Chizh B A, Göhring M, Tröster A, Quartey G K, Schmelz M, Koppert W
Clinical Pharmacology and Discovery Medicine, GlaxoSmithKline, Addenbrooke's Centre for Clinical Investigation, Addenbrooke's Hospital, Hills Road, Cambridge CB2 2GG, UK.
Br J Anaesth. 2007 Feb;98(2):246-54. doi: 10.1093/bja/ael344.
Central sensitization is an important mechanism of neuropathic pain; its human models could be useful for early detection of efficacy of novel treatments. The electrical hyperalgesia model invokes central sensitization by repetitive stimulation of the skin. To assess its predictive value, we have investigated pregabalin, a standard neuropathic pain treatment, and aprepitant, an NK(1) antagonist, as an example of a drug class active in animal models but not in neuropathic pain patients. Furthermore, we explored if combinations of either of these drugs with the COX-2 inhibitor parecoxib could improve its efficacy.
This was a double-blind, two-period, placebo-controlled study using incomplete block design. Thirty-two healthy volunteers received either oral pregabalin (titrated to 300 mg) or aprepitant (titrated to 320 mg), or matching placebo over 6 days before testing. Sensitization was assessed over 3 h; at 2 h, subjects received either parecoxib (40 mg) or saline i.v.
Pregabalin significantly reduced the areas of punctate mechanical hyperalgesia and dynamic touch allodynia vs placebo (both P < 0.0001); no significant reduction in the area of hyperalgesia or allodynia vs placebo was observed with aprepitant. In the pregabalin + parecoxib treated group, the area of allodynia was significantly reduced (P < 0.0001) and the area of hyperalgesia insignificantly attenuated (P = 0.09) vs placebo + parecoxib; no efficacy improvement was observed with aprepitant + parecoxib.
The model can serve to predict analgesic efficacy in early human development and investigate the mechanism of action. The model could also be used to explore efficacy of analgesic combinations to provide a rationale for patient studies.
中枢敏化是神经性疼痛的重要机制;其人体模型可能有助于早期检测新疗法的疗效。电痛觉过敏模型通过重复刺激皮肤引发中枢敏化。为评估其预测价值,我们研究了普瑞巴林(一种标准的神经性疼痛治疗药物)和阿瑞匹坦(一种NK(1)拮抗剂),以作为在动物模型中有活性但在神经性疼痛患者中无活性的一类药物的示例。此外,我们探讨了这两种药物中的任何一种与COX - 2抑制剂帕瑞昔布联合使用是否能提高其疗效。
这是一项采用不完全区组设计的双盲、两阶段、安慰剂对照研究。32名健康志愿者在测试前6天接受口服普瑞巴林(滴定至300毫克)或阿瑞匹坦(滴定至320毫克),或匹配的安慰剂。在3小时内评估敏化情况;在2小时时,受试者静脉注射帕瑞昔布(40毫克)或生理盐水。
与安慰剂相比,普瑞巴林显著减少了点状机械性痛觉过敏和动态触觉异常性疼痛的面积(两者P < 0.0001);阿瑞匹坦与安慰剂相比,痛觉过敏或异常性疼痛面积无显著减少。与安慰剂 + 帕瑞昔布相比,普瑞巴林 + 帕瑞昔布治疗组的异常性疼痛面积显著减少(P < 0.0001),痛觉过敏面积略有减少(P = 0.09);阿瑞匹坦 + 帕瑞昔布未观察到疗效改善。
该模型可用于预测早期人体研究中的镇痛疗效并研究作用机制。该模型还可用于探索镇痛联合用药的疗效,为患者研究提供理论依据。