# Understanding the Intricate Pathophysiology of Psoriasis and Related Skin Disorders
## 4 Sporiasis and Associated Dermatologic Disorders
The key interleukin IL-17, with IL-17A being particularly influential, appears to play a significant role in the progression of both diseases. [PERSON] et al. reported seven cases of SLE and PsA coexistence. In five out of seven, PsA occurred before the development of SLE, while in the remaining two cases, SLE was diagnosed before PsA [39]. Managing patients with both SLE and psoriasis is complex. The medications must be meticulously assessed to prevent the worsening of either condition and to reduce associated morbidities. One of the main treatment methods for psoriasis, UV radiation, may induce and/or exacerbate not only skin lesions but also the course of SLE [40]. In turn, antimalarial drugs, which are fundamental in the treatment of SLE, may induce or exacerbate psoriatic skin lesions and have even been linked to the induction of psoriasis. [PERSON] et al. reported a case of annular pustular psoriasis induced by hydroxychloroquine in a patient with a gain-of-function mutation in caspase recruitment domain family member 14 (CARD14). Several mechanisms have been proposed, including the suppression of the epidermal barrier function via inhibition of transglutaminase activity, induction of keratinocyte proliferation via IL-17 production, and interference with cholesterol metabolism. The gain-of-function CARD14 mutation causes psoriatic disease through the activation of nuclear factor-xB, suggesting the involvement of CARD14 mutation in the pathogenesis of APP. In this case, hydroxychloroquine administration was considered to have induced APP based on CARD14 mutation, a genetic predisposition for psoriatic diseases, but the relation between SLE and CARD14 mutation remains to be elucidated [41]. Regarding biologics, the development of SLE as a result of treatment with TNF-\(\alpha\) inhibitors is relatively rare--0.19-0.22% for infliximab, 0.18% for etanercept, and 0.10% for adalimumab--and the autoantibodies induced are typically IgM and are not pathogenic [42]. The biologics targeting the Th17 pathway, including vstekinumab and secukinumab, have been successfully used in the treatment of patients with concomitant psoriasis and LE. [PERSON] et al. report the case of a 23-year-old female patient with psoriasis and SLE that improved after receiving secukinumab treatment [34]. However, several case reports presented new-onset SLE or the deterioration of pre-existing SLE during or after Th17-targeted treatment [43]. [PERSON] et al. reported a patient with aggravation of discoid lupus erythematosus (DLE) after secukinumab treatment for psoriasis. Symptoms of psoriasis and PsA almost resolved after 150 mg secukinumab every four weeks for 2 years, but lesions of DLE enlarged and became generalized [44]. A few cases of concomitant psoriasis, PsA, and SLE have been successfully treated with vstekinumab, following advances in research into the roles of IL-17 and IL-23 in its pathophysiology [45]. Ustekinumab has shown a positive response in treating cutaneous lupus, including subacute cutaneous lupus erythematosus (SCLE) and DLE, regardless of the presence of concomitant psoriasis. A randomized, placebo-controlled, phase II trial involving 102 patients with active SLE reported that vstekinumab, when added to standard therapy, significantly improved the SLE Responder index (SRI-4), with 60% of patients achieving this outcome compared to 31% in the placebo group. Additionally, significant reductions in the SLEDAI-2K were observed at week 24. Ustekinumab shows promise as a treatment for SLE and could be a valuable option for patients with concurrent SLE and psoriasis. However, despite positive reports regarding the effectiveness of vstekinumab in treating cutaneous LE and SLE, there have been instances of adverse reactions associated with the treatment. For example, [PERSON] et al. reported a case of a patient with both psoriasis and SLE who experienced exacerbations of cutaneous LE and developed acute class IV lupus nephritis after receiving five doses of vstekinumab [46].