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Prurigo nodularis (PN) is an inflammatory skin condition characterized by intensely pruritic nodules on the skin. Patients with PN suffer from an intractable itch–scratch cycle leading to impaired sleep, psychosocial distress and a significant disruption in quality of life. The pathogenesis of PN is associated with immune and neural dysregulation, mediated by inflammatory cytokines [such as interleukin (IL)-4, -13, -17, -22 and -31] and neuropeptides (such as substance P and calcitonin gene-related peptide). There is a role for type 2 inflammation in PN in addition to T-helper (Th)17 and Th22-mediated inflammation. The neuroimmune feedback loop in PN involves neuropeptides released from nerve fibres that cause vasodilation and further recruitment of inflammatory cells. Inflammatory cells, particularly mast cells and eosinophils, degranulate and release neurotoxins, as well as nerve growth factor, which may contribute to the neuronal hyperplasia seen in the dermis of patients with PN and neural sensitization. Recent studies have also indicated underlying genetic susceptibility to PN in addition to environmental factors, the existence of various disease endotypes centred around degrees of type 2 inflammation or underlying myelopathy or spinal disc disease, and significant race and ethnicity-based differences, with African Americans having densely fibrotic skin lesions. Dupilumab became the first US Food and Drug Administration-approved therapeutic for PN, and there are several other agents currently in development. The anti-IL-31 receptor A inhibitor nemolizumab is in late-stage development with positive phase III data reported. In addition, the oral Janus kinase (JAK) 1 inhibitors, abrocitinib and povorcitinib, are in phase II trials while a topical JAK1/2 inhibitor, ruxolitinib, is in phase III studies. [ABSTRACT FROM AUTHOR]

There is concern for increased risk of adverse events, particularly periprosthetic joint infection (PJI), following total joint replacement (TJR) in patients with hidradenitis suppurativa (HS) because of a compromised skin barrier and bacterial colonization of lesions. We used the TriNetX health research database to identify patients who had undergone TJR with (n = 1760) and without (n = 1760) HS matched by age, sex, ethnicity, race and risk factors for PJI. Multivariate analysis was performed and revealed that 90-day risk of PJI, reoperation, wound dehiscence, delayed wound healing, emergency room visits and readmission were not increased among patients with HS who underwent TJR. Given these findings, dermatologists and orthopaedists should not defer TJR access for patients with HS, as risk of postoperative complications is not prohibitive. [ABSTRACT FROM AUTHOR]