Ständer Sonja, Steinhoff Martin
Department of Dermatology and Ludwig Boltzmann Institute for Cell Biology and Immunobiology of the Skin, University of Münster, Münster, Germany.
Exp Dermatol. 2002 Feb;11(1):12-24. doi: 10.1034/j.1600-0625.2002.110102.x.
Pruritus is an essential feature of atopic dermatitis (AD) and the diagnosis of active AD cannot be made without the history of itching. Because of the high impact on life quality, most of the patients measure the severity of eczema by the intensity of pruritus rather than appearance of skin lesions. However, although pruritus is a cardinal symptom of AD, its mechanism and association with the cutaneous nervous system is not completely understood. Recently, a considerable progress has been achieved in clarifying the complex pathophysiology of pruritus in AD. As a cutaneous sensory perception, itch requires excitation of neuropeptide-containing free nerve endings of unmyelinated nociceptor fibers. It is well known that histamine and acetylcholine provoke itch by direct binding to 'itch receptors' and several mediators such as neuropeptides, proteases or cytokines indirectly via histamine release. Interestingly, some variations of these complex mechanisms could be demonstrated in patients with AD. This review highlights the recent knowledge of different mechanisms which may be involved in regulating pruritus in patients with AD potentially leading to new therapeutic applications for the treatment of itch in AD.
瘙痒是特应性皮炎（AD）的一个基本特征，没有瘙痒病史就无法做出活动性AD的诊断。由于对生活质量影响很大，大多数患者通过瘙痒强度而非皮肤病变外观来衡量湿疹的严重程度。然而，尽管瘙痒是AD的主要症状，但其机制以及与皮肤神经系统的关联尚未完全明确。最近，在阐明AD中瘙痒的复杂病理生理学方面取得了相当大的进展。作为一种皮肤感觉，瘙痒需要无髓伤害性感受器纤维中含神经肽的游离神经末梢被激活。众所周知，组胺和乙酰胆碱通过直接结合“瘙痒受体”引发瘙痒，而一些介质如神经肽、蛋白酶或细胞因子则通过组胺释放间接引发瘙痒。有趣的是，这些复杂机制的一些变体在AD患者中得到了证实。本综述重点介绍了可能参与调节AD患者瘙痒的不同机制的最新知识，这可能会为AD瘙痒治疗带来新的治疗应用。
