الفهرس 
IntroductionOnly 14 pages are availabe for public view
 |  | from | 72 |  |  |
| | | from | 72 | | |
Abstract
Psoriasis is a common chronic inflammatory dermatosis with varying
incidence between 0.5% to 11.5% of population.
Several variants of psoriasis are present with chronic plaque psoriasis,
which is the most common variant.
The etiology of psoriasis is unknown, but evolving evidence suggests that
it is a complex disorder caused by interaction of multiple factors includes
immunological, environmental and genetic factors.
Psoriasis pathogenesis is also characterized by dysregulated angiogenesis
and vascular remodeling. New blood vessel formation is seen in early stages of
psoriatic lesions and neo-vascularization disappears with clearance of skin
disease. Immune processes and inflammatory cascades are well known inducers
of angiogenesis and vice versa.
Also keratinocytes producing proangiogenic signals as vascular
endothelial growth factor (VEGF), von Willebrand Factor (vWF), nerve growth
factor (NGF) demonstrated in the study.
These cytokines are said to stimulate angiogenesis in psoriatic skin
lesions. Studies have suggested that lymphocytes secrete angiogenic factors such
asVEGF which induces capillary proliferation and vasodilatation. Newer
angiogenic factors namely vWF and nerve growth factor (NGF), are said to
stimulate angiogenesis in psoriatic skin lesions.
Von Willebrand factor (vWF) is a plasma glycoprotein synthesized mainly
in endothelial Cells. It is a marker of endothelial activation. That plays an
essential role in initial hemeostasis, mediating adhesion of platelets to
subendothelial surfaces at sites of vascular injury and acting as a carrier protein
for factor VIII.
Von Willebrand factor is considered a marker of endothelial dysfunction
and injury, elevated plasma level of vWF reflects the damage to endothelial cells.
Elevated plasma level also was found in patient with cerebrovascular disease and
inflammatory vascular diseases the higher concentration of vWF is an index of
increasd risk of thrmbogenesis and atherosclerosis.
Recent studies demonstrated that endothelial dysfunction that present in
psoriatic lesions contributes to local procoagulation that mediated via (vWF) that
further enhance inflammation.
The aim of the work to assess immunohistochemical expression of vWF as
angiogenic, hypercoagulable and inflammatory marker in cases of psoriasis
vulgaris patients with various degrees of severity and healthy controls to evaluate
its possible role in the pathogenesis and prongnosis of the disease.
This study was conducted in the period from December 2018 to October
2019. Cases of psoriasis vulgaris were selected from Dermatology Outpatient
Clinic, Faculty of Medicine, Menoufia University Hospital. They were compared
to control healthy voluntears.
Histopathological and immunohistochemical evaluation were carried out
in Pathology Department, Faculty of Medicine, Menoufia University. This
SUMMARY
46
prospective case-control study was carried out on a total number of 45 subjects,
they included 30 patients with chronic plaque psoriasis and 15 age and gender
matched apparently normal subjects as a control group.
Patients were collected randomly from Dermatology Outpatient Clinic,
Menoufia University Hospital in the period between periods from December 2018
to October 2019. Control subjects were selected from apparently healthy persons.
Written consent form, approved by Local Ethical Research Committee in Faculty
of Medicine, Menoufia University was obtained from every participant prior to
study initiation.
The patients included in this study were selected according to inclusion
and exclusion criteria. All studied cases were subjected to complete history
taking, clinical, general and dermatological examination including assessment of
PASI score. Immunohistochemical expression of von Willebrand Factor was done
for all subjects in this study.
In our stydy showed significant difference regarding epidermal expression
of vWF between cases and control. Our results could be explained as
keratinocytes have be identified as the main source of angiogenic growth factors
as VEGF, NGF and vWF is one of the new angiogenic growth factor that could
also be released from keratinocytes and contributes to psoriasis angiogenesis.
This study show significant difference regarding dermal expression of
vWF in endothelial cells between cases and control.
Our finding supported that psoriasis charachterized by vascular
proliferation, tortuosity and elongation of vessels which reflected by increased
microvessel density and increased vascular marker expression including vWF.
The strong vWF expression found in the capillary microvessels of the psoriatic
sections is in line with the observation of marked endothelial dysfunction within
psoriatic plaques.
This study show statistically high significant difference regarding
expression of vWF in dermal inflammatory cells between cases and control. To
our knowlage no previous study reported vWF exoression in inflammatory cells
but in the same line with this study that was carried by Rashed et al., (2012) that
recorded that angiogenic growth factor named vascular endothelial grwth factor
(VEGF) was positively expressed in the dermal inflammatory cells in psoriatic
patients compared to control. This may reflect the interaction between vascular
response and inflammation.
This study showed statistically significant difference between vWF
expression and duration of the disease. This denoting that the more the duration of
the disease the more expression of vWF.
In the present study there was no statistically significant correlation
between PASI score and immunohistochemical expression of vWF (p=>0.05).
This might be in the same line with the studies done on serum and
immunohistochemical expression of VEGF that showed that only serum level of
VEGF is what significantly correlates with PASI and considered as a severity
marker.