الفهرس 
Etiology of Rheumatoid arthritisOnly 14 pages are availabe for public view
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Abstract
Rheumatoid arthritis (RA) is a chronic, inflammatory, systemic
autoimmune disease of the joints that affects about 1% of the world
population. It’s of unknown etiology but it is thought to result from the
interaction of genetic, immunological, and environmental factors.
It’s characterized by a chronic inflammatory process that leads to
destruction of the synovial membrane, cartilage and bone causing
deformities, severe disability .It is also associated with extra articular and
systemic effects that worsen quality of life and reduced life expectancy.
Cardiovascular diseases (CVDs), are two to three times more
common in patients with RA and account for 30% to 50% of all deaths.
Recent studies showed that atherosclerosis lesions occur earlier and have a
more rapid evolution in patients with RA than in the general population.
Endothelial dysfunction (ED) is thought to be a key event in the
development of atherosclerosis. Some of the explanations may be that
pathogenic mechanisms in RA increase CV risk, or that RA and CVD share a
common risk factor.
Chitotriosidase (CHIT1), one of the most quantitative proteins
secreted by activated macrophages, is a human chitinase member of family
18 glycosyl hydrolases. The rate of synthesis and secretion of CHIT1 by
human macrophages is one of the most important indices for evaluation of
their activity. CHIT1 has been also implicated in the pathogenesis of many
human diseases through the improper induction of inflammation and faulty.