Effect of Alterations in Apoptotic pathway on Development of Metabolic Syndrome in Patients with Psoriasis Vulgaris

Objectives The purpose of this study is to evaluate the role of changes in gene expression of apoptosis activators (BAX, cytocrome-c [cyt-c], and caspase-3) and apoptosis inhibitors (BCL2, survivin, cyclin D1 [CCND1], SOD, catalase 3 [CAT], glutathione synthetase [GS], heat shock protein [HSP]27, HSP60, HSP70, and HSP90) on the development of metabolic syndrome (MetS) in patients with psoriasis vulgarins. Methods Fifty patients with psoriasis were enrolled in the study, 25 of whom had MetS. Twenty-five healthy people and 25 people with only MetS were included in the study as a control group. Serum fasting blood glucose (FBG), urea, creatinine, total cholesterol, high density lipoprotein cholesterol (HDL-C), low density lipoprotein-cholesterol (LDL-C), triglycerides (TG), thyroid stimulating hormone (TSH), fraction of thyroxine (T4), fasting insulin, and high sensitive C-reactive protein (hsCRP) levels were measured in all participants. In addition, the expressions of genes BAX, cyt-c, and caspase 3, BCL2, survivin, CCND1, and SOD, CAT, GS, HSP27, HSP60, HSP70, and HSP90 were measured in peripheral blood. Clinical activation of patients with psoriasis was calculated by using Psoriasis Area and Severity Index (PASI) scores. Results In patients with MetS, there was an increase in the expression of genes for cyt-c, survivin, HSP27, HSP60, and HSP90 and a decrease in the expression of the CCND1 genes identified. Furthermore, the levels of expression of CCND1 genes were identified to be an independent risk factor for MetS development in psoriatic patients. Conclusion The increase in expression of the apoptosis inhibitors surviving, HSP27, HSP60, and HSP90 and the decrease in CCND1 gene expression—which plays a role in the activation of mitochondria—may be an important mechanism in the development of MetS in psoriatic patients. This article is protected by copyright. All rights reserved.