From the Division of Urogynecology and Pelvic Reconstructive Surgery, University of Pennsylvania.
Pelvic and Sexual Health Institute, Philadelphia, PA.
Female Pelvic Med Reconstr Surg. 2021 Feb 1;27(2):e418-e422. doi: 10.1097/SPV.0000000000000951.
The pathogenesis of bladder pain is poorly understood. Our hypothesis is that in women with urinary urgency without incontinence, bladder pain is associated with the presence of neurogenic inflammation in the bladder wall and neuroinflammatory biomarkers in the urine.
We conducted a prospective cross-sectional study of women with urinary urgency without incontinence. Urinary symptoms were measured using Female Genitourinary Pain Index. Neuropathic pain, a clinical biomarker of neuroinflammation, was measured using the PainDETECT questionnaire. Inflammatory neuropeptides measured in the urine included nerve growth factor (NGF), brain-derived neurotrophic factor, vascular endothelial growth factor, and osteopontin. Neuropathic pain scores and urinary neuropeptide levels were compared between patients with and without bladder pain using univariable and multivariable analyses.
In 101 women with urinary urgency without incontinence, 62 (61%) were in the bladder pain group (visual analog scale score, ≤ 3), whereas 39 (39%) were in the no bladder pain group. Urinary symptom scores (5.0 ± 3.1 versus 3.5 ± 2.4, P < 0.001) and neuropathic pain scores (13.3 ± 8.6 vs 5.1 ± 4.8, P < 0.001) were significantly higher for the bladder pain group than for the no bladder pain group. On multivariable analysis after controlling for age, body mass index, and severity of urinary urgency, bladder pain score was significantly associated with elevated urinary levels of vascular endothelial growth factor (P = 0.04) and osteopontin (P = 0.02), whereas the neuropathic pain score was significantly associated with an increased NGF level (P = 0.03).
In women with urinary urgency without incontinence, bladder pain is associated with the presence of clinical and urinary biomarkers of neuroinflammation.
膀胱疼痛的发病机制尚不清楚。我们的假设是,在没有尿失禁的急迫性尿失禁女性中,膀胱疼痛与膀胱壁的神经炎症和尿液中的神经炎症生物标志物的存在有关。
我们对没有尿失禁的急迫性尿失禁女性进行了前瞻性横断面研究。使用女性泌尿生殖疼痛指数(Female Genitourinary Pain Index)测量尿症状。使用疼痛检测问卷(PainDETECT questionnaire)测量神经性疼痛,这是神经炎症的临床生物标志物。尿液中测量的炎性神经肽包括神经生长因子(NGF)、脑源性神经营养因子、血管内皮生长因子和骨桥蛋白。使用单变量和多变量分析比较有和无膀胱疼痛的患者之间的神经性疼痛评分和尿液神经肽水平。
在 101 名没有尿失禁的急迫性尿失禁女性中,62 名(61%)为膀胱疼痛组(视觉模拟评分,≤3),39 名(39%)为无膀胱疼痛组。与无膀胱疼痛组相比,膀胱疼痛组的尿症状评分(5.0±3.1 比 3.5±2.4,P<0.001)和神经性疼痛评分(13.3±8.6 比 5.1±4.8,P<0.001)显著更高。在控制年龄、体重指数和尿急严重程度后进行多变量分析,膀胱疼痛评分与血管内皮生长因子(P=0.04)和骨桥蛋白(P=0.02)尿液水平升高显著相关,而神经性疼痛评分与 NGF 水平升高显著相关(P=0.03)。
在没有尿失禁的急迫性尿失禁女性中,膀胱疼痛与临床和尿液神经炎症生物标志物的存在有关。