الفهرس 
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Abstract
Psoriasis vulgaris is a common, chronic immune-mediated skin disease characterized by red, scaly patches, papules, and plaques, affects 1-3% of world’s population. It is thought to result from a combination of genetic, epigenetic, and environmental influences. Histologically, psoriasis is characterized by abnormal keratinocytes proliferation and infiltration of immune cells, predominantly T lymphocytic cell and dendritic cells. Psoriasis considered not only skin disease but also it is associated with several comorbidities such as metabolic syndrome. The main cause of mortality in psoriatic patients is cardiovascular events which suggests an association between psoriasis and traditional cardiovascular risk factors.
Autophagy is an intracellular degradation system; in which a part from the cytoplasm is degraded by the lysosomes to form auto-phagosomes. It is essential for survival, differentiation, development, and homeostasis. Impaired autophagy may contribute to the pathogenesis of several dermatological diseases as psoriasis, vitilligo, and systemic lupus erythematosus. Also; it may have a role in metabolic diseases, including DM and its complications, metabolic syndrome and obesity.
The current study was conducted on 54 subject who divided into two groups; group I: 38 psoriasis vulgaris patients who were 27 males (71.1%) and 11 females (28.9%) with a mean of age 48.45±14.94 years; and group II: 16 healthy control was equal in sex n=8 with a mean of age 45.38±14.04 years.
Measurement of waist circumference, blood pressure, serum fasting blood glucose, serum triglyceride and serum high-density lipoprotein (HDL) cholesterol were done for all subjects. Also; evaluation of psoriasis severity in patients by “Psoriasis Area and Severity Index” (PASI) score and assessment of MetS using JIS definition for all subjects were done.
Also; 4 mm punch skin biopsy was taken from the lesional and perilesional skin of patients and from normal skin of controls to measure expression of LC3 in tissues by immunohistochemistry.
There was a high statistically significant difference between patients and controls as regard LC3 expression; as LC3 expression was nearly absent, in epidermis of lesional skin of psoriasis vulgaris patients while it was strong among control group. LC3 expression in lesional skin of psoriasis vulgaris patients was lower than its expression in perilesional.
However, there was no correlation between LC3 expression in patients and PASI score. No significant variation in lesional expression of LC3 between patients with MetS and patients without MetS. LC3 expression in perilesional skin of psoriasis vulgaris patients is highly correlated with diastolic blood pressure.
The prevalence of the metabolic syndrome was 42.1% among psoriasis patients and 25% among control. The most common abnormal metabolic feature, among studied patients were decreased serum HDL (81.57%), followed by abdominal obesity (52.63%) and hypertriglyceridemia and elevated blood pressure each of them represent (44.73%). No elements of the MetS was present in 5.26% of studied patients. The disturbances in lipid profiles and obesity were most important factors leading to the increased prevalence of the metabolic syndrome in this study. However, the prevalence of MetS in the studied patients showed no correlation with duration and severity of psoriasis.
In conclusion, our findings suggest that autophagy marker LC3 expression is decreased in psoriatic lesion and some changes occur in perileional. Also; LC3 expression is nearly not changed regardless severity and presence or absence of MetS. The current study points to a potential link between psoriasis vulgaris and autophagy marker LC3 with lower skin expression in patients than in controls. Such a link may help to further explore the complex pathogenesis of psoriasis. Autophagy enhancer may be used as a beneficial therapeutic agent in autoimmune and inflammatory skin disorders.
Future studies with larger sample size, different clinical presentation may be needed to obtain reliable data regarding relation between LC3 and psoriasis. In addition, future studies may be needed to find the expression of other autophagy markers.