الفهرس 
Psoriasis vulgaris
Factors affecting epidemiologyOnly 14 pages are availabe for public view
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Abstract
Psoriasis affects nearly 2-3% of the world’s population. Its profound
effect on the patients’ quality of life as well as its associated co-morbidities
caused it to be one of the most studied dermatological diseases.
Psoriasis is a chronic inflammatory skin disease characterized by
hyper proliferation of keratinocytes, dilation and growth of dermal
capillary vasculture, and cellular infiltrate of activated T cells, dendritic
cells, monocytes, and neutrophils. Increased production of numerous
cytokines, chemokines and growth factor has been found to be present
within the skin as well as in the circulation in psoriasis patients.
Nowadays, it is believed that psoriasis is most likely a Th1/Th17
induced inflammatory disease, with interplay between genetic
susceptibility, defects in skin barrier and dysregulation of innate and
adaptive immunity. Environmental factors also play a role in the
pathogenesis of psoriasis including drugs, skin trauma, infection and stress.
High mobility group box-1 (HMGB1), initially described as a non
histone nuclear protein with transcriptional regulatory properties, is now
recognized as a late mediator in septic shock as well as a pro- inflammatory
cytokines. HMGB1 is expressed by almost all cells, and usually located in
the nucleus. However, it has been reported that HMGB1 can be
translocated to the cytosol and then released into the extracellular space.
There are two pathways in which HMGB1 can be released
extracellularly. One is an active process which occurs when cells exposed
to inflammatory mediators, such as lipopolysaccharide (LPS), (TNF)- α,
and (IFN)-γ ; the other a passive process during cellular necrosis. With the discovery of HMGB1 as a potent mediator of inflammation
and the presence of extranuclear HMGB1 in several inflammatory
conditions, investigations of possible beneficial effects of
HMGB1-targeted therapies were initiated.
Many recent studies have concluded that HMGB1 is a key player in
the pathogenesis of several autoimmune diseases such as rheumatoid
arthritis, systemic lupus erythematosus and psoriasis vulgaris.
It was suggested that HMGB1 may constitute a proinflammatory loop
and may act as an important player in the inflammatory processes in
psoriasis vulgaris. Activated HMGB1 mediates cellular responses including
chemotactic cell movement and release of proinflammatory cytokines such
as tumor necrosis factor-, IL-1 β, and IL-6, and effects on various immune
cells, such as macrophages, monocytes, T cells, and B cells.
This study included 20 randomly selected psoriasis vulgaris cases of
different clinical variants and 20 healthy control subjects. Each patient was
subjected to a detailed history taking and examination. Skin biopsies were
taken from all subjects. Tissue levels of HMGB1 were assessed using an
enzyme-linked immunosorbent assay before and after treatment. NB-UVB
treatment sessions were given for the patient group three times per week
for 3 months. Tissue HMGB1 levels and PASI scores were measured at the
beginning of the study and after 3 months of treatment.
Results assessed revealed a statistically significant increase in the
mean tissue HMGB1 level in patients with psoriasis vulgaris compared to
healthy control subjects which supports the possible role of HMGB1 in
psoriasis vulgaris. Tissue HMGB1 levels in patients with high PASI score
before treatment were statistically higher than those with low PASI score
after treatment which indicates that HMGB1 may be used in psoriasis vulgaris as marker of activity and a prognostic factor. No significant
association between tissue HMGB1 level and the age or the sex of patients.
With reference to duration of disease, there was significant positive
correlation between tissue HMGB1 levels and the disease duration.