Complete primary treatment failure of adalimumab in a patient with photoaggravated psoriasis

Kulapatrapa, Chanika; Rünger, Thomas M.

doi:10.1111/phpp.12132

Cited by 1 publication

(2 citation statements)

References 9 publications

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“…There are reports that neutralizing TNF with infliximab (transiently) or etanercept can be effective in clearing PP (and also pityriasis rubra pilaris). However, in one case of PP, after complete primary treatment failure with the anti‐TNF monoclonal adalimumab, the anti‐IL‐23 antibody ustekinumab was highly effective in clearing psoriatic lesions . Together with the report that pityriasis rubra pilaris was responsive to ustekinumab, these studies suggest that directly interfering with the Th17/IL‐23 pathway may be advantageous in PP.…”

Section: Perspectivesmentioning

confidence: 93%

“…A better understanding of the pathophysiology of PP should help improve therapeutic concepts. Although patients with PP often do respond to classical antipsoriatic therapeutics such as PUVA and cyclosporine, they may not always benefit equally well from biologics . There are reports that neutralizing TNF with infliximab (transiently) or etanercept can be effective in clearing PP (and also pityriasis rubra pilaris).…”

Section: Perspectivesmentioning

confidence: 99%

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Desired response to phototherapy vs photoaggravation in psoriasis: what makes the difference?

Wolf

Weger

Patra

et al. 2016

Experimental Dermatology

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Psoriasis commonly responds beneficially to UV radiation from natural sunlight or artificial sources. Therapeutic mechanisms include the proapoptotic and immunomodulating effects of UV, affecting many cells and involving a variety of pro-and anti-inflammatory cytokines, downregulating the Th17/IL-23 response with simultaneous induction of regulatory immune cells. However, exposure to UV radiation in a subset of psoriasis patients leads to exacerbation of the disease. We herein shed light on the predisposing factors of photosensitive psoriasis, including genetics (such as HLACw*0602 or CARD14), gender and coexisting photodermatoses such as polymorphic light eruption (PLE) in the context of potential molecular mechanisms behind therapeutic photoresponsiveness or photoaggravation. UV-induced damage/pathogenassociated molecular patterns, damage to self-coding RNA (signalling through Toll-like receptors), certain antimicrobial peptides and/or inflammasome activation may induce innate immunity, leading to psoriasis at the site of UV exposure when there is concomitant, predisposing resistance against UV-induced suppression of the adaptive immune response (like in PLE) that otherwise would act to reduce psoriasis. K E Y W O R D S

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Section: Perspectivesmentioning

confidence: 93%

Section: Perspectivesmentioning

confidence: 99%