頑固性間質性膀胱炎/骨盆腔疼痛症候群病患使用體外震波治療之症狀及尿液生化標記之治療效果

沈元琦¹、Pradeep Tyagi²、李偉嘉¹、Michael Chancellor³、莊燿吉¹

¹高雄長庚紀念醫院 泌尿科

²Department of Urology, School of Medicine, University of Pittsburgh, USA

³Department of Urology, Beaumont Health System Oakland University William Beaumont School of Medicine Royal, USA

Improves symptoms and urinary biomarkers in refractory interstitial cystitis/bladder pain syndrome patients randomized to extracorporeal shock wave therapy versus placebo

Yuan-Chi Shen¹、Pradeep Tyagi²、Wei-Chia Lee¹、Michael Chancellor³、Yao-Chi Chuang¹

¹Department of Urology, Kaohsiung Chang Gung Memorial Hospital, Kaohsiung, Taiwan

²Department of Urology, School of Medicine, University of Pittsburgh, USA

³Department of Urology, Beaumont Health System Oakland University William Beaumont School of Medicine Royal, USA

Purpose:

Extracorporeal shock wave therapy (ESWT) has been shown to improve symptoms in patients with interstitial cystitis/bladder pain syndrome (IC/BPS); however, there is a lack of objective evidence. We measured change of urinary biomarker levels and symptoms in 25 patients with IC/BPS received ESWT or placebo once a week for 4 weeks.

Material and methods:

Urines were collected from participants at baseline,4 and 12 weeks post treatment. A representative 41 inflammatory growth factors, cytokines, and chemokines in urine were measured using a MILLIPLEX immunoassay kit. Symptom bother was assessed by O’Leary-Sant symptom scores (OSS), and visual analog scale (VAS) for pain.

Results:

The ESWT group exhibited a significant reduction in the OSS and VAS compared to the placebo group 4 weeks post-treatment (P < 0.05), and the effects were persistent at 12 weeks. The difference in urinary markers change in ESWT versus placebo was P = 0.054 for IL4, P = 0.013 for VEGF, and P = 0.039 for IL9 at 4 weeks. The change of urine biomarker was not significant in other biomarkers or all the measured proteins at 12 weeks.

Conclusion:

The current data suggest that IL4, IL9, and VEGF mediation may be involved in its pathophysiologic mechanisms and response to LESW treatment.