This study aimed to investigate the immunoreactivity of asprosin in tissue samples of patients diagnosed with plaque psoriasis and pustular psoriasis by means of immunohistochemical analysis

In this study, a total of 60 skin samples were used, including 20 from patients diagnosed with plaque psoriasis, 20 from patients diagnosed with pustular psoriasis, and 20 healthy skin samples obtained from areas adjacent to diseased tissue without any pathological findings, serving as the control group. Skin samples from patients diagnosed with other dermatological diseases, malignancies, or diabetes mellitus were excluded from the study. Following the confirmation of diagnoses, tissue sections of 5–6 µm thickness were obtained from paraffin-embedded blocks, and indirect immünohistochemical staining for asprosin was performed. In this method, the tissues were incubated with the primary antibody in a humid environment, followed by the application of a biotinylated secondary antibody and incubation with a streptavidin-conjugated enzyme (peroxidase or alkaline phosphatase). Subsequently, chromogens such as 3-Amino-9-Ethylcarbazole (AEC) or 3,3′-Diaminobenzidine (DAB) were applied as enzyme substrates. A histoscore was calculated based on the extent of immünoreactivity (0.1: <25%, 0.4: 26–50%, 0.6: 51–75%, 0.9: 76–100%) and staining intensity (0: none, +0.5: very weak, +1: weak, +2: moderate, +3: strong). The formula histoscore = extent × intensity was used for these calculations. The obtained data were analyzed using the Statistical Package for the Social Sciences (SPSS, version 22.0) (Chicago, IL, USA). After performing the Kolmogorov-Smirnov and Shapiro-Wilk normality tests, independent samples t-test was used for comparisons between two groups, and analysis of variance (ANOVA) was used for comparisons involving more than two groups. A p-value of <0.05 was considered statistically significant. In this study, the mean asprosin histoscore of the control group was found to be 0.530 ± 0.146, whereas the mean histoscore of the psoriasis patient group was 0.570 ± 0.146. The mean asprosin histoscore of the pustular psoriasis group was 1.605 ± 0.392. İmmünohistochemical analysis of asprosin immünoreactivity revealed no statistically significant difference between the plaque psoriasis group and the control group (p = 0.874). However, a statistically significant increase in asprosin immünoreactivity was observed in the pustular psoriasis group compared to the control group (p < 0.001). Additionally, when compared to the plaque psoriasis group, the pustular psoriasis group showed a statistically significant increase in asprosin immünoreactivity (p < 0.001). The aim of this study was to evaluate the immünohistochemical expression of the asprosin molecule in healthy skin and in two subtypes of psoriasis: plaque and pustular psoriasis. While asprosin immünoreactivity was significantly increased in pustular psoriasis, it remained at levels comparable to healthy skin in plaque psoriasis. This difference suggests that the elevated levels of asprosin in pustular psoriasis may be associated with the intense neutrophilic inflammation characteristic of this subtype, which is dominated by autoinflammatory pathways such as IL-1 and IL-36. In conclusion, asprosin may be considered a potential biomarker reflecting the severity of inflammation, particularly in pustular psoriasis. Further studies are needed to clarify its role and diagnostic value. Key words: Psoriasis, pustular psoriasis, asprosin