Inflammatory vascular

Blake, D.R., Winyard, P., Scott, D.G.I., Brailsford, S., Blann, A. and Lunec, J. (1985). Endothelial cell cytotoxicity in inflammatory vascular diseases - the possible role of oxidised lipoproteins. Ann. Rheum. Dis. 44, 176-182. 

JAMs. Members of an immunoglobulin subfamily expressed by leukocytes, platelets, and endothelial cells, regulates leukocyte/platelet/endothelial cell interactions in the immune system, and promotes inflammatory vascular responses... 

Atherothromboembolism ntracranial small vessel disease Leukoaraiosis Dissection (Table 6.4) Fibromuscular dysplasia Congenital arterial anomalies Moyamoya syndrome Embolism from arterial aneurysms Inflammatory vascular diseases Irradiation... 

Futrell N (1995). Inflammatory vascular disorders diagnosis and treatment in ischemic stroke. Current Opinions in Neurology 8 55-61... 

Giant cell arteritis (or other inflammatory vascular disorders) (Ch. 6) Structural intracranial lesion (Chs. 8 and 9) intracranial venous thrombosis (Ch. 29)... 

Fever is unusual in the first few hours after stroke onset, and endocarditis or other infections, inflammatory vascular disorders or cardiac myxoma should be considered. Later fever is quite common and usually reflects a complication of the stroke (Ch. 16). 

Spinal subarachnoid hemorrhage is very rare. It is caused by a vascular malformation, hemostatic failure, coarctation of the aorta, inflammatory vascular disease, mycotic aneurysm or a vascular tumor such as ependymoma. Accumulating hematoma may compress the spinal cord. Suspicion is aroused if the cerebral angiogram is negative and the patient develops spinal cord signs. 

The regeneration of normal filament structure of restored tissues was observed by immunohistochemical methods after PHB devices implantation [66]. The immunohistochemical demonstration of cytokeratine, an intermediate filament, which is a constituent of epithelial and mesodermal cells, agreed with observations on intact mesothelium. Heparin sulfate proteoglycan, a marker of basement membrane, was also identified [66]. However, in spite of good tissue reaction to implantation of cardiovascular PHB patches, PHB endovascular stents in the rabbit iliac arteria caused intensive inflammatory vascular reactions [80]. 

When exposure is repeated, the allergen binds between two adjacent IgE molecules. This causes release of inflammatory mediators (histamine, leukotrienes, chemotactic factors). These act locally and cause smooth muscle contraction, increased vascular permeability, mucous gland secretion, and infiltration of inflammatory cells (neutrophils and eosinophils). However, histamine can also be released by non-IgE-mediated mechanisms (e.g., due to exposure to certain fungi). 463... 

Human bodies are constantly exposed to a plethora of bacteria, viruses, and other inflammatory substances. To combat these infections and toxic agents, the body has developed a carefully regulated inflammatory response system. Part of that response is the orderly migration of leukocytes to sites of inflammation. Leukocytes literally roll along the vascular wall and into the tissue site of inflammation. This rolling movement is mediated by reversible adhesive interactions between the leukocytes and the vascular surface. 

Current evidence suggests that PPAR activation may limit inflammation and hence atherosclerosis. Both PPAR-a and PPAR-y can reduce T-cell activation, as shown by decreased production of EFN-y. PPAR-a agonists also rqness endothelial VCAM-1 expression and inhibit the inflammatory activation of vascular SMCs, while PPAR-y agonists repress endothelial chemokine expression and decrease macrophage MMP production. 

Furthermore, there is some evidence for pleiotrophic effects (e.g., effects on hemostasis, vascular function, anti-inflammatory effects, and stabilizing effects on atherosclerotic plaques) of statins. The clinical relevance of this (and the potential difference between the various statins) is at present uncertain but subject to intense investigation. 

Diseases affecting skeletal muscle are not always primary diseases of muscle, and it is necessary first to determine whether a particular disorder is a primary disease of muscle, is neurogenic in origin, is an inflammatory disorder, or results from vascular insufficiency. A primary disease of muscle is one in which the skeletal muscle fibers are the primary target of the disease. Neurogenic disorders are those in which weakness, atrophy, or abnormal activity arises as a result of pathological processes in the peripheral or central nervous system. Inflammatory disorders may result in T-cell mediated muscle damage and are often associated with viral infections. Vascular insufficiency as a result of occlusion in any part of the muscle vasculature can cause severe disorders of muscle, especially in terms of pain, metabolic insufficiency, and weakness. 

Muscle dysfