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Copyright of Journal der Deutschen Dermatologischen Gesellschaft is the property of Wiley-Blackwell and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Journal der Deutschen Dermatologischen Gesellschaft is the property of Wiley-Blackwell and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Chronic pruritus (CP) is a highly prevalent, difficult-to-treat, and burdensome condition. Today, multiple topical and systemic therapy concepts are available for the treatment of CP. Current guidelines recommend, besides topical treatments, the use of a vast array of mostly off-label systemic drugs with different mechanisms, including antihistamines, gabapentinoids, antidepressants, immunosuppressive drugs, and μ‑opioid receptor antagonists. The choice of the right agent depends on the indication, the safety profile of the drug, and patient-specific features, such as comorbidities and comedication. Thanks to a deeper understanding of the pathophysiology of CP, novel drugs have been developed and have already shown antipruritic efficacy in clinical studies and case reports. Of note, phosphodiesterase‑4 inhibitors as topical agents and monoclonal antibodies, neurokinin‑1 receptor antagonists, Janus kinase inhibitors, and opioid receptor modulators as systemic agents are in the frontline of innovative CP treatment. Other promising targets include structures of the peripheral and central nervous system which are involved in itch signaling. This article provides an overview of currently available topical and systemic therapies for CP and their indications and discusses novel innovative agents and promising new targets in CP.

The care of patients with chronic pruritus as a symptom of a wide variety of underlying diseases continues to confront dermatologists with diagnostic and therapeutic challenges. However, a structured history and a physical examination may already substantially help in narrowing down the number of potential differential diagnoses. Apart form reducing the intensity of pruritus, identification and appropriate treatment of the underlying disease are important needs of patients. If these goals doesn't lead to improvement of itch, current guidelines provide a number of topical and systemic therapies for symptomatic treatment. Various skin lesions (for example, xerosis caused by irritant substances, secondary scratch lesions) prompt patients to consult a dermatologist, but most cases require an interdisciplinary therapeutic approach to identify potential internal medicine, neurologic, or psychosomatic aspects. Although great strides have been made in basic research, specific therapies are still rare, and a precise knowledge of the legal framework for the implementation of guidelines (for example, off-label use) is essential. This CME article gives an overview of the causes of and treatment options for chronic pruritus and discusses both advances in basic research as well as progress in clinical knowledge., (© 2015 Deutsche Dermatologische Gesellschaft (DDG). Published by John Wiley & Sons Ltd.)

The pathogenesis of acute and chronic (> 6 weeks duration) pruritus is complex and involves in the skin a network of resident cells (e. g., mast cells, keratinocytes, sensory neurons) and transient inflammatory cells (e. g., eosinophils). Though pruritus and pain show overlapping mechanisms, recent studies have provided evidence that pruritus and pain pathogenesis differ in important points. In the skin, the sensory C-nerve fibers have been investigated intensively. Several classes of histamine-sensitive or histamine-insensitve C-fibers have been described. Epidermal and dermal sensory nerve fibres are now assumed to be of major importance in pruritus induction. They interact with keratinocytes, inflammatory cells such as T lymphocytes, eosinophils and basophils which have been shown to release multiple pruritogenic mediators (e.g., nerve growth factor, interleukin-31) which lead to activation, sensitization and sprouting of skin nerves. Specific receptors have been discovered on cutaneous and spinal neurons to be exclusively involved in the processing of pruritic signals. Just recently, the gastrin-releasing peptide receptor (GRPR) was identified on spinal neurons that are crucially involved in pruritus but not pain processing. Chronic pruritus is notoriously difficult to treat. Newer insights into the underlying pathogenesis of pruritus have enabled novel treatment approaches that target the pruritus-specific pathophysiological mechanism. For example, kappa-opioid receptor agonists and neurokinin-1 antagonists have been found to relieve chronic pruritus., (© The Authors • Journal compilation © Blackwell Verlag GmbH, Berlin.)

