查看文章

VOL. 102 NO. 5S I NOVEMBER 2018 19 WWW. MDEDGE. COM/CUTIS is caspase recruitment domain family member 14, CARD14 (formerly PSORS2), a gene encoding a scaffolding protein important in the activation of NF-κβ. 10, 11 Missense CARD14 mutations cause upregulation of NF-κβ through formation of a complex with adapter protein B-cell lymphoma 10 (BCL10) and mucosa-associated lymphoid tissue lymphoma translocation protein 1 (MALT1), 12 which, in turn, causes increased transcription of cytokines IL-8, CC motif chemokine ligand 20 (CCL-20), and IL-36 gamma in the keratinocyte. 13 Mutations in CARD14 alone lead to psoriasiform skin in mice through amplified activation of the IL-23/IL-17 axis. 14, 15 Patients with a mutation in a CARD14 variant (p. Arg820Trp) have demonstrated better response to tumor necrosis factor (TNF) inhibitors. 16 Further characterization of the genetic pathogenesis of psoriasis might lead to better targeted therapies, including the possibility of MALT1 inhibitors as a treatment option. 12

Infection Streptococcus—The association between streptococcal infection and psoriasis was first documented more than 100 years ago, specifically the onset of acute guttate psoriasis. 17, 18 Although classically described following throat infection, psoriasis also occurs following streptococcal vulvovaginitis and perianal streptococcal infection. 19, 20 This type of psoriasis is typically self-limited but can recur with subsequent streptococcal infections or initiate a more chronic plaque psoriasis. Patients have a 1 in 3 risk of developing chronic psoriasis within 10 years of a single episode of acute guttate psoriasis. 21 …