cutaneous trauma can trigger pediatric PsO. Upper respiratory tract infection, particularly group A β-hemolytic streptococcal pharyngitis, and some drugs (eg, propranolol, antimalarials, terbinafine, and lithium as well as following withdrawal of systemic corticosteroids) are other well-recognized triggers.11,32 Environmental exposure to tobacco smoke and stressful life events have also been associated with pediatric PsO.33-35 Paradoxical PsO refers to an emerging subtype of PsO first recognized in adults but increasingly reported in children.36-40 This subtype develops in patients treated with a biologic agent that blocks tumor necrosis factor (TNF). Agents that target this pathway are effective, FDA-approved medications for PsO but when used for other indications (inflammatory bowel disease [IBD] or arthritis) can trigger PsO.
Pathophysiology
Well-defined, but not mutually exclusive, inflammatory pathways distinguish plaque PsO from AD, as supported by the evolving pipeline of targeted biologic therapy. In vitro studies initially identified the helper T (TH) 1 pathway as the most important signaling pathway in the pathophysiology of PsO.41,42 Early clinical trials that followed this discovery demonstrated that blocking TNF alpha led to significant improvement in PsO, but subsequent studies yielded even better improvements with agents that block interleukin (IL)-17 and IL-23.43 In contrast, TH2 inflammation is the major immunologic pathway that impacts AD, as supported by successful treatment with biologic agents that block IL-4 and IL-13.44
Assessment of Pediatric PsO
A common assessment tool for determining PsO disease severity is total body surface area (BSA) involvement using the "rule of 9's" measurement, with adjustment of relative proportions of regions based on age.32,45 The rule of 9's general guidelines are that the head and each arm comprise 9% of the total BSA, each leg and the front and back of the torso, respectively, each make