Objective: This study investigated whether dermatology inpatients with chronic pruritus benefit from an 1-hour psychoeducational group therapy, adapted from educational programmes for patients with atopic dermatitis. Such a symptom-specific intervention for patients with chronic pruritus has not been evaluated before., Method: 91 of the 315 group participants (28.9 %) and 175 of the 318 patients who had been admitted to the hospital without group therapy (55.0 %) were examined at admission and discharge using standardised questionnaires (Adjustment to Chronic Skin Diseases Questionnaire, Itch-Cognition Questionnaire) and a Visual Analogue Scale for itch intensity (randomized pre-post study)., Result: Evaluation of the standardised questionnaires and of the change in pruritus intensity indicated no additive benefit of group intervention, both for the whole sample and for subgroups with chronic pruritus., Discussion: The results indicate either that group intervention in this form is not effective or that the dermatological medical treatment of the patients is so efficient that the intervention brings no added benefit. Perhaps an intervention of 1 hour is simply too short. Further conceptual developments of the psychoeducational programme are necessary.

Background: Aquagenic pruritus (AP) can be induced by systemic diseases. The distribution of underlying diseases in a representative patient collective has not been investigated. This retrospective study aimed to determine the frequency and pruritus-specific parameter of systemic diseases in a series of patients., Patients and Methods: Data of 39 patients with AP (24 f, 15 m; mean age: f: 51.3 ± 20.1, m: 57.2 ± 15.0 years) were obtained and statistically evaluated as follows: demographic data, pruritus characteristics, underlying diseases, family history., Results: 30.8 % of patients exhibited polycythemia vera or myelofibrosis (Group 1: G1), in 69.2 % (G2) no underlying disease was found. 25.6 % had lactose intolerance as possible contributing factor. Women were significantly more common in G2 (p < 0.01), with a lower mean age (p < 0.01) and longer duration of AP (18.9 years, p < 0.01)., Conclusions: AP occurs frequently with polycythemia vera. Other underlying diseases are rare; in over half of the patients no cause can be detected. In 25 % lactose intolerance is present which possibly acts as co-factor. Demographic parameters (age, gender) allow estimation of the possible underlying disease in AP. Pruritus characteristics are similar in all groups and not helpful in determining the origin of AP., (© The Authors • Journal compilation © Blackwell Verlag GmbH, Berlin.)

Background: Postherpetic neuralgia is a frequent adverse event in herpes zoster patients and difficult to treat. Conventional analgetic therapy often fails to reduce the burning pain transmitted by unmyelinated nerve fibers. These nerves express cannabinoid receptors which exert a role in modulation of nociceptive symptoms. Therefore, topical therapy with cannabinoid receptor agonist seems likely to suppress local burning pain., Patients and Methods: In an open-labeled trial, 8 patients with facial postherpetic neuralgia received a cream containing the cannabinoid receptor agonist N-palmitoylethanolamine. The course of symptoms was scored with the visual analog scale., Results: 5 of 8 patients (62.5 %) experienced a mean pain reduction of 87.8 %. Therapy was tolerated by all patients. No unpleasant sensations or adverse events occurred., Conclusions: Topical cannabinoid receptor agonists are an effective and well-tolerated adjuvant therapy option in postherpetic neuralgia.

Background: Prurigo nodularis shows intense itching nodules, which are often persistent and therapy refractory. Histological alterations include fibrosis of collagen fibers and presence of inflammatory infiltrate, which partly explains the clinical persistence of lesions. Inflammatory cells may directly contribute to induction and maintenance of pruritus at nerve fibers. Cyclosporine microemulsion (ME) suppresses the migration and proliferation of inflammatory cells and may thereby interfere with pathogenesis of prurigo nodularis. The aim of this investigation was to assess the antipruritic efficiency of cyclosporine ME in therapy of prurigo nodularis., Patients and Methods: 14 patients with prurigo nodularis of diverse origin and failure to previous therapy were treated with oral cyclosporine ME (3 to 5 mg per kg daily). Blood pressure, liver enzymes, renal function and differential blood count were monitored., Results: In 13 of 14 prurigo patients (92.9 %) there was a significant response to monotherapy with cyclosporine ME. The maximal antipruritic effect occurred after 2 weeks to 12 months. Prurigo nodules also healed during therapy. Seven patients (50.0 %) described side effects. In one case the therapy was stopped., Conclusions: Oral cyclosporine ME is an effective therapy for prurigo nodularis of diverse origin. It appears to function by inhibiting dermal inflammatory cells.

Neurotropic invasion of keratoacanthoma (KA) is rare and can easily be missed histologically. A 36-year-old woman developed a KA on the upper lip four weeks after CO(2) laser skin resurfacing; it showed microscopic evidence of perineural invasion. Despite repeated treatment with intralesional methotrexate, the KA recurred after 6 months. She was then treated with ionizing radiation (56 Gy) and has been tumor-free for more than 3 years. Immunohistochemistry showed decreased expression of desmoglein 1 as it is seen in squamous cell carcinomas. In most cases not much importance is attached to perineural invasion which is frequently seen in KA because of the high rate of spontaneous regression. Our case suggests that perineural invasion may be an indicator for aggressive growth of head-and-neck KAs so that histologically-controlled excision is recommended.

Pustular psoriasis is a severe form of psoriasis with a generalized pustular eruption. Since TNF-alpha plays an important role in pustular psoriasis, we treated two patients who had not responded to established therapy regimens with the TNF-alpha antagonist infliximab. Both patients showed significant improvements of their skin eruption and their general condition within three days after treatment and without any side effects. We suggest that infliximab is a therapeutic option for severe therapy-resistant pustular psoriasis because a single well-tolerated dose significantly ameliorates the patient's condition.

Itching is one of the most common complaints affecting the skin. A differentiation is made between pruritus in the absence of inflamed skin lesions, which is frequently associated with a systemic disease, and pruritus caused by inflamed skin, as a symptom of a skin disease. Treatment is directed initially to the underlying illness, and both topical and systemic antipruritic medications are available as flanking measures.

Erythrokeratodermia variabilis (EKV) is a rare autosomal dominant genodermatosis with disturbed epidermal differentiation. Its clinical picture varies from transient, fast moving erythema to persistent brown hyperkeratoses. The gene defect in EKV was recently located on the short arm of chromosome 1 encoding the gap junction protein connexin 31. We report on a 48-year-old patient with sharply circumscribed, scaling erythema on the extremities, buttocks and trunk starting since 30 years of age. Histological investigation showed orthokeratotic hyperkeratosis with focal parakeratosis overlying an acanthotic epidermis. Immunohistochemistry revealed a decreased expression of the gap junction protein connexin 31 as well as increased expression of connexin 43. At the ultrastructural level, widened intercellular spaces in the upper epidermis were present with regular desmosomes, adherens junctions and gap junctions. Epidermal cell proliferation and differentiation are regulated by gap junctions. The mutation in connexin 31 is regarded therefore as causal for the clinical picture of the EKV. The unique upregulation of connexin 43 may occur as a consequence of the Cx31 mutation and temporarily compensate for this defect.

Interstitial granulomatous dermatitis is a rare entity characterized by cutaneous linear strands (the "rope sign") and rheumatoid arthritis. In the past years, 12 other cases have been described with variable cutaneous symptoms. All showed similar histological features, resembling those of granuloma annulare or 'palisaded neutrophilic and granulomatous dermatitis', suggesting a wide spectrum for a single entity. A 60-year-old patient presented with erythematous patches with an indurated, violaceous border resembling the "rope sign" on both flanks. The histological investigation revealed dense diffuse interstitial inflammatory infiltrates composed of eosinophils, neutrophils, lymphocytes, macrophages and multinucleated giant cells in the superficial and deep dermis. In the deep dermis, prominent eosinophilic degenerated collagen fibres with surrounding macrophages ('floating sign') occurred. In contrast to most previously described patients, our patient did not have arthralgias. The skin findings cleared following therapy with hydroxychloroquine.

Pruritus is an unpleasant sensory perception of the skin associated with the desire to scratch. As a physiological nociception, pruritus leads to the removal of harmful agents such as parasites and plants from the skin surface. More often, pruritus occurs as a severe and therapy-refractory symptom of various underlying dermatological and systemic diseases. Comparable to chronic pain, chronic pruritus worsens the general condition and may lead to physical and psychological exhaustion. Until the 1990s, pruritus had been regarded as an incomplete pain sensation. Only recently, itch was defined as a separate, pain-independent sensation with its own mediators, spinal neurons and cortical areas. These observations led to the development of new therapeutic modalities. This paper gives an overview of itch pathophysiology, clinical types and therapies.