Jack Birch Unit of Molecular Carcinogenesis, Department of Biology, University of York, Heslington, York YO10 5DD, UK.
Acta Neuropathol Commun. 2013 Oct 8;1:64. doi: 10.1186/2051-5960-1-64.
There is an emerging association between ketamine abuse and the development of urological symptoms including dysuria, frequency and urgency, which have a neurological component. In addition, extreme cases are associated with severe unresolving bladder pain in conjunction with a thickened, contracted bladder and an ulcerated/absent urothelium. Here we report on unusual neuropathological features seen by immunohistology in ketamine cystitis.
In all cases, the lamina propria was replete with fine neurofilament protein (NFP+) nerve fibres and in most patients (20/21), there was prominent peripheral nerve fascicle hyperplasia that showed particular resemblance to Morton's neuroma. The nerve fascicles, which were positive for NFP, S100 and the p75 low-affinity nerve growth factor receptor (NGFR), were generally associated with a well-developed and in places, prominent, epithelial membrane antigen+/NGFR+ perineurium. This peripheral nerve fascicle hyperplasia is likely to account for the extreme pain experienced by ketamine cystitis patients. Urothelial damage was a notable feature of all ketamine cystitis specimens and where urothelium remained, increased NGFR expression was observed, with expansion from a basal-restricted normal pattern of expression into the suprabasal urothelium.
The histological findings were distinguishing features of ketamine cystitis and were not present in other painful bladder conditions. Ketamine cystitis afflicts predominantly young patients, with unknown long-term consequences, and requires a strategy to control severe bladder pain in order to remove a dependency on the causative agent. Our study indicates that the development of pain in ketamine cystitis is mediated through a specific neurogenic mechanism that may also implicate the urothelium.
氯胺酮滥用与泌尿系统症状的发展之间存在着一种新兴的关联,包括尿痛、尿频和尿急,这些症状都有神经学成分。此外,极端情况下还与严重的无法缓解的膀胱疼痛有关,同时伴有膀胱增厚、收缩和尿路上皮溃疡/缺失。在这里,我们报告氯胺酮膀胱炎中通过免疫组化观察到的不寻常的神经病理学特征。
在所有病例中,固有层都充满了细神经丝蛋白(NFP+)神经纤维,在大多数患者(20/21)中,存在明显的周围神经束状增生,特别类似于莫顿神经瘤。神经束状增生对 NFP、S100 和 p75 低亲和力神经生长因子受体(NGFR)呈阳性,通常与发育良好且在某些部位突出的上皮膜抗原+/NGFR+神经周膜相关。这种周围神经束状增生可能是氯胺酮膀胱炎患者经历极度疼痛的原因。尿路上皮损伤是所有氯胺酮膀胱炎标本的显著特征,在尿路上皮仍然存在的情况下,观察到 NGFR 表达增加,从基底受限的正常表达模式扩展到基底上尿路上皮。
组织学发现是氯胺酮膀胱炎的鉴别特征,在其他疼痛性膀胱疾病中不存在。氯胺酮膀胱炎主要影响年轻患者,其长期后果未知,需要采取策略来控制严重的膀胱疼痛,以消除对致病剂的依赖。我们的研究表明,氯胺酮膀胱炎中疼痛的发展是通过一种特定的神经源性机制介导的,这也可能涉及尿路上皮。