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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.
Nonselective inhibition of cyclooxygenase (COX) by nonsteroidal anti-inflammatory matory drugs frequently induces renal failure in decompensated cirrhosis. Studie s in an experimental cirrhosis suggest that selective inhibitors of the inducible i soform COX- 2 do not adversely affect renal function. However, very limited information 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 A significant reduction (P <0 .05) in g lularular filtration rate (113 ± 27 to 84 ± 22 mL / min), renal plasma flow (5 92 ± 158 to 429 ± 106 mL / min) and urina ry prostaglandin E2 excretion (3430 ± 430 to 2068 ± 549 pg / min) and suppression of the diuretic (urine volume: 61 ± 128 to 414 ± 107 mL / h) and natriuretic (urine sodium: 53 ± 13 to 34 ± 10 mEq / h) 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 that that short- term administration of celecoxib does not impair platelet and renal function and the response to diu retics in decompensated cirrhosis.