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Prurigo nodularis (PN) is a chronic skin dermatosis with hyperkeratotic and intensely pruritic nodules. Managing PN-associated itch is difficult because its aetiology is still unknown. This study aimed to investigate the correlation between itch intensity in PN and the expression of a pruritogenic cytokine interleukin (IL)-31, its receptor complex components IL-31 receptor α (IL-31RA) and oncostatin M receptor β (OSMRβ), and oncostatin M (OSM), which is a ligand of OSMR β, through immunofluorescence staining examination. Itch intensity in PN was closely correlated with the number of dermal IL-31(+) cells (Spearman's r = 0.551, p 0.05), dermal IL-31RA(+) cells (r = 0.475, p 0.05) and dermal OSM(+) cells (r = 0.505, p 0.05). In addition, the number of dermal OSMRβ (+) cells was increased in PN (t test, p 0.05), despite not being correlated with itch intensity (Spearman's r = 0.375, p 0.05). Major cellular sources of dermal IL-31 were T cells (27.0% of total IL-31-expressing cells) and macrophages (35.0%), while those of OSM were mainly T cells (49.8%) and mast cells (26.8%). IL-31RA-expressing dermal cells were mostly mast cells (49.3%) and macrophages (36.6%), and OSMRβ was mainly expressed by macrophages (51.8%) in the dermis. These findings indicate that IL-31 (mainly from macrophages and T cells) and OSM (principally from T cells and mast cells) stimulate dermal cells expressing IL-31RA and OSMRβ (e.g. macrophages), which may further promote itch and inflammation in PN. This complex dermal milieu of cell/cytokine/receptor network can be a therapeutic target for PN-associated itch.

Objective Chronic itch can be a debilitating, unrelenting symptom. Over the years, we have advanced our knowledge about immune-mediated itch (eg, atopic dermatitis) and have developed several treatments targeting these immune pathways. Chronic itch that is noninflammatory in nature is more elusive. However, we have gained some understanding of the neural component mediating itch and have made progress in treating this challenging symptom. Data Sources A comprehensive literature search was conducted, and data and literature were reviewed on the topics of chronic itch, its pathophysiology, and nonimmunological treatments for chronic itch that work on the nerves. Study Selections Basic science papers, review articles, case reports, and clinical trial data were considered. Results A variety of topical and systemic therapies targeting the nerves have shown effectiveness in treating patients with chronic itch of different types. Conclusion Treating chronic itch may be challenging, but an arsenal of treatments are available and many are on the horizon as we expand our knowledge of mechanisms of itch and the neural receptors involved.

This article seeks to review the current literature on post-burn pruritus and its treatments, as well as to propose new treatments that may be of potential benefit for these patients. Post-burn pruritus has been reported to affect as many as 93% of patients after a burn injury. Pruritus is extremely distressing to these patients, yet the current state of treatment, mostly antihistamines and emollients, is still widely ineffective in providing relief of itch. Therapies that are effective in treating pruritus and that may act as superior treatment options for patients suffering from post-burn pruritus include gabapentin and pregabalin, topical ketamine-lidocaine-amitriptyline, opioid medications, neurokinin-1 inhibitors, antidepressants, anti-cytokines, PAR-2 inhibitors, and botulinum toxin among others.

Friction alopecia is a non-scarring alopecia that causes hair breakage and may cause trichorrhexis nodosa. We report a case of a 15-year-old girl with self-inflicting friction alopecia that demonstrated broken hairs and proximal trichorrhexis nodosa on dermoscopy. We review various causes of friction alopecia and clinical findings, as well as trichorrhexis nodosa.