Pathophysiology and therapy of pruritus in allergic and atopic diseases

被引:97
作者
Buddenkotte, J. [3 ]
Steinhoff, M. [1 ,2 ]
机构
[1] Univ Calif San Francisco, Dept Dermatol, San Francisco, CA 94143 USA
[2] Univ Calif San Francisco, Dept Surg, San Francisco, CA 94143 USA
[3] Univ Hosp Munster, Dept Dermatol, Boltzmann Inst Cell & Immunobiol, Munster, Germany
关键词
atopic dermatitis; itch; nerve; pathophysiology; pruritus; therapy; HISTAMINE-INDUCED ITCH; PLATELET-ACTIVATING-FACTOR; MUSCARINIC ACETYLCHOLINE-RECEPTORS; HUMAN EPIDERMAL-KERATINOCYTES; POSITRON-EMISSION-TOMOGRAPHY; INTERFERON-GAMMA-THERAPY; BLOOD MONONUCLEAR-CELLS; RANTES MESSENGER-RNA; SUBSTANCE-P RECEPTOR; SENSORY NERVE-FIBERS;
D O I
10.1111/j.1398-9995.2010.01995.x
中图分类号
R392 [医学免疫学];
学科分类号
100102 ;
摘要
P>Pruritus (itch) is a major characteristic and one of the most debiliating symptoms in allergic and atopic diseases and the diagnostic hallmark of atopic dermatitis. Pruritus is regularly defined as an unpleasant sensation provoking the desire to scratch. Although we achieved rather good knowledge about certain inducers of itch such as neuropeptides, amines, mu-opioids, cytokines and proteases, for example, less is known about the pathophysiological specifities among the different diseases, and the therapeutic consequences which may derive thereoff. This review dissects the role of mediators, receptors and itch inhibitors on peripheral nerve endings, dorsal root ganglia, the spinal cord and the CNS leading to the amplification or - vice versa - suppression of pruritus. As the treatment of pruritus in allergic and atopic skin disease is still not satisfactory, knowing these pathways and mechanisms may lead to novel therapeutic approaches against this frequently encountered skin symptom.
引用
收藏
页码:805 / 821
页数:17
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