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Impaired diffuse noxious inhibitory controls: an additional mechanism of pain in chronic pancreatitis?

机译:弥漫性有毒抑制对照障碍:慢性胰腺炎疼痛的额外机制?

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摘要

In general, treatment of underlying pain mechanisms yields the best results. The study by Olesen et al reported in this issue of Clinical Gastro enter ology and Hepatology suggests there may be more than a single mechanism present in chronic pancreatitis (CP) patients. There clearly is evidence of end-organ damage in CP, but how this damage is sensed may be different in these patients than in other tissue damage-related disorders. Olesen et al showed impaired endogenous pain control systems are present in subjects with CP by showing reduced diffuse noxious inhibitory controls (DNICs). In doing this, Olesen et al place CP in the company of painful disorders such as irritable bowel syndrome, fibromyalgia, chronic fatigue syndrome, temporomandibular disorder, atypical facial pain, chronic tension headaches, and other hypersensitivity disorders with limited identifiable pathology2"5 that have similar deficits in DNIC and separates CP from other disorders such as rheumatoid arthritis,6 which has DNIC mechanisms intact.
机译:一般来说,潜在的疼痛机制的治疗产生了最佳结果。 Olesen等人在这个问题上报道了临床胃肠进入物学和肝脏的研究表明,可能存在慢性胰腺炎(CP)患者中存在的单一机制。显然存在CP中末端器官损伤的证据,但是如何感测到这种伤害在这些患者中可能不同于其他组织损伤相关疾病。 Olesen等人显示出在CP的受试者中存在受损的内源性疼痛控制系统,通过显示降低的弥漫性有毒抑制控制(DNIC)。在这样做的情况下,奥尔森等人在公司的痛苦疾病中,例如肠症综合征,纤维肌痛,慢性疲劳综合征,颞下颌疾病,非典型面部疼痛,慢性紧张性疾病和其他具有有限的识别病理2“5的过敏障碍的患者DNIC中的类似缺陷并将CP与类风湿性关节炎等其他疾病分离,6,其中具有DNIC机制。

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