The association between psoriasis and insulin

The association between psoriasis and insulin resistance is known, and many studies in have been published in this area. However, none of these studies has evaluated irisin levels in patients with psoriasis. Our study is the first study to examine irisin levels in psoriasis aimed at understanding etiopathogenesis of the disease. In our study, by measuring irisin levels in patients with psoriasis, which is a disease associated with increased insulin resistance, we evaluated whether irisin levels show any correlation with severity of the disease. We hope our results would also aid in establishing a protocol aimed at understanding the etiopathogenesis and treatment of psoriasis.
Materials and methods This study was conducted by the Dermatology Department of Mugla Sitki Kocman University Faculty of Medicine. The study included patients diagnosed with psoriasis vulgaris (n = 30), who presented to the dermatology outpatient clinic and were not receiving systemic treatment (receiving topical therapy). The control group included voluntary participants who did not have any disease (n = 30). Individuals in both groups were informed about the study protocol, and all participants provided written consent. Comparison of parameters between the two groups were made with Kolmogorov–Smirnov test and Student t test. Correlation of parameters were analyzed with Spearman correlation test and p values less than 0.05 was accepted as the level of significance.
Results There were 15 males (50%) and 15 females (50%) in the patient group, and 15 males (50%) and 15 females (50%) in the control group. There was no statistically significant difference between the two groups in distribution of sex (p > 0.05). Mean age was 39.67 ± 9.30 years in the patient group, whereas it was 39.76 ± 15.74 years in the control group. Mean BMI was 27.73 ± 4.17 kg/m2 in the patient group, and 26.17 ± 3.81 kg/m2 in the control group. There was no statistically significant difference between the patient and control groups regarding mean age and BMI (p > 0.05). PASI scores in the patient group varied between 0.4 and 15.8, and the mean PASI score was 4.71 ± 3.52. The DLQI value in the patient group varied between and 26. The mean DLQI value was 10.73 ± 7.82. Table 1 summarizes biochemical parameters, insulin and buy Talabostat mesylate A1c (HbA1c) levels, and HOMA-IR scores in the patient and control groups. Serum irisin and salivary irisin levels were significantly lower in the patient group when compared with the control group (p < 0.05; Figure 1). The patient group had significantly higher serum glucose and triglyceride levels, and significantly lower HDL levels when compared with the control group (p < 0.05; Figure 2). The patient group had significantly higher HbA1c levels and HOMA-IR scores when compared with the control group (p < 0.05; Figure 3). In the patient group, serum irisin levels showed a positive correlation with salivary irisin levels (r = 418; p = 0.022) and a negative correlation with PASI (r = −437; p = 0.016) and DLQI (r = −424; p = 0.02) values. Salivary irisin levels had a negative correlation with PASI, but these correlations were not statistically significant (r = −351; p = 0.058). In addition, serum irisin levels had a negative correlation with serum triglyceride levels and HOMA-IR scores and a positive correlation with serum HDL levels; however, these correlations were also not statistically significant.
Discussion Although the pathogenesis of psoriasis is not fully understood, activation of T lymphocytes and keratinocyte hyperproliferation are given particular emphasis in pathogenesis. In addition, there is evidence indicating a role of endothelial cells in pathogenesis in the early period of psoriasis. The most commonly emphasized mechanism concerning pathogenesis of psoriasis involves activation of T cells of the immune system. Activated T cells release cytokines such as interferon-γ or tumor necrosis factor-α (TNF-α), and increase concentration of other immune effector cells, including neutrophils, in the inflammation site. TNF-α additionally stimulates vascular endothelial cell growth factor production in keratinocytes, and induces secondary proliferation of epidermal and vascular cells. Various studies have been performed to determine the pathogenesis of psoriasis; however, its etiology is not yet clear. Many studies have emphasized chronic inflammation in psoriasis. Recently, a strong association has been suggested to exist between psoriasis and metabolic syndrome as well as one of its components, insulin resistance. It has been suggested that cytokines that are released during the chronic inflammation in psoriasis may lead to the development of metabolic syndrome. One study emphasized the presence of a strong correlation between severity of psoriasis and insulin resistance. Furthermore, it drew attention to psoriasis not only as a disease of the skin, but also as a metabolic disease.