Assistant Professor, University of Kentucky, College of Medicine, Department of Anesthesiology, 800 Rose Street Suite, N 201, Lexington, KY 40536, USA.
Expert Rev Clin Pharmacol. 2008 Mar;1(2):291-7. doi: 10.1586/17512433.1.2.291.
Opioid-induced pain or opioid tolerance should be considered when opioid therapy fails to provide expected analgesic effects or when there is unexplainable pain exacerbation following opioid treatment. As a result, an increase in the opioid dosage may not be the solution to ineffective opioid therapy for chronic pain management. A decrease in the opioid mass may actually provide pain relief in many instances. At one time, it was anticipated that opioid-induced pain was related to upregulation of NMDA receptors with a downregulation of mu receptors. However, there is growing evidence to suggest the opioid receptor-based hyperalgesic mechanism may be directly modulated by the NMDA receptor. Furthermore, the mechanism that causes opioid tolerance may be the same mechanism that causes opioid-induced pain. Current evidence suggests that opioid-induced pain sensitivity could be prevented by interrupting the cellular and molecular changes associated with the development of opioid tolerance. Continued research may lead the way to a new period in which patients prone to opioid-induced pain could be identified, allowing one to tailor pharmacologic pain therapy to each patient.
当阿片类药物治疗未能提供预期的镇痛效果，或者在阿片类药物治疗后出现无法解释的疼痛加剧时，应考虑阿片类药物引起的疼痛或阿片类药物耐受。因此，增加阿片类药物剂量可能不是治疗慢性疼痛管理中无效阿片类药物治疗的解决方案。在许多情况下，减少阿片类药物的剂量实际上可以缓解疼痛。曾经，人们预计阿片类药物引起的疼痛与 NMDA 受体的上调和 mu 受体的下调有关。然而，越来越多的证据表明，基于阿片受体的痛觉过敏机制可能直接受到 NMDA 受体的调节。此外，导致阿片类药物耐受的机制可能与导致阿片类药物引起的疼痛的机制相同。目前的证据表明，通过中断与阿片类药物耐受发展相关的细胞和分子变化，可以预防阿片类药物引起的疼痛敏感性。进一步的研究可能会开创一个新的时期，使那些容易发生阿片类药物引起的疼痛的患者能够被识别出来，从而使每个人都能根据每个患者的情况量身定制药物治疗疼痛。
