塞内昔布和奈普生对肝硬化伴腹水的非氮质血症患者肾功能的影响

作     者：Clària J. Kent J.D. López- Parra M. V. Arroyo 杨瑗 

作者机构：Liver Unit Institut de Malalties Digestives Hospital Clinic Villarroel 170 Barcelona 08036 Spain 

出 版 物：《世界核心医学期刊文摘（胃肠病学分册）》 (Core Journals in Gastroenterology)

年 卷 期：2005年第1卷第7期

页      面：37-38页

学科分类：1002[医学-临床医学] 100201[医学-内科学(含：心血管病、血液病、呼吸系病、消化系病、内分泌与代谢病、肾病、风湿病、传染病)] 10[医学] 

主　　题：塞内昔布 氮质血症 奈普生 肾功能 萘普生 腹水患者 安慰剂对照 肾脏功能 血小板功能 尿钠增多 

摘      要：Nonselective inhibition of cyclooxygenase (COX) by nonsteroidal anti- inflam matory drugs frequently induces renal failure in decompensated cirrhosis. Studie s in experimental cirrhosis suggest that selective inhibitors of the inducible i soform COX- 2 do not adversely affect renal function. However, very limited inf ormation is available on the effects of these compounds on renal function in hum an cirrhosis. This investigation consists of a double- blind, randomized, place bo- controlled trial aimed at comparing the effects of the selective COX- 2 in hibitor celecoxib (200 mg every 12 hours for a total of 5 doses) on platelet and renal function and the renal response to furosemide (40 mg intravenously) with those of naproxen (500 mg every 12 hours for a total of 5 doses) and placebo in 28 patients with cirrhosis and ascites. A significant reduction (P 0 .05) in g lomerular filtration rate (113 ± 27 to 84 ± 22 mL/min), renal plasma flow (5 92 ± 158 to 429 ± 106 mL/min) and urinary prostaglandin E2 excretion (3430 ± 430 to 2068 ± 549 pg/min) and suppression of the diuretic (urine volume: 5 61 ± 128 to 414 ± 107 mL/h) and natriuretic (urine sodium: 53 ± 13 to 34 ± 10 mEq/h) responses to furosemide were observed in the group of patients tre ated with naproxen but not in the other two groups. Naproxen, but not celecoxib or placebo, significantly inhibited platelet aggregation (72% ± 8% to 47% ± 8% , P 0 .05) and thromboxane B2 production (41 ± 12 to 14 ± 5 pg/mL, P 0.05). In conclusion, our results indicate that short- term administration of celecoxib does not impair platelet and renal function and the response to diu retics in decompensated cirrhosis.