PN does not seem to represent a characteristic symptom of one disease only. Multiple pruritogenic diseases are linked to evolution and improvement of PN upon treatment. Atopic predisposition is a major factor in nearly half of PN patients. The large collective of the present study helped detect a broad range of underlying diseases and thus to provide recommendations for rational diagnostics.

Chronic pruritus, one of the main symptoms in dermatology, is often intractable and has a high impact on patient's quality of life. Beyond dermatologic disorders, chronic pruritus is associated with systemic, neurologic as well as psychologic diseases. The pathogenesis of acute and chronic (＞6 weeks duration) pruritus is complex and involves in the skin a network of resident (e.g., sensory neurons) and transient inflammatory cells (e.g., lymphocytes). In the skin, several classes of histamine-sensitive or histamine-insensitve C-fibers are involved in itch transmission. Specific receptors have been discovered on cutaneous and spinal neurons to be exclusively involved in the processing of pruritic signals.Chronic pruritus is notoriously difficult to treat. Newer insights into the underlying pathogenesis of pruritus have enabled novel treatment approaches that target the pruritusspecific pathophysiological mechanism. For example, neurokinin-1 antagonists have been found to relieve chronic pruritus. (Ann Dermatol 23(1) 1∼11, 2011)

In the present study, a RCLASI was developed by experts, and reliability studies supported the validity and applicability of the revised scoring instrument for CLE. Thus, the RCLASI is a valuable instrument in multicentre studies and for the clinical evaluation of activity and damage in different disease subtypes.

Phototherapy has still great importance in the treatment of atopic dermatitis, though costs, compliance, and long-term risks narrow its relevance. In spite of its long history, up to now, the therapeutic regimes are mostly empirical. Narrowband UVB und UVA1 are the most frequently applied regimens in atopic dermatitis with proven efficacy. However, even for these modalities randomized prospective and controlled studies are still pending. Advances in photoimmunology and molecular biology had demonstrated that phototherapy targets inflammatory cells, alters cytokine production, and has a significant antimicrobial effect within atopic skin. This paper summarizes the current literature on the different regimes of phototherapy and also discusses therapeutic modalities like photochemotherapy and extracorporeal photopheresis. These more complex regimes should be restricted to severe cases of atopic dermatitis, which are refractory to topical treatment.

Pruritus is an integral part of the patient's symptoms in numerous dermatological and systemic diseases in humans and animals. Comparable to chronic pain, pruritus can have a dramatic impact on the quality of life of the patient. In recent years, pruritus has been defined as an autonomous, pain-independent sensation, and itch-specific neurons, mediators, spinal neurons and cortical areas have been identified. These observations have not only improved our understanding of the neurobiology of itch but will also lead to improved diagnosis and to the development of new and more efficient therapeutic options. This article reviews the role of itch fibres and their response to various mediators of pruritus including histamine, vasoactive intestinal peptide (VIP), calcitonin gene-related peptide (CGRP), and substance P (SP), and opioids. Substances that may be involved in the induction or modulation of itch may be termed pruritogenic mediators and examples discussed include proteases, lipid mediators, neuropeptides, opioids and various cytokines. There is no single, generally accepted clinical classification of chronic pruritus. In the past pruritus has been classified on the basis of the neuroanatomical origin and on the potential underlying disease. Therapeutic options for the management of pruritus are discussed including topical and systemic therapies, assuming that trigger factors have been eliminated where possible. Topical agents may include capsaicin, the calcineurin inhibitors tacrolimus and pimecrolimus, and cannabinoid agonists such as N-palmitoyl ethanolamine. Systemic therapies may include antihistamines, anticonvulsants, opiate receptor antagonist or agonists, antidepressants, ciclosporin, and UV light.