الفهرس 
Review of LiteratureOnly 14 pages are availabe for public view
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Abstract
P
soriasis is a chronic relapsing dermatological disease that affects around 1–3% of the world’s population and the prevalence has been increasing globally over the past years.
Besides skin affection, patients with psoriasis have higher risk to develop several comorbidities, including psoriatic arthritis, metabolic syndrome, cardiovascular events, anxiety, and depression.
The diagnosis of psoriasis is mainly clinical. The chronic plaque type is the most common presentation in the form of well-demarcated erythematous plaques with silvery laminated scales mainly over the extensor surfaces of the elbows and knees. While the hallmark of the disease histopathology is epidermal acanthosis, hyperkeratosis, and parakeratosis, associated with dilated tortuous blood vessels reaching into the tips of the dermal papillae, which correlate clinically with the Auspitz sign, and mixed inflammatory infiltrates in the dermis and epidermis.
A complex multifactorial etiology is suggested to be the underlying mechanism, involving both genetic and environmental factors that can initiate psoriatic inflammation, including mild trauma, sunburn, or chemical irritants. The interaction between these factors can disrupt the epidermal homeostasis, which triggers a viscous inflammatory circle that leads to epidermal hyperplasia and psoriasis.
Over the past years, accumulating evidence established that TNF-α, IL23, IL17 and IL22 are the major players in the pathogenesis of the disease. This inflammatory cascade is the outcome of interaction between epidermal DCs, T lymphocytes and keratinocytes. However, the initial stimulus for DCs stimulation and T cells differentiation is still unclear.
In psoriasis, there is a hormonal disturbance in the form of defective GC secretion associated with HPA axis dysfunction that is claimed to be one of the causative links between stress and psoriasis.
Recently, accumulating evidence established the presence of cutaneous steroidogenesis, and several studies proved a significant correlation between several steps of this pathway and the ongoing inflammation in psoriasis. The most important of this pathway is the final step controlled by 11βHSD. This enzyme by its 2 types can control local levels of activated GCs in the skin.
The balance between 11βHSD1 and 11βHSD2 enzymes, which convert active cortisol/inactive cortisone, is the key to maintain skin barrier function, hence a healthy skin.
Our study showed that 11βHSD1 activity was significantly decreased in psoriasis patients in comparison to healthy volunteers. Besides, 11βHSD1 enzyme level was found to be decreased in lesional than non lesional skin in psoriasis patients.
Further histopathological assessment revealed that the lower enzyme levels are associated with greater epidermal acanthosis and higher degree of immunostaining by anti-FGF-2, which indicates the major role of 11βHSD1 in controlling psoriatic inflammation. This was supported by the positive correlation between the non lesional enzyme level and the longest period of remission that we detected in our patients.
Surprisingly, there was no significant correlation between the lesional nor the non lesional enzyme levels and the PASI score. Yet, the calculation of PASI score depends on several external factors that should be considered.
Interestingly, PSS was not correlated with 11βHSD1 level in psoriasis patients but was negatively correlated with the enzyme level only in healthy controls. This supports the role of stress in modifying enzyme activity, however, in psoriasis epidermal proliferation and the presence of inflammatory infiltrate definitely affect the enzyme level.
Better understanding of the complex symphony between all the players of psoriasis pathogenesis will reveal the role of 11βHSD1 and factors affecting its level in psoriasis vulgaris.