Abstract PD-1 (programmed Death-1) immune checkpoint inhibitors have provided significant benefits to tumor patients. However, a considerable proportion of the patients develop immune-related adverse events (irAEs), of which cutaneous irAEs (cirAEs, e.g., psoriasis) occur relatively early. This review provides an overview of the current progress in psoriasis de novo or exacerbation by PD-1 checkpoint inhibitors. It not only describes the relevant influencing factors but also theoretically analyzes the immunological mechanisms that lead to the onset or exacerbation of psoriasis. Finally, the authors present guidelines for the treatment of psoriasis de novo or exacerbation by PD-1 checkpoint inhibitors. The review is intended to assist dermatologists in the early recognition and effective individualized management of such cirAE, which is helpful to continue or adjust the tumor-targeted immunotherapy on the basis of ensuring the quality of life of tumor patients. PD1 PD 1 PD- programmed Death1 Death Death-1 However immunerelated related irAEs, , (irAEs) cirAEs, cirAEs (cirAEs eg e g e.g. Finally cirAE tumortargeted targeted Death- (irAEs e.g

Abstract Background There is an obvious need for more prompt and specific biomarkers of bacterial infections in generalized pustular psoriasis patients. Objective The aim of this study was to evaluate the diagnostic properties and define appropriate cut-off values of procalcitonin and C-reactive protein in predicting bacterial infection in generalized pustular psoriasis patients. Methods Sixty-four generalized pustular psoriasis patients hospitalized from June 2014 to May 2017 were included in this retrospective study. The values of procalcitonin, C-reactive protein, details of infection, and other clinical parameters were analyzed. Results Receiver operating characteristic curve analysis generated similar areas (p = 0.051) under the curve for procalcitonin 0.896 (95% CI 0.782-1.000) and C-reactive protein 0.748 (95% CI 0.613-0.883). A cut-off value of 1.50 ng/mL for procalcitonin and 46.75 mg/dL for C-reactive protein gave the best combination of sensitivity (75.0% for procalcitonin, 91.7% for C-reactive protein) and specificity (100% for procalcitonin, 53.8% for C-reactive protein). Procalcitonin was significantly positively correlated with C-reactive protein levels both in the infected (r = 0.843, p = 0.040) and non-infected group (r = 0.799, p = 0.000). Study limitations The sample size and the retrospective design are limitations. Conclusions The serum levels of procalcitonin and C-reactive protein performed equally well to differentiate bacterial infection from non-infection in generalized pustular psoriasis patients. The reference value of procalcitonin and C-reactive protein applied to predicting bacterial infection in most clinical cases may not be suitable for generalized pustular psoriasis patients. C-reactive protein had better diagnostic sensitivity than procalcitonin; however, the specificity of procalcitonin was superior to that of C-reactive protein.

Psoriasis vulgaris is defined by a series of linked cellular changes in the skin: hyperplasia of epidermal keratinocytes, vascular hyperplasia and ectasia, and infiltration of T lymphocytes, neutrophils and other types of leukocytes in the affected skin. Catechol-O-methyltransferase ( COMT ) 158 polymorphism can reduce the activity of the COMT enzyme that may trigger defective differentiation of keratinocytes in psoriasis. Immunocytes can degrade and inactivate catecholamines via monamine oxidase (MAO) and COMT in the cells. We hypothesized that the COMT-158 G > A polymorphism was associated with the risk of psoriasis vulgaris in Han Chinese people. In a hospital-based case-control study, 524 patients with psoriasis vulgaris and 549 psoriasis-free controls were studied. COMT-158 G > A polymorphism was genotyped using the PCR sequence-specific primer (PCR-SSP) technique. We found no statistically significant association between the COMT-158 allele A and the risk of psoriasis vulgaris (p = 0.739 adjusted OR = 1.03; 95% CI = 0.81-1.31). This suggests that the COMT-158 G > A polymorphism may not contribute to the etiology of psoriasis vulgaris in the Han Chinese population.