ABSTRACT
Pruritus, regularly defined as an unpleasant sensation provoking the desire to scratch,1 is a diagnostic hallmark of atopic dermatitis (AD).2,3 As a cutaneous sensory perception, itch is excited on neuropeptide-containing free nerve endings of unmyelinated nociceptor fibres. It is known that several mediators such as neuropeptides, proteases, or cytokines provoke itch by direct binding to itch receptors or indirectly via histamine release. Although great efforts have been made during the last years, the pathophysiology of pruritus in AD is not fully understood but several facts explain its intensity and therapy refractoricity demanding a specific management.
