الفهرس 
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Abstract
Psoriasis is a genetically determined disease of the skin characterized by profound epidermal hyperproliferation and marked inflammation of epidermis and dermis, vascular changes and dermal inflammatory infiltrate. Many pathological features of psoriasis can be attributed to alternations in the growth and maturation of epidermal keratinocytes.
Epidermal keratinocytes are also crucial to cutaneous inflammatory and immune responses in psoriasis by elaborating various cytokines, adhesion molecules, and chemotactic factors. However, the regulatory and effector mechanisms underlying epidermal and immunological activation in psoriasis remain incompletely understood.
Recent concepts of the pathogenesis of psoriasis focus on the importance of the innate immune system and the role of dendritic cells, neutrophils, and antimicrobial peptides.
Various exogenous and endogenous factors such as streptococcal pharyngitis (with guttate psoriasis), stressful life events, humidity, HIV infection, trauma, smoking, drugs (beta-blockers, lithium, anti-malarial, Interferon), cold weather, diet and obesity have been shown to be associated with psoriasis. Psoriasis vulgaris is the most common variety of psoriasis, representing about 70% to 80% of psoriatic patients.
Psoriasis is initiated and maintained through the multifaceted interplay of keratinocytes, blood vessels, immune system mediators and expressed genes. Some gene polymorphisms have been shown to be associated with psoriasis.
Angiopoietins are part of a family of vascular growth factors that play a role in embryonic and postnatal angiogenesis. Two major isoforms regulate vascular homeostasis, namely ANGPT-1and ANGPT-2. ANGPT-1binds Tie2 resulting in decreased vascular permeability and promotion of vessel maturation and stabilization. ANGPT-2, on the other hand, antagonizes ANGPT-1 and induces neovascularization by destabilizing endothelial cell-pericyte junctions and promotes endothelial cell survival, migration, and proliferation. The aim of the current study was to investigate the association between SNPs of ANGPT2 (rs 2442598) in patients with psoriasis vulgaris compared with age and gender matched healthy controls. This study was conducted on 40 patients with psoriasis vulgaris and 40 age and gender matched healthy subjects as a control group.
Inclusion criteria included cases diagnosed with psoriasis vulgaris irrespective of age and gender. Patient stopped topical treatment 2 weeks and systemic treatment 6 months prior to blood sampling.
Exclusion criteria included patients with other dermatological diseases except psoriasis vulgaris, patients with autoimmune diseases as SLE, patients with chronic diseases as chronic renal failure and liver failure, patients having infectious conditions at the time of blood sampling as bacterial infection.
Patients and controls were subjected to history taking and clinical examination. Assesment of disease severity was done according to PASI score. PASI score was calculated and assessment SNPs in ANGPT-2 gene by PCR and restriction enzyme.
In the present study, significant difference between cases and controls regarding ANGPT-2 genotypes (rs2442598) (P < 0.001), significant difference between cases and controls regarding Angiopoietin 2 alleles (P <0.001).There was no significant relationship between Angiopoietin 2 genotypes (rs2442598) and clinical data of studied cases (P >0.05 for all). There was no statistical significant relationship between Angiopoietin 2 alleles (rs2442598) and clinical data of cases (P >0.05 for all).