Abstract

Vasculitis is a class name of the disease, because the immune system attacks the vascular
tissue cause. Vasculitis can be roughly divided into large vessels, small vasculitis. Some
vasculitis confined to the skin, there is no systemic performance. And severe systemic vasculitis
usual manifestations of fever, fatigue, skin rash, hemoptysis, hematuria, proteinuria or neuralgia
etc. (neuralgia and general joint pain is different, mainly burning, numbness, tingling, sensory
abnormalities).Because the symptoms of the disease varied and rare, so difficult to
diagnose. Course of repeated treatment also difficult. Such disease is relatively rare, the level of
medical institutions for treatment is a major challenge.vasculitis secondary to
infection,malignancy and drugs are not common among children,but association with Kawasaki
syndrome and Henoch-schonlein purpura and Behcets diseases needs citation ,these classical
triad of pediatric diseases represent the involvement of amyloid deposition,glomerulonephritis
and tubule interstital involvement ,due course in the absence of treatment may lead to renal
failure
Introduction
Almost all primary vasculitis involve either of arterial or venous system, but in the behcets
disease involving both system and affecting vessels of any size made superimpostry.Kawasaki
Disease predominantly causes vasculitis in medium-sized arteries, with a striking predilection
for the coronary arteries progressed by early inflammatory infiltration of the vascular wall by
polymorpho nuclear cells followed by plasma cells and CD8+Tcells,as it is progress invading
systemic organs including kidney ending up with acute renal failure with the involvement of
tubule interstitial nephritis, immune complex mediated nephropathy and hemolytic uremic
syndrome
Etiology and pathogenesis
Vasculitis can have a variety of different etiology mechanism, but it is very limited histologic
abnormalities in acute diseases, mainly of inflammatory cells polymorpho nuclear leukocytes; in
chronic degenerative conditions, then mainly lymphocytes Additionally, neutrophil segmental
inflammation, so most parts of the vessel branches can be normal, but contain sporadic
significant inflammatory lesions. in the affected area, in one or more layers of the vessel wall
visible varying degrees of inflammatory cell infiltration, necrosis or scarring. muscular artery
inflammation of the middle easily destroy the internal elastic layer of the vessel wall
inflammation of any part of the outcome is often fibrosis and intimal thickening.
Sometimes, you can see changes of certain specific tissue (such as a large number of
Cytomegalovirus or patchy fibrinoid necrosis, inflammation of the entire vessel wall sections
were destroyed and liquefaction). No matter what part of the emergence of inflammation in the
vessel wall, can be expected due to the intimal thickening or thrombosis occurs secondary pipe
cavity occlusion. Furthermore, once the integrity of the vessel wall damage, red blood cells and
fibrin exudation to be perivascular connective tissue.
Any vessel can be violated inflammatory response, including arteries, arterioles, veins,
venules and capillaries. However, due to a variety of pathophysiological changes caused by
vasculitis, most can be summarized as arterial inflammation, which can happen arteritis

complete or partial occlusion of blood vessels, and tissue necrosis ensues.

Total due to vascular inflammation showed segmental or focal lesions, when clinically
suspicious tissue biopsy, not be able to get the exact histological evidence of vasculitis.
However endometrial inflammatory lesions of the vessel wall caused and fibrotic reaction
around the outer membrane, often inward and outward expansion from the primary tumor, thus
intimal thickening and fibrosis or surrounding adventitia go far histologic findings suggestive of
vasculitis is often nearby