Diminished neurokinin-1 receptor availability in patients with two forms of chronic visceral pain.
Diminished neurokinin-1 receptor availability in patients with two forms of chronic visceral pain.
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DOI：
10.1016/j.pain.2013.02.026
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发表时间：
2013-07
期刊：
影响因子：
7.4
通讯作者：
Mayer EA
中科院分区：
文献类型：
--
作者：
Jarcho JM;Feier NA;Bert A;Labus JA;Lee M;Stains J;Ebrat B;Groman SM;Tillisch K;Brody AL;London ED;Mandelkern MA;Mayer EA
中枢敏感化和外周P物质和神经激肽-1受体（NK-1 R）信号转导失调与炎症性肠病（IBD）和肠易激综合征（IBS）的慢性腹痛相关。虽然正电子发射断层扫描（PET）已经证明，损伤相关的慢性疼痛患者的大脑中NK-1 R的可用性降低，但尚不清楚这些缺陷是否存在于IBD和IBS患者中，这些患者具有病因学上不同的非损伤相关慢性疼痛形式。本研究的目的是确定IBD或IBS患者相对于健康对照（HC）是否表现出NK-1 R脑表达的缺陷，患者人群中表达模式的差异程度，以及这些模式是否与临床参数差异相关。使用含[18 F]SPA-RQ的PET通过定量3组中的结合潜力（BP）来测量NK-1 R的可用性。进行探索性相关分析，以检测NK-1 R BP和身体症状之间的关联。与HC相比，IBD患者在广泛的皮质和皮质下区域网络中存在NK-1 R BP缺陷。IBS患者有类似的，但不太明显的缺陷。这些区域的子集中的BP与每个患者人群中的离散临床参数稳健相关。NK-1 R BP的广泛缺陷发生在IBD中，在较小程度上，IBS;然而，在每个患者人群中，离散的临床参数与NK-1 R BP相关。这表明靶向NK-1 R信号传导的潜在药理学干预可能对治疗IBD和IBS的不同症状最有效。
Central sensitization and dysregulation of peripheral substance P and neurokinin-1 receptor (NK-1R) signaling are associated with chronic abdominal pain in inflammatory bowel disease (IBD) and irritable bowel syndrome (IBS). Although positron emission tomography (PET) has demonstrated that patients with injury-related chronic pain have diminished NK-1R availability in the brain, it is unknown whether these deficits are present in IBD and IBS patients, who have etiologically distinct forms of non-injury-related chronic pain. This study's aim was to determine if patients with IBD or IBS exhibit deficits in brain expression of NK-1Rs relative to healthy controls (HCs), the extent to which expression patterns differ across patient populations, and if these patterns differentially relate to clinical parameters. PET with [18F]SPA-RQ was used to measure NK-1R availability by quantifying binding potential (BP) in the 3 groups. Exploratory correlation analyses were performed to detect associations between NK-1R BP and physical symptoms. Compared to HCs, IBD patients had NK-1R BP deficits across a widespread network of cortical and subcortical regions. IBS patients had similar, but less pronounced deficits. BP in a subset of these regions was robustly related to discrete clinical parameters in each patient population. Widespread deficits in NK-1R BP occur in IBD and, to a lesser extent, IBS; however, discrete clinical parameters relate to NK-1R BP in each patient population. This suggests that potential pharmacological interventions that target NK-1R signaling may be most effective for treating distinct symptoms in IBD and IBS.
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