Journal of Clinical and Aesthetic Dermatology

Updates on Psoriasis & Cutaneou Oncology

An evidence-based, peer-reviewed journal for practicing clinicians in the field of dermatology

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S14 P r o c e e D i n G s JCAD jOUrnAl Of ClInICAl And AEsthEtIC dErMAtOlOgy september 2017 • volume 10 • number 9 • supplement lymphocytes, monocytes, keratinocytes, fibroblasts, and endothelial cells in response to interferon-γ (ifnγ) and tnf. 21 it has been speculated that cxcl10 may be a potential biomarker for Psa. in a prospective study of patients with skin psoriasis but without Psa, baseline levels of serum cxcl10 messenger rna were evaluated as a potential biomarker for Psa. 2 2 Patients in whom Psa developed were designated in this study as "converters," compared to "nonconverters" (who did not develop Psa). cxcl10 serum levels were signifcantly higher in converters (493pg/ml) than nonconverters (371pg/ml), p=0.005, but serum levels of c-reactive protein were similar between groups. 2 2 after Psa developed, patients exhibited lower levels of cxcl10. this both implicates cxcl10 as a predictive biomarker for Psa in psoriasis patients and suggests that it may play a role in the pathogenesis of Psa. a new population-based study by lewinson et al 23 has found depression increases the risk that a patient with cutaneous psoriasis will develop Psa. since systemic ingammation increases the risk of Psa in psoriasis patients and since major depressive disorder (MDD) is associated with increased levels of systemic ingammation, investigators hypothesized that patients with psoriasis who suder from MDD were more at risk of developing Psa than those without MDD. a retrospective analysis using the Health improvement network identifed psoriasis patients (n=73,447) who were followed for 25 years until either Psa was diagnosed or the censor date. using cox proportional hazards models, those psoriasis patients who developed MDD had a signifcantly increased risk of subsequently developing Psa compared to those psoriasis patients who did not have MDD (Hr: 1.37, 95% ci: 1.05–1.80, p=0.021). 23 there are numerous treatment options for Psa, including adjunctive treatments (e.g., nonsteroidal anti-ingammatory drugs [nsaiDs]), physical therapy, topical agents (e.g., topical corticosteroids), disease-modifying antirheumatic drugs (DMarDs) (e.g., methotrexate), biologics, and new experimental agents (e.g., Janus-kinase [JaK] inhibitors, α-il- 23 monoclonal antibodies, and other anti-il-17 agents). early and edective treatment of Psa is crucial to reduce joint damage, improve outcomes, prevent disability, and enhance patient quality of life. as many as 20 to 50 percent of patients with Psa are unemployed and 16 to 39 percent are legally disabled. 24 Patients with Psa who are employed may suder from presenteeism (i.e., ability to go to work but at a diminished capacity), absenteeism (i.e., taking time od from work for medical reasons), and productivity loss (i.e., combination of presenteeism plus abstenteeism). 25 a multicenter, observational cohort study enrolled patients with Psa who were either starting or switching to an anti-tnf therapy or conventional synthetic DMarD (csDMarD) for Psa. 25 at baseline, 57 percent of the study population was employed and 24 percent of those of working age were not employed. at six months of therapy, there were signifcant improvements in the csDMarD group (n=164) in terms of presenteeism (10%, p=0.007) and work-related productivity (15%, p=0.001). the improvements were more pronounced in the anti-tnf therapy group (n=65), with proportions of patients achieving signifcantly less presenteeism (30%, p<0.001) and greater work productivity (40%, p<0.001). clinical improvement was greater in the anti-tnf group compared to the csDMarD group. 25 obesity is a frequently observed comorbidity with Psa and may exacerbate its course. 27 obesity is associated with ingammation, and studies of other rheumatic patients suggest that anti-tnf therapy adherence is low in patients with obesity. 26,27 an observational cohort study evaluated patients with Psa over a median 1.5 years (n=1,943). 28 of this population, 32 percent were obese (n=408), defned as body mass index (BMi) of 30kg/m 2 or more. adherence was defned as the number of years that the patient maintained treatment with the frst tnf inhibitor, although temporary interruptions in treatment (<3 months) were allowed. tnf inhibition therapy was shorter in patients with obesity compared to patients without obesity (2.5 years vs. 5.9 years). Good or moderate response on the european league against rheumatism (eular) scale was achieved by 55 percent of obese and 65 percent of nonobese patients at six months (p=0.02), and obesity was associated with greater degree of disease activity, increased risk of discontinuation of tnf inhibition therapy, and decreased treatment response. obesity had a signifcant edect on patients in this study irrespective of sex, particular type of tnf inhibitor, and patient nationality. 28 Biologics able to inhibit the il-17a pathway have been explored for their potential role in treating Psa as well as other disorders. il-17a has been implicated in the pathogenesis of multiple immunoingammatory diseases, including psoriasis, Psa, and rheumatoid arthritis (ra). 29 i l-17 is a cytokine family of six subunits (a, B, c, D, e, f). il-17a may be described as a principal edector of t-helper type (th) 17 cells; high levels may be found at diseased cutaneous sites and in diseased joints. 29 in results presented at the 2016 meeting of the american college of rheumatology, secukinumab at multiple dosages odered sustained improvements in signs and symptoms in various clinical domains at three years in 606 Psa patients. 30 other il-17a inhibitors currently being evaluated for Psa treatment include ixekizumab, bimerkizumab (this monoclonal antibody antagonizes both il-17a and il-17f), a dual-

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