Clinical Effects of Cycloxygenase-2 Inhibitor on Nocturia.
- Author:
Hyun Suk YOON
1
;
Jae Yeong YOO
;
Kye Min CHUN
;
Hana YOON
Author Information
1. Department of Urology, College of Medicine, Ewha University, Seoul, South Korea. wowhana@ewha.ac.kr
- Publication Type:Original Article
- Keywords:
Nocturia;
COX-2 inhibitor
- MeSH:
Cholinergic Antagonists;
Cyclooxygenase 2 Inhibitors;
Deamino Arginine Vasopressin;
Drug Therapy;
Follow-Up Studies;
Humans;
Nocturia*;
Vasopressins
- From:Journal of the Korean Continence Society
2009;13(1):67-72
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
PURPOSE: This study aimed to examine the effects of cyclooxgenase-2 inhibitors on patients with nocturia, whose symptoms persisted after the use of first-line drug therapy, such as alpha blockers and/or anticholinergics. MATERIALS AND METHODS: Thirty-three patients whose symptoms persisted after more than three months of first-line drug therapy were chosen to receive additional COX-2 inhibitors or antidiuretic hormones orally. Seven patients (group 1) were given 80mg of zaltoprofen at night, while 15 (group 2) were given 100mg of nimesulide at night. Desmopressin acetate (0.2mg) was administered at night to 11 patients (group 3) as a control group. Median follow up was 35 days (range, 28~90 days). RESULTS: In 25 patients (75.8%), the severity of nocturia was reduced. The median decline of nocturia in the COX-2 inhibitor groups (groups 1 and 2) was once, and it was statistically significant (p<0.001), while the median decline in each of these groups was twice (p=0.026) and once (p=0.002), respectively. The reduction of nocturia in the control group was once (p=0.011). The differences in reduction between the COX-2 inhibitor group and the control group were not statistically significant (p=0.418). CONCLUSIONS: The effects of the COX-2 inhibitors were not significantly different from those of desmopressin. Combination therapy with COX-2 inhibitors can effectively reduce nocturia in patients with refractory nocturia, following first-line drug therapy.
