sodium, as is the case with other members of the proton pump inhibitor (PPI) class of compounds, is metabolised through the cytochrome P450 (CYP450) hepatic drug metabolising system. In vitro studies with human liver microsomes indicated that rabeprazole sodium is metabolised by isoenzymes of CYP450 (CYP2C19 and CYP3A4). In these studies, at expected human plasma concentrations rabeprazole neither induces nor inhibits CYP3A4; and although in vitro studies may not always be predictive of in vivo status these findings indicate that no interaction is expected between rabeprazole and cyclosporin. In humans the thioether (M1) and carboxylic acid (M6) are the main plasma metabolites with the sulphone (M2), desmethyl-thioether (M4) and mercapturic acid conjugate (M5) minor metabolites observed at lower levels. Only the desmethyl metabolite (M3) has a small amount of anti-secretory activity, but it is not present in plasma.
Following a single 20mg 14C labelled oral dose of rabeprazole sodium, no unchanged drug was excreted in the urine. Approximately 90% of the dose was eliminated in urine mainly as the two metabolites: a mercapturic acid conjugate (M5) and a carboxylic acid (M6), plus two unknown metabolites. The remainder of the dose was recovered in faeces.
Gender: Adjusted for body mass and height, there are no significant gender differences in pharmacokinetic parameters following a single 20mg dose of rabeprazole.
Renal dysfunction: In patients with stable, end-stage, renal failure requiring maintenance haemodialysis (creatinine clearance ≤5ml/min/1.73m2), the disposition of rabeprazole was very similar to that in healthy volunteers. The AUC and the Cmax in these patients was about 35% lower than the corresponding parameters in healthy volunteers. The mean half-life of rabeprazole was 0.82 hours in healthy volunteers, 0.95 hours in patients during haemodialysis and 3.6 hours post dialysis. The clearance of the drug in patients with renal disease requiring maintenance haemodialysis was approximately twice that in healthy volunteers.
Hepatic dysfunction: Following a single 20mg dose of rabeprazole to patients with chronic mild to moderate hepatic impairment the AUC doubled and there was a 2-3 fold increase in half-life of rabeprazole compared to the healthy volunteers. However, following a 20mg dose daily for 7 days the AUC had increased to only 1.5-fold and the Cmax to only 1.2-fold. The half-life of rabeprazole in patients with hepatic impairment was 12.3 hours compared to 2.1 hours in healthy volunteers. The pharmacodynamic response (gastric pH control) in the two groups was clinically comparable.
Elderly: Elimination of rabeprazole was somewhat decreased in the elderly. Following 7 days of daily dosing with 20mg of rabeprazole sodium, the AUC approximately doubled, the Cmax increased by 60% and t½ increased by approximately 30% as compared to young healthy volunteers. However there was no evidence of rabeprazole accumulation.
CYP2C19 Polymorphism: Following a 20mg daily dose of rabeprazole for 7 days, CYP2C19 slow metabolisers, had AUC and t½ which were approximately 1.9 and 1.6 times the corresponding parameters in extensive metabolisers whilst Cmax had increased by only 40%.
5.3 Preclinical safety data
Non-clinical effects were observed only at exposures sufficiently in excess of the maximum human exposure that make concerns for human safety negligible in respect of animal data.
Studies on mutagenicity gave equivocal results. Tests in mouse lymphoma cell line were positive, but in vivo micronucleus and in vivo and in vitro DNA repair tests were negative. Carcinogenicity studies revealed no special hazard for humans.
6. Pharmaceutical particulars
6.1 List of excipients
Core tablet: Mannitol, magnesium oxide, low-substituted hyprolose, hyprolose, magnesium stearate
Undercoating: ethylcellulose, magnesium oxide
Enteric coating: hypromellose phthalate, diacetylated monoglycerides, talc, titanium dioxide (E171), red iron oxide (E172) – 10mg only, yellow iron oxide (E172) – 20mg only, carnauba wax
Printing ink – Pariet 10mg: White Shellac, black iron oxide (E172), Dehydrated Ethyl Alcohol, 1-Butanol.
Printing ink – Pariet 20mg: White Shellac, Red Iron Oxide (E172), Carnauba wax, Glycerine fatty acid ester, Dehydrated Ethyl Alcohol, 1-Butanol.
6.2 Incompatibilities
Not applicable.
6.3 Shelf life
3 years.
6.4 Special precautions for storage
Do not store above 25°C. Do not refrigerate
6.5 Nature and contents of container
Blister strips (aluminium/aluminium)
Pack sizes: 1,5, 7, 14, 15, 25, 28, 30, 50, 56, 75, 98, 112, or 120 tablets
Not all pack sizes may be marketed.
6.6 Special precautions for disposal and other handling
No special requirements.
7. Marketing authorisation holder
Eisai Limited, European Knowledge Centre, Mosquito Way, Hatfield, Hertfordshire, AL10 9SN, United Kingdom
8. Marketing authorisation number(s)
Pariet 10mg: PL 10555/0010 (10mg tablets)
Pariet 20mg: PL10555/0008 (20mg tablets)
9. Date of first authorisation/renewal of the authorisation
8 May 1998/May 2008
10. Date of revision of the text
21 March 2013
11. Legal category
POM – Medicinal product subject to medical prescription
Pariet获欧盟批准用于消灭幽门螺旋杆菌
Pariet(雷贝拉唑钠)－是一种疗效很强的“质子泵抑制剂”(PPI)，最近在欧盟获得了批准，将用于消灭消化道溃疡病患者的幽门螺旋杆菌(H.pylori)。
对于与幽门螺旋杆菌有关的胃和十二指肠溃疡来说，抑制酸性对提高杀菌疗效非常重要。临床数据显示，通过创造一个弱酸环境，雷贝拉唑钠能够克服pH值障碍，从而消灭幽门螺旋杆菌(1)(2)。
主要专家都对这种新的指征表示欢迎，它向感染幽门螺旋杆菌的患者提供了迅速而且可预测的酸性抑制和抗生素值的最佳组合，从而达到完全消灭机体细菌的效果。
在欧洲，Pariet*(雷贝拉唑钠)已经获得批准与相应的抗菌治疗方案一道，用于消灭消化道溃疡病患者的幽门螺旋杆菌。建议使用以下剂量进行7天的治疗：Pariet*(雷贝拉唑钠)20毫克，每日两次；克拉霉素500毫克，每日两次；羟氨苄青霉素1克，每日两次。
Pariet*(雷贝拉唑钠)已经被指定用于治疗症状腐蚀性或溃疡性GORD，作为腐蚀性或溃疡性GORD的维持疗法，以及用于治疗活动期十二指肠溃疡和活动期良性胃溃疡。与其它PPI(3)相比，Pariet*(雷贝拉唑钠)已经显示了更快、更强和更加持久的酸性抑制作用，(4)从第一天开始(5)(6)(7)就使GORD患者缓解症状。
注意：
雷贝拉唑钠是由卫材有限公司发现的，杨森制药公司与卫材有限公司已达成一项战略联盟，根据这项联盟，卫材公司与杨森－齐拉格公司联手在德国和英国促销这种药物。在美国，雷贝拉唑钠由卫材公司与杨森制药公司共同促销，品牌名称为Aciphex(注册标)。Pariet 在日本和亚洲以外的其它大部分国家及地区可通过杨森－齐拉格公司购买。
*Pariet/Aciphex(注册商标)是日本东京卫材有限公司的商标。