瑞巴派特联合兰索拉唑对胃溃疡愈合质量的影响

目的探讨瑞巴派特联合兰索拉唑对胃溃疡愈合质量的影响。方法72例经内镜诊断并检测证实幽门螺旋杆菌（HP）阳性的活动性胃溃疡患者,随机分成治疗组和对照组。治疗第1周,两组患者均予HP根除三联疗法,第2～8周,治疗组给予瑞巴派特联合兰索拉唑,对照组仅用兰索拉唑治疗。8周疗程结束后,两组患者复查胃镜,观察胃溃疡愈合率（S1期＋S2期）,S2期获得率及两组患者治疗后的胃黏膜组织学变化,评价对胃溃疡愈合质量的影响。结果治疗组胃溃疡愈合率和S2期获得率分别为88．8％和583％,对照组分别为83．3％和30．6％,两组胃溃疡愈合率差异无显著性（P〉0．05）,S2期获得率治疗组显著高于对照组（P〈0．05）。两组组织学观察指标较治疗前均有不同程度的好转（P〈0．05）。治疗组显著高于对照组（P〈0．05）。结论瑞巴派特联合兰索拉唑治疗明显增加s2期获得率,显著提高组织学愈合质量,促进高质量的溃疡愈合,提示瑞巴派特在胃溃疡愈合中,特别是提高溃疡愈合质量中起重要作用。     

兰索拉唑在消化性溃疡病人中的药代动力学研究

目的在消化性溃疡病人中观察兰索拉唑的药代动力学的变化，进一步了解该药的代谢规律。方法选取经胃镜检查确诊为消化性溃疡的患者为试验组（Ｇ组，ｎ＝６）及健康志愿者为对照组（Ｃ组，ｎ＝６），口服兰索拉唑胶囊３０ｍｇ，定时取血通过高压液相方法测定血药浓度。利用３Ｐ８７药代动力学程序模拟药时曲线，计算药代动力学参数。结果兰索拉唑符合一房室模型。试验组中，５位患者的吸收速率常数Ｋα较对照组的Ｋα明显增加，吸收半衰期Ｔ１２α及达峰时间Ｔｍａｘ明显减少。血药浓度高峰Ｃｍａｘ有明显提高。而清除速率常数Ｋβ、清除半衰期Ｔ１２β也有较明显的差别，其表观分布容积Ｖ／Ｆ、清除率ＣＬ／Ｆ及血药浓度曲线下面积ＡＵＣ差别均不显著。１位幽门不全梗阻患者的药代动力学曲线表明吸收明显延迟。结论兰索拉唑口服后，分布广泛，代谢迅速。消化性溃疡患者应用时，其吸收速率和其排泄明显加快。血药浓度高峰明显增加，对于治疗该病可能具有重要的意义。     

Role of sensory neurons in restitution and healing of gastric ulcers

It has been shown that capsaicin-sensitive afferent fibers play a crucial role in acute gastroprotection. Release of neurotransmitters such as calcitonin gene-related peptide (CGRP) and the consequent increase in mucosal blood flow have been identified as key factors in the protective effect of the stimulation of these fibers by capsaicin. Conversely the involvement of sensory nerves in the process of tissue repair after acute and chronic gastric mucosal damage has remained largely unexplored. Some studies, however, while demonstrating that the process of rapid repair (restitution) of the gastric mucosa damaged by ethanol is unaffected by capsaicin pretreatment, have shown that the recovery of gastric integrity after mucosal damage induced by sodium taurocholate or monochloramine, a known cytotoxic agent present in H. pylori patients, requires an intact sensory function and the maintenance of an adequate blood supply. In addition, a delayed healing (up to 1 week) of HCl-induced gastric lesions has been reported in capsaicin-deafferented rats, in association with a selective impairment of the hyperemic response to acid. Healing of gastric lesions induced by indomethacin, ischaemia and reperfusion, water restraint stress or concentrated ethanol was delayed in animals with functional ablation of sensory nerves. In a well-validated model, such as chronic gastric ulcers induced in rats by subserosal injection of acetic acid whose lesions last up to 4 weeks, the chemical ablation of sensory neurons negatively interferes with the process of chronic ulcer healing. The delay in ulcer healing was found to be associated with a persistent decrease in tissue levels of gastric CGRP and with a change of inflammatory mediators and growth factors, while gastric secretion and emptying were not concomitantly affected. Taken together, these data suggest that capsaicin-sensitive afferent nerves may play a role in the process of ulcer healing by mediating the hyperemic response through the release of CGRP and facilitating the acid disposal in the mucosa. From a therapeutic perspective, it is obvious that the compound acting on this system could have a role in the healing processes of the stomach damage.     

Role of thromboxane A2 in healing of gastric ulcers in rats

We investigated the role of thromboxane (TX) A2 in gastric ulcer healing in rats. Acetic acid ulcers were produced in male Donryu rats. TXA2 synthesis in the stomachs with ulcers was significantly elevated in ulcerated tissue, but not in intact tissue, compared with that in the gastric mucosa of normal rats. Indomethacin inhibited both TXA2 and prostaglandin E2 (PGE2) synthesis in ulcerated tissue, while NS-398 (selective cyclooxygenase-2 inhibitor) reduced only PGE2 synthesis. OKY-046 (TXA2 synthase inhibitor) dose-relatedly inhibited only TXA2 synthesis. The maximal effect of OKY-046 (80% inhibition) was found at more than 30 mg/kg. When OKY-046 was administered for 14 days, the drug at more than 30 mg/kg significantly accelerated ulcer healing without affecting acid secretion. The maximal reduction of ulcerated area by OKY-046 was about 30%, compared with the area in the control. Histological studies revealed that regeneration of the mucosa was significantly promoted by OKY-046, but neither maturation of the ulcer base nor angiogenesis in the base were affected. OKY-046 and TXB2 had no effect on proliferation of cultured rat gastric epithelial cells, but U-46619 (TXA2 mimetic) dose-relatedly prevented the proliferation without reducing cell viability. These results indicate that the increased TXA2, probably derived from cyclooxygenase-1 in ulcerated tissue, exerts a weak inhibitory effect on ulcer healing in rats. The effect of TXA2 might be due partly to prevention of gastric epithelial cell proliferation at the ulcer margin.     

Role of endogenous glucocorticoids in the healing of gastric erosions and chronic gastric ulcers in rats

To investigate the role of endogenous glucocorticoids in the healing of gastric lesions, we compared the healing of indomethacin- or cold-restraint-induced gastric erosions as well as aceticacid-induced ulcers in sham-operated rats, adrenalectomized rats and adrenalectomized rats with corticosterone replacement. Adrenalectomy was performed immediately after the formation of gastric erosions (4 h after indomethacin administration or 6 h after the onset of cold-restraint stress) or chronic ulcers (in 3 days after ingestion of acetic acid into the luminal side of the stomach). All ulcerogenic stimuli caused an increase in corticosterone production. Adrenalectomy created corticosterone deficiency and delayed the healing of gastric erosions and chronic ulcers. Replacing corticosterone reversed the deleterious effect of adrenalectomy on healing of gastric damage in adrenalectomized rats. These results suggest that glucocorticoids participate in natural healing processes of injured gastric mucosa. The data obtained also indicate that participation of glucocorticoid in the healing of gastric lesions is more evident under prostaglandin deficient conditions.     

Dose-related healing of duodenal ulcer with the proton pump inhibitor lansoprazole

Lansoprazole (AG 1749) is a novel substituted benzimidazole which inhibits gastric acid secretion by blocking H+,K(+)-ATPase. This randomized, double-blind multicentre trial studied the dose-response relationship of lansoprazole on ulcer healing and compared it with ranitidine in 314 out-patients with endoscopically assessed, symptomatic duodenal ulcer. Cumulative healing rates with Lansoprazole 7.5, 15, and 30 mg o.m. were 48, 59, and 74% at 2 weeks and 75, 84, and 95% at 4 weeks, respectively (intention-to-treat); the difference of the healing rates between 7.5 and 30 mg groups was significant (P less than 0.001). Corresponding healing rates for 300 mg ranitidine nocte were 51 and 89%. Pain relief was similar in all treatment groups. Lansoprazole was well tolerated. During a follow-up of 6 months relapse rates after lansoprazole 7.5, 15, and 30 mg were 21, 29, and 22%, respectively; the relapse rate after ranitidine 300 mg was 20%. In conclusion, lansoprazole provides faster healing of duodenal ulcer than ranitidine and a similar relapse pattern. For further trials in peptic ulcer disease a daily dose of lansoprazole 30 mg o.m. is recommended.     

Effect of omeprazole on delayed healing of acetic acid-induced gastric ulcers in rats

Omeprazole, a gastric mucosal proton pump inhibitor, significantly and dose-dependently prevented the delayed healing of acetic acid-induced gastric ulcers in response to repeatedly administered indomethacin to rats. Both basal and histamine-stimulated gastric acid secretions in rats with acetic acid-induced ulcers that were given indomethacin were markedly and persistently (greater than 24 hr) inhibited after 4 weeks treatment with omeprazole. The prevention of delayed ulcer healing by omeprazole appears to be due to its long-lasting antisecretory activity.     

Effect of dopamine on the healing of acetic acid-induced gastric ulcers in rats

Dopamine, as a neurotransmitter in the brain, is also present in the gastroduodenal mucosa and has been implicated in several functions in these tissues. Recent study showed that dopamine acts as a potent antitumor/angiogenic activity through suppression of growth factor expression. Since growth factors are known to play a crucial role in the mechanism of wound healing, it is possible that dopamine has a deleterious influence on the healing of gastric ulcers. In the present study, we examined the effect of dopamine on the healing of acetic acid-induced gastric ulcers in rats. Gastric ulcers were induced in male SD rats by serosal application of acetic acid for 60 sec. Dopamine was subcutaneously given twice daily for 7 days, starting 3 days after ulceration. In some case, the osmotic mini-pump filled with dopamine was implanted into the dorsal subcutaneous space in rats for 7 days. VEGF and Flk-1 mRNA expressions were determined by RT-PCR. Dopamine (3, 10 and 30 mg/kg) given subcutaneously for 7 days did not significantly affect the healing of gastric ulcers. The expression of VEGF and Flk-1 mRNA in the ulcerated mucosa was up-regulated after ulceration, and these expressions were not affected by dopamine. Likewise, dopamine (0.6 mg/kg/hr) infused continuously using the osmotic mini-pump also had no effect on the healing of these ulcers. These results suggest that dopamine, although reportedly shows a potent antitumor/angiogenic activity, does not cause any influence on the healing of the pre-existing gastric ulcers in rats. Received 3 August 2006; accepted 10 November 2006     

Molecular mechanisms of epithelial regeneration and neovascularization during healing of gastric and esophageal ulcers

In this paper we reviewed and updated current views on the cellular and molecular mechanisms of gastric and esophageal ulcer healing. Gastric ulcer healing encompasses inflammation, cell proliferation, epithelial regeneration, gland reconstruction, formation of granulation tissue, neovascularization (new blood vessel formation), interactions between various cells and the matrix and tissue remodeling, resulting in scar formation. All these events are controlled by the cytokines and growth factors, GI hormones including gastrin, CCK, and orexigenic peptides such as ghrelin, orexin-A and obestatin as well as Cox2 generated prostaglandins. These growth factors and hormones trigger cell proliferation, migration, and survival utilizing Ras, MAPK, PI-3K/AKT, PLC-γ and Rho/Rac/actin signaling pathways. Hypoxia triggers activation of some of these genes (e.g., VEGF) via hypoxia inducible factor (HIF). Growth factors: EGF, HGF, IGF-1, their receptors and Cox2 are important for epithelial cell proliferation, migration, re-epithelialization and regeneration of gastric glands during gastric ulcer healing. Serum response factor (SRF) is also essential for re-epithelialization and muscle restoration. VEGF, bFGF, angiopoietins, nitric oxide, endothelin, prostaglandins and metalloproteinases are important for angiogenesis, vascular remodeling and mucosal regeneration within gastric ulcer scar. SRF is critical limiting factor for VEGF-induced angiogenesis. Esophageal ulcer healing follows similar pattern to gastric ulcer, but KGF and its receptor are the key players in regeneration of the epithelium. In addition to local mucosal cells from viable mucosa bordering necrosis, circulating bone marrow derived stem and progenitor cells are potentially important for ulcer healing, contributing to the regeneration of epithelial and connective tissue components and neovascularization.     

奥美拉唑与兰索拉唑对成人活动期胃溃疡患者的临床疗效及溃疡愈合质量的影响

目的探讨奥美拉唑与兰索拉唑对成人活动期胃溃疡的临床疗效及对溃疡愈合质量的影响。方法将2010年1月至2012年12月在我院治疗的64例活动期胃溃疡患者随机分为兰索拉唑组和奥美拉唑组,每组32例,兰索拉唑组每日1次口服兰索拉唑30 mg,奥美拉唑组每日1次口服奥美拉唑20 mg。观察两组患者的溃疡愈合率、临床症状改善情况以及溃疡愈合的质量。结果兰索拉唑组治疗总有效率为93.75%,奥美拉唑组为90.63%,两组比较差异无统计学意义(χ2=0.676,P>0.05);治疗后两组症状积分与治疗前比较均明显改善(P<0.05);治疗后两组间相比,症状积分差异无统计学意义(P>0.05)。治疗8周后,兰索拉唑组腺体密度和腺管形态恢复情况均显著优于奥美拉唑组,两组比较差异具有统计学意义(P<0.05)。结论兰索拉唑对活动期胃溃疡患者的临床症状改善程度和疗效与奥美拉唑相当,但是兰索拉唑对溃疡愈合的质量更好,值得临床推广。     

Effect of H2-receptor blockade by ranitidine on ulcer healing and gastric acid secretion in patients with gastric and duodenal ulcers

The effect of treatment for 4 weeks with the H2-receptor antagonist ranitidine 200 mg daily on ulcer healing, clinical symptoms and antacid consumption, and on gastric acid secretion, was studied in a double blind trial in 48 patients with a total of 50 endoscopically confirmed duodenal, prepyloric or corporeal gastric ulcer. Patients whose ulcers did not show complete healing within 28 days were continued openly on ranitidine for up to a further 4 weeks. Endoscopy, basal gastric acid secretion (BAO) and pentagastrin-stimulated maximal secretion (PAO) studies were performed at 2-week intervals. After four weeks, 73% of the gastro-duodenal ulcers in the ranitidine group showed complete healing versus 42% in the placebo group (p less than 0.05). Gastric acid secretion was considerably inhibited both under basal (89%; p less than 0.001) and maximal challenge (71%; p less than 0.001) conditions. The inhibitory effect was still pronounced 13-15 h after administration of ranitidine 100 mg. Symptoms and the need for antacids were significantly reduced. Ranitidine appears to be an efficacious, safe and well tolerated medicine principle for the treatment of gastro-duodenal ulcer disease.     

Alendronate gastric ulcers

BACKGROUND: It appears likely that drugs other than NSAIDs may cause ulcers and ulcer complications (e.g. potassium chloride). Alendronate (Fosamax) is used in the treatment and prevention of metabolic bone disease and has also been associated with severe oesophageal damage and stricture. We have previously shown that the dose of alendronate used for Paget's disease (40 mg) causes gastric damage similar to NSAIDs. The usual dose for the treatment of postmenopausal osteoporosis is 10 mg per day. AIM: To investigate whether the 10 mg dose of alendronate causes gastric ulcers. METHODS: We performed an endoscopist-blind, crossover, randomized, single-centre comparison of 10 mg of alendronate/day and placebo in volunteers aged 40 years or more. Video-endoscopy was used to evaluate the presence and degree of mucosal damage to the oesophagus, stomach, or duodenal bulb after 7 and 14 days of treatment. RESULTS: Twenty-four healthy volunteers participated, including 15 women and nine men, ranging in age from 41 to 52 years. Visible gastric mucosal damage was present in nine (38%) who received alendronate compared to three (13%) in the placebo group. There was a marked difference in the severity of mucosal damage; there were no ulcers or large erosions in those receiving placebo. In contrast, potentially clinically significant gastric mucosal injury was seen in six subjects receiving alendronate (two developed antral ulcers and four had large (4-8 mm) superficial antral erosions) compared to none in the placebo group (P = 0.0219). One subject developed oesophageal damage in the form of multiple linear superficial erosions in the mid and distal oesophagus. Duodenal injury was not seen. CONCLUSION: Alendronate causes gastric ulceration, suggesting that alendronate use may be associated with ulcer complications such as acute upper gastrointestinal bleeding. The results of this study suggest the need for post-marketing surveillance to clarify the nature, frequency and magnitude of any potential gastrointestinal side-effects associated with the use of this drug.     

Effects of cimetidine and atropine sulfate on gastric secretion and healing of gastric and duodenal ulcers in rats.

Cimetidine, a new histamine H2-receptor antagonist (50 or 100 mg/kg) and atropine sulfate (15 mg/kg) given intraduodenally, markedly inhibited gastric secretion in pylorus-ligated rats. Cimetidine (100 or 200 mg/kg/day) given for 10 or 12 consecutive days orally in two divided doses, significantly promoted the healing rate of both gastric and duodenal ulcers induced in rats. Atropine (30 mg/kg/day) also significantly accelerated the healing of duodenal ulcers but failed to affect gastric ulcers.     

兰索拉唑联用达喜治疗胃溃疡的临床疗效分析

目的探讨兰索拉唑联用达喜（铝碳酸镁）治疗胃溃疡临床的疗效。方法选自我院门诊198例胃溃疡的患者,分为治疗组105例,对照组93组,两组根除幽门螺杆菌（H．Pylori）三联治疗方法。1周后,治疗组用兰索拉唑和达喜治疗;对照只用兰索拉唑。1疗程为8周。结果治疗组的痊愈率和总有效率分别为61．91％和93．33％;对照组的痊愈率和总有效率分别为40．09％和80．65％,两组的痊愈率和总有效率比较差异有统计学意义俨〈0．05）。药物未见明显不良反应。结论兰索拉唑联用达喜治疗胃溃疡,疗效较单用兰索拉唑显著。     

Does omeprazole-induced hypergastrinaemia contribute to the enhanced healing of aceticacid-induced gastric ulcers in rats?

We examined the effects of omeprazole and SDZ CO-611 (an orally active somatostatin analogue) alone and in combination, on ulcer healing, gastric acid secretion and the serum gastrin level in rats. Two or 4-weeks’ treatment with oral omeprazole significantly enhanced spontaneous healing and/or prevented delayed healing (caused by indomethacin) of acetic acid ulcers, with the inhibition of gastric acid secretion and hypergastrinaemia. While oral SDZ CO-611 had no effect on spontaneous ulcer healing, it significantly prevented delayed ulcer healing. On SDZ CO-611 treatment, gastric acid secretion was significantly inhibited but basal gastrin level remained unchanged. Hypergastrinaemia induced by a single treatment with oral omeprazole was markedly suppressed by SDZ CO-611 for >12 h. SDZ CO-611, administered together with omeprazole for 2 or 4 weeks, did not affect the enhanced ulcer healing or the antisecretory effect of omeprazole, despite a greater than 60% decrease. We conclude that omeprazole-induced hypergastrinaemia does not contribute to the mechanism by which omeprazole enhances ulcer healing. This paper was presented at the Section of IUPHAR GI Pharmacology Symposium on ‘Biochemical pharmacology as an approach to gastrointestinal disorders (basic science to clinical perspectives)’, October 12–14, 1995, Pécs, Hungary.     

Long-term maintenance treatment of gastric ulcers with ranitidine

One hundred and twenty patients with gastric ulcer disease, who had been receiving maintenance treatment with ranitidine (150 or 300 mg/day) for periods up to 7 years, were studied retrospectively. The proportion of patients remaining free from symptomatic recurrence of ulcer during maintenance treatment was 97% after 1 year; 90% after 3 years; and 79% after 5 years. No patient developed haemorrhage or perforation during maintenance treatment. None of the demographic features was shown to be associated with a significantly increased risk of ulcer recurrence during maintenance treatment. Comparison of the recurrence rates during maintenance treatment with those during periods without active anti-ulcer therapy, using life table and incidence density analysis, showed a significant difference in favour of maintenance treatment. We conclude that maintenance treatment with ranitidine for 5 years significantly reduces the risk of symptomatic ulcer recurrence in patients with gastric ulcer.     

Prostaglandin content in the rat gastric mucosa during healing of chronic ulcers induced by acetic acid

Non-steroidal anti-inflammatory compounds delayed the regeneration of chronic gastric ulcers induced by acetic acid in the rat. The delayed regeneration was connected with a decreased PGE2 content in the proliferating tissue. Glucocorticoid influenced neither the regeneration of mucosal damages nor the gastric PGE2 content. The carboanhydrase inhibitor, acetazolamide, also did not alter the restoration of gastric mucosa after being damaged. From the clinical point of view, the safe use of NOSAC will be emphasized in patients with ulcer anamnese. The findings with prednisolone did not confirm a similar safe use of this drug in patients.     

A trial of lansoprazole in refractory gastric ulcer.

BACKGROUND: The proton-pump inhibitor, lansoprazole, a more potent gastric acid inhibitor with a longer action than H2-receptor antagonists, should heal refractory gastric ulcers more effectively. METHODS: Lansoprazole's efficacy in healing refractory gastric ulcer(s) (i.e. after 6 weeks of treatment with H2-receptor antagonists, antacids or sucralfate at recommended dosages, and/or a relapse within 1 year of documented gastric ulcer), was compared by a two-dose regimen in a four- centre, randomized, parallel group study. One hundred and eighteen patients (59 per group) with an endoscopically confirmed gastric ulcer > or = 3 mm, received lansoprazole 30 or 60 mg daily. We assessed efficacy endoscopically at 4 and 8 weeks, and again after documented healing during a maintenance phase of lansoprazole 30 mg/day at 2 and 4 months. RESULTS: Demographic and anthropometric data were comparable. Healing rates at 4 weeks were 63% (30 mg) vs. 66% (60 mg) (95% CI, -14 to 21%) and cumulatively at 8 weeks, 83% (30 mg) vs. 81% (60 mg) (95% CI, -12 to 16%). Two and 4 months after documented healing, 86% and 78% of intention-to-treat patients remained in remission. CONCLUSION: Lansoprazole 30 or 60 mg/day appear equally effective in healing refractory gastric ulcers, while maintenance therapy of 30 mg/day effectively prevented an ulcer relapse.     

胃得安胶囊联合兰索拉唑治疗胃溃疡的临床研究

目的探讨胃得安胶囊联合兰索拉唑治疗胃溃疡的临床效果。方法选取2016年7月—2018年7月天津市第五中心医院收治的胃溃疡患者96例,随机分成对照组(48例)和治疗组(48例)。对照组早餐前30 min口服兰索拉唑肠溶胶囊,30 mg/次,1次/d。治疗组在对照组基础上口服胃得安胶囊,2粒/次,3次/d。两组患者均连续治疗6周。观察两组患者临床疗效,同时比较治疗前后两组患者上腹痛评分、反酸评分、前列腺素(PG)E2、C反应蛋白(CRP)、白介素-17(IL-17)、超氧化物歧化酶(SOD)和脂质过氧化物(LPO)水平以及幽门螺杆菌根除率、溃疡愈合率及复发率。结果治疗后,对照组临床有效率为87.5%,显著低于治疗组的100.0%,两组比较差异有统计学意义(P0.05)。治疗后,两组患者中上腹痛评分和反酸评分均显著降低(P0.05),且治疗组患者中上腹痛评分和反酸评分明显低于对照组(P0.05)。治疗后,两组患者胃液中PGE2浓度及血清SOD水平均显著升高(P0.05),血清CRP、IL-17、LPO浓度则均显著降低(P0.05),且治疗组患者这些指标水平明显好于对照组(P0.05)。治疗后,治疗组幽门螺杆菌根除率、溃疡愈合率分别为93.8%、75.0%,均显著高于对照组(P0.05)。随访6个月,治疗组复发率为8.3%,比对照组的25%明显显著降低(P0.05)。结论胃得安胶囊联合兰索拉唑治疗胃溃疡的整体疗效切实,促进溃疡愈合,增强胃黏膜的防御功能及机体的抗氧化能力。     

Clinical trial: healing of NSAID-associated gastric ulcers in patients continuing NSAID therapy - a randomized study comparing ranitidine with esomeprazole

BACKGROUND: The use of non-steroidal anti-inflammatory drugs (NSAID) is associated with an increased risk of gastric ulcer (GU) development. METHODS: This multicentre, randomized, double-blind, parallel-group trial compared endoscopic healing rates at 4 and 8 weeks after treatment with oral esomeprazole 40 or 20 mg once daily, or ranitidine 150 mg twice daily, in patients with 1 baseline GU > or = 5 mm but no GUs or duodenal ulcers >25 mm in diameter who received continued cyclooxygenase-2-selective or non-selective NSAID therapies. The primary outcome was the percentage of patients in each treatment group who had no GUs at week 8. RESULTS: Four hundred and forty patients were randomized to treatment. At week 8, GU healing rates (95% CI) with esomeprazole 40 mg, esomeprazole 20 mg and ranitidine were 85.7 (79.8-91.7)%, 84.8 (78.8-90.8)% and 76.3 (69.2-83.3)%, respectively; between-group differences were not statistically significant. Week-4 GU healing rates were 70.7 (62.9-78.4)% and 72.5 (65.0-79.9)% with esomeprazole 40 and 20 mg, respectively, and were significantly higher (P < 0.01 for both doses) than those with ranitidine [55.4 (47.1-63.7)%]. CONCLUSION: In patients who require continued NSAID therapy, GU healing rates at 8 weeks numerically favoured esomeprazole but were not significantly different from ranitidine.