Uvelius Bengt, Andersson Karl-Erik
Department of Urology, Skåne University Hospital, Malmö, Sweden.
Department of Clinical Sciences, Lund University, Lund, Sweden.
Int Neurourol J. 2024 Jun;28(2):75-82. doi: 10.5213/inj.2448134.067. Epub 2024 Jun 30.
Transurethral resection of the prostate, or other methods to decrease outlet resistance usually leads to relief of symptoms in patients with bladder outlet obstruction (BOO). If symptoms of underactivity persist after normalization of outflow conditions, treatment options are limited. In this review, we hypothesize, based on results from basic research, what might become treatment options for such patients in the future. The primary local treatment will still aim at reducing outlet obstruction. We speculate that local secondary treatment in the future might include transplantation of stem cells or mature bladder ganglion cells into the bladder wall. There has been some success in transplanting ganglion cells into the rat bladder. The ganglion cells will sprout into the surrounding tissue but functional connections between the axons of the transplanted neurons, and the detrusor smooth muscle have so far not been demonstrated. Neurotrophins or neurotrimin might be injected into the bladder wall to increase the sprouting of existing or transplanted neurons. Stem cell transplantation has been performed and improves detrusor function, but it has so far, been difficult to demonstrate transplanted stem cells. BOO, persisting detrusor underactivity, and decreased nerve density are often combined with inflammatory activity of the lower urinary tract. NLR family pyrin domain containing 3 (NLRP3) and its messenger RNA (mRNA) as well as cyclooxygenase-2 (Cox-2) mRNA are increased in obstructed bladders. Systemic treatment with the NLRP3 inhibitor glyburide normalized nerve density in rat bladder, and, to some extent, bladder function. It is unclear whether Cox-2 is involved in the decreased nerve density following obstruction, but Cox-2 mRNA increases 5-fold in obstructed bladder. Future therapy against bladder underactivity remaining following relief of obstruction includes either systemic treatment, perhaps by anti-inflammatory drugs, or local treatment by injection of stem cells, mature ganglion cells, and/or neurotrophins or neurotrimin into the bladder wall.
经尿道前列腺切除术或其他降低出口阻力的方法通常可缓解膀胱出口梗阻(BOO)患者的症状。如果在流出道状况恢复正常后,膀胱逼尿肌活动不足的症状仍然持续存在,治疗选择就会很有限。在本综述中,我们基于基础研究的结果推测,未来这类患者可能的治疗选择是什么。主要的局部治疗仍将旨在减轻出口梗阻。我们推测,未来的局部辅助治疗可能包括将干细胞或成熟的膀胱神经节细胞移植到膀胱壁。将神经节细胞移植到大鼠膀胱已取得了一些成功。神经节细胞会向周围组织发出新芽,但到目前为止,尚未证实移植神经元的轴突与逼尿肌平滑肌之间存在功能连接。神经营养因子或神经调节素可能会被注入膀胱壁,以增加现有或移植神经元的新芽生长。干细胞移植已经实施并改善了逼尿肌功能,但到目前为止,很难证实移植的干细胞。BOO、持续的逼尿肌活动不足和神经密度降低通常与下尿路的炎症活动同时存在。在梗阻的膀胱中,含NLR家族pyrin结构域3(NLRP3)及其信使核糖核酸(mRNA)以及环氧化酶-2(Cox-2)mRNA均增加。用NLRP3抑制剂格列本脲进行全身治疗可使大鼠膀胱神经密度正常化,并在一定程度上改善膀胱功能。目前尚不清楚Cox-2是否参与梗阻后神经密度的降低,但在梗阻的膀胱中,Cox-2 mRNA增加了5倍。针对梗阻缓解后仍存在的膀胱活动不足的未来治疗方法包括全身治疗,可能通过抗炎药物,或通过将干细胞、成熟神经节细胞和/或神经营养因子或神经调节素注入膀胱壁进行局部治疗。