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  • Title: Use of cyclooxygenase-2 inhibitor for prevention of urethral strictures secondary to transurethral resection of the prostate.
    Author: Sciarra A, Salciccia S, Albanesi L, Cardi A, D'Eramo G, Di Silverio F.
    Journal: Urology; 2005 Dec; 66(6):1218-22. PubMed ID: 16360446.
    Abstract:
    OBJECTIVES: To analyze whether the addition of a cyclooxygenase (COX)-2 inhibitor after transurethral resection of the prostate (TURP) offers an advantage compared with TURP alone in reducing postoperative urethral strictures. At urethroscopy, stenosis of the urethra with a circumference of less than 19 mm was defined as stricture. METHODS: This was a prospective, unblinded, randomized, single-center study. Between December 2001 and December 2003, 96 consecutive men with benign prostatic hyperplasia underwent TURP. After TURP, patients were randomly assigned to receive or not receive a COX-2 inhibitor (rofecoxib 25 mg/day). In the group given the COX-2 inhibitor, the therapy was started at catheter removal and continued for 20 days. Follow-up was performed on an outpatient basis after 1 month. A diagnosis of postoperative urethral stricture was assessed during a follow-up of 12 months. RESULTS: At the 1-month visit, the mean and median improvement in the peak urinary flow rate from preoperative values was +6.25 +/- 3.76 mL/s (median 7.30) in the no COX-2 inhibitor group and +9.42 +/- 3.06 mL/s (median 8.75) in the COX-2 inhibitor group. The improvement was significantly (P < 0.0001) greater for the group treated with the COX-2 inhibitor. At 1 year of follow-up, a urethral stricture had been diagnosed in 8.3% of all cases; in particular, in 17% and 0% of cases in the no COX inhibitor group and COX-2 inhibitor group, respectively. Post-TURP COX-2 inhibitor therapy was significantly (P = 0.0039) and inversely (r = -0.2876) associated with urethral stricture development. CONCLUSIONS: We suggest that limited postoperative treatment with a COX-2 inhibitor can effectively prevent post-TURP urethral stricture development by specifically interfering with the inflammatory processes that can precede scar formation.
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