Abstract
Itch is a major symptom of atopic dermatitis, for which there are no sufficiently effective therapies. Recent studies have shown that sensitization for itch plays a crucial role in pruritus of atopic dermatitis. Several inflammatory mediators and neurotrophic factors have been demonstrated to sensitize peripheral neurons. Moreover, continuous activation of peripheral C-nerves leads to sensitization of secondary afferent neurons in the spinal cord. Sensitization leads not only to lowering of itch sensation but also to attenuated inhibition of itch by pain. Therefore, even such stimuli that normally evoke pain and suppress itch would cause itch. This could explain the vicious itch-scratch cycle observed in patients with atopic dermatitis. Our recent study has shown that inflammatory pain mediators like bradykinin and serotonin also evoke itch in atopic dermatitis, which cannot be suppressed by antihistamines. This implies that anti-inflammatory medications like topical application of corticosteroid should be the most promising anti-pruritic strategy in atopic dermatitis.
