Research Information System
Thesis Type: Expertise In Medicine
Institution Of The Thesis: Gazi Üniversitesi, Tıp Fakültesi, Turkey
Approval Date: 2014
Student: VOLKAN TEKTAŞ
Supervisor: AYLA GÜLEKON
Abstract:Psoriasis is a complex chronic inflammatory disease with 2-3% prevalence. 6-8% of patients presenting to Dermatology clinics are comprised of psoriasis patients. Psoriasis is an autoimmune skin disorder characterized by increased keratinocyte proliferation and activated T cell accumulation as a response to an unknown antigenic stimulant. Oxidative stress is one of the factors thought to have a role in the beginning or chronicity of psoriasis. Recently, in studies performed with an objective to determine oxidative stress parameters, tissue or blood levels of both oxidant system elements such as malondialdehyde (MDA), 8-hydroxy-2-deoxyguanosine (8-OHdG) and nitric oxide (NO) and enzymes of antioxidant system such as superoxide dismutase (SOD) and glutathione peroxidase (GPx) have been pointing out to a disruption of the oxidant/antioxidant equilibrium. The risk of developing psoriasis in smokers is markedly increased compared to the normal population. Smoking is considered to have a role in both development and flaring of psoriasis by inducing production of free oxygen radicals and inflammatory cytokine expression. A total of 33 patients followed up in our department with clinical and histopathological diagnosis of psoriasis vulgaris, of which 17 were smokers and 16 were nonsmokers were included in our study. The control group was of 31 volunteers; 12 smokers and 19 nonsmokers, having neither psoriasis nor any other inflammatory skin disease. By measuring blood levels of NO, MDA, 8-OHdG, SOD, GPx frequently used as oxidative stress markers and tissue levels of NO and MDA in psoriasis patients and healthy controls, we aimed to evaluate the role of oxidative stress in the etiopathogenesis of psoriasis vulgaris and to investigate the association of smoking with this mechanism. In our study, median SOD and GPx levels in the patients were lower than the control group. Low SOD and GPx levels in patients with psoriasis have been thought to be caused by insufficiency of the antioxidant system. The DNA damage induced by reactive oxygen species (ROS), causes mutations in genes regulating cell growth, leading to abnormal apoptosis by disruption in cell cycle control and DNA repair mechanisms. 8-OHdG is accepted as a marker of DNA oxidation. In our study, median plasma 8-OHdG level of the case group was statistically higher than that of the control group. The increased level of 8-OHdG in psoriasis patients was thought to be an important finding as it shows genomic instability. In our study, median plasma and blood NO levels of the case groups were found to be statistically higher than the control group. High NO levels we determined in both tissue and plasma suggest that NO might be an effective second messenger in disease etiopathogenesis. Median plasma and tissue MDA levels were higher in the patients group were higher than the control group. Increased tissue and plasma MDA levels in psoriasis patients are good indicators of increased lipid peroxidation due to ROS. In our study these levels were high in the patients group and indicate increased lipid peroxidation. In our study, between smokers and nonsmokers in the patients group, no statistically significant difference concerning median plasma SOD; GPx, 8- 147 OHdG, MDA, NO and median tissue MDA and NO levels were observed. Contrary to the publications pointing out to the effect of smoking through oxidative stress at the beginning of the disease, no effect of smoking through ROS was determined. This suggests smoking might be effective in the triggering of the disease through other mechanisms than oxidative stress, or these results may be associated with the paucity of patient number. While all these results point out to increased oxidative stress in psoriasis etiopathogenesis, these parameters should be supported by studies in wider patient series to assess the role of oxidative stress and the effect of smoking on the etiopathogenesis of psoriasis.