In this comprehensive exploration, we delve into the intricate pathophysiology of Prurigo Nodularis (PN), highlighting the pivotal roles of neuronal sensitization, inflammation, and pruritus. This challenging dermatological condition is characterized by dermatological condition histopathologic alterations, including enhanced hypervascularization, epidermal hyperkeratosis, and dermal fibrosis. Explore the connection between PN and the proinflammatory Th2 cytokine IL-13, shedding light on its binding to IL-4R across various skin components.

TTP is a life-threatening thrombotic microangiopathy (TMA) that requires quick diagnosis and urgent treatment. ^1,2

Exact pathophysiology of PN is currently not understood. Based on the evolving literature, type 2 inflammation may play a role in PN.

This systematic review and network meta-analysis revealed that the use of low-molecular-weight heparin (LMWH) may be more effective than unfractionated heparin (UFH) in reducing incidence of deep vein thrombosis (DVT) among critically ill patients.