Gómez B J, Caunedo A, Redondo L, Esteban J, Sáenz-Dana M, Blasco M, Hergueta P, Rodríguez-Téllez M, Romero R, Pellicer F J, Herrerías J M
Gastroenterology Service, Virgen Macarena University Hospital, Seville, Spain.
Int J Clin Pharmacol Ther. 2006 Apr;44(4):154-62. doi: 10.5414/cpp44154.
To assess the effect of a 2-week treatment with dexibuprofen, in comparison with ibuprofen and diclofenac, on pepsinogen plasma concentrations and gastrointestinal mucosa, as well as the correlation of these changes with gastrointestinal mucosal injury.
60 patients with rheumatologic disease in chronic therapy with NSAID, were included. After a 7-day run-in period patients were randomly assigned to receive a 14-day treatment with dexibuprofen (Group A; Day 1 - 3 = 400 mg t.i.d; Day 4 - 14 = 400 mg b.i.d.), ibuprofen (Group B; Day 1 - 3 = 800 mg t.i.d; Day 4 -14 = 800 mg b.i.d.) or diclofenac (Group C; Day 1 - 3 = 50 mg t.i.d; Day 4 - 14 = 50 mg b.i.d.). Upper gastrointestinal endoscopy (Day 15), capsule-endoscopy (Day 16, 7 patients of each group) and determination of pepsinogen plasma concentrations were performed (basal and Day 15). A semiquantitative scale was designed for the assessment of the gastrointestinal mucosa.
No differences in plasma pepsinogen were found between treatment groups or gastrointestinal injury grades or between basal and post-therapy determinations. Dexibuprofen showed gastroduodenal mucosal injury in fewer patients (42.1%) than was the case with ibuprofen (5%; p = 0.003) and diclofenac (30%; p = N.S.). Dexibuprofen administration was also associated with more patients having no intestinal mucosal damage (42.86% vs. 28.7% in the diclofenac group and 14.29% in the ibuprofen group; p = 0.0175). The rate of clinical adverse events was similar in Groups A, B and C (28%, 38% and 34%).
Dexibuprofen showed a lower rate of gastroduodenal and intestinal mucosal injury. This effect was not mediated by modifications of plasma pepsinogen levels.
比较右布洛芬与布洛芬和双氯芬酸进行为期2周的治疗，对胃蛋白酶原血浆浓度和胃肠道黏膜的影响，以及这些变化与胃肠道黏膜损伤的相关性。
纳入60例正在接受非甾体抗炎药（NSAID）慢性治疗的风湿性疾病患者。经过7天的导入期后，患者被随机分配接受为期14天的右布洛芬治疗（A组；第1 - 3天=每日3次，每次400mg；第4 - 14天=每日2次，每次400mg）、布洛芬治疗（B组；第1 - 3天=每日3次，每次800mg；第4 - 14天=每日2次，每次800mg）或双氯芬酸治疗（C组；第1 - 3天=每日3次，每次50mg；第4 - 14天=每日2次，每次50mg）。在第15天进行上消化道内镜检查，在第16天进行胶囊内镜检查（每组7例患者），并测定胃蛋白酶原血浆浓度（基础值和第15天的值）。设计了一个半定量量表用于评估胃肠道黏膜。
治疗组之间、胃肠道损伤分级之间或基础值与治疗后测定值之间，血浆胃蛋白酶原水平均无差异。与布洛芬（5%；p = 0.003）和双氯芬酸（30%；p = 无显著差异）相比，右布洛芬组出现胃十二指肠黏膜损伤的患者较少（42.1%）。使用右布洛芬治疗的患者中，没有肠道黏膜损伤的比例也更高（42.86%，双氯芬酸组为28.7%，布洛芬组为14.29%；p = 0.0175）。A、B、C三组的临床不良事件发生率相似（分别为28%、38%和34%）。
右布洛芬导致胃十二指肠和肠道黏膜损伤的发生率较低。这种作用不是由血浆胃蛋白酶原水平的改变介导的。
