Antiproliferative activity is present in bladder but not renal pelvic urine from interstitial cystitis patients

被引:31
作者
Keay, S
Warren, JW
Zhang, CO
Tu, LM
Gordon, DA
Whitmore, KE
机构
[1] Univ Maryland, Sch Med, Vet Adm Med Ctr, Dept Med,Div Infect Dis, Baltimore, MD 21201 USA
[2] Baltimore Vet Affiars Maryland Hlth Care Syst, Res Serv, Baltimore, MD USA
[3] Allegheny Univ Hlth Sci, Grad Hosp, Philadelphia, PA 19102 USA
[4] Univ Penn, Philadelphia, PA 19104 USA
关键词
interstitial cystitis; cytotoxin;
D O I
10.1016/S0022-5347(05)68345-0
中图分类号
R5 [内科学]; R69 [泌尿科学(泌尿生殖系疾病)];
学科分类号
1002 ; 100201 ;
摘要
Purpose: To determine whether an antiproliferative urine factor that we previously discovered to be specific for urine from interstitial cystitis (IC) patients originated in the lower urinary tract or a more proximal site. Materials and Methods: Sequential catheterized urine specimens were collected under sterile conditions from the bladder and renal pelvis of 20 IC patients and one control patient (with stress incontinence). Antiproliferative activity was determined by H-3-thymidine incorporation of primary normal adult bladder epithelial cells cultured with pH- and osmolality-corrected bladder or ureteral urine specimens; significant inhibition was defined as a change in H-3-thymidine incorporation greater than 2 standard deviations from the mean of control cells. Results: Bladder urine specimens from 19 of 20 IC patients significantly inhibited H-3-thymidine incorporation as compared to cell medium alone (mean change for bladder specimens = -68.7 +/- 7.5%), while a renal pelvic specimen from only 1 of 20 IC patients inhibited proliferation significantly (mean change for renal pelvic specimens = 3.2 +/- 3.4%) (p <.001 by Fisher's exact test). The one inhibitory IC renal pelvic specimen inhibited by 31% while a bladder specimen obtained during the same procedure inhibited by 94%. In comparison, neither bladder nor renal pelvic urine from the control patient had inhibitory activity. Conclusions: The antiproliferative factor previously found in the urine of IC patients appears to be made and/or activated in the distal ureter or urinary bladder.
引用
收藏
页码:1487 / 1489
页数:3
相关论文
共 10 条
[1]  
*DIV KIDN UR HEM D, 1989, AM J KIDNEY DIS, V13, P353
[2]  
Held PJ, 1990, Interstitial Cystitis, P29, DOI 10.1007/978-1-4471-3293-6_4
[3]  
HOHLBRUGGER G, 1987, EUR UROL, V13, P83
[4]   CLINICAL-FEATURES AND SPECTRUM OF LIGHT MICROSCOPIC CHANGES IN INTERSTITIAL CYSTITIS [J].
JOHANSSON, SL ;
FALL, M .
JOURNAL OF UROLOGY, 1990, 143 (06) :1118-1124
[5]   A hypothesis for the etiology of interstitial cystitis based upon inhibition of bladder epithelial repair [J].
Keay, S ;
Warren, JW .
MEDICAL HYPOTHESES, 1998, 51 (01) :79-83
[6]   Decreased H-3-thymidine incorporation by human bladder epithelial cells following exposure to urine from interstitial cystitis patients [J].
Keay, S ;
Zhang, CO ;
Trifillis, AL ;
Hise, MK ;
Hebel, JR ;
Jacobs, SC ;
Warren, JW .
JOURNAL OF UROLOGY, 1996, 156 (06) :2073-2078
[7]   A diagnostic in vitro urine assay for interstitial cystitis [J].
Keay, S ;
Zhang, CO ;
Hise, MK ;
Hebel, JR ;
Jacobs, SC ;
Gordon, D ;
Whitmore, K ;
Bodison, S ;
Gordon, N ;
Warren, JW .
UROLOGY, 1998, 52 (06) :974-978
[8]   EPITHELIAL DYSFUNCTION IN NONBACTERIAL CYSTITIS (INTERSTITIAL CYSTITIS) [J].
PARSONS, CL ;
LILLY, JD ;
STEIN, P .
JOURNAL OF UROLOGY, 1991, 145 (04) :732-735
[9]  
RUGGIERI MR, 1994, UROL CLIN N AM, V21, P163
[10]  
TRIFILLIS AL, 1993, IN VITRO CELL DEV-AN, V29A, P908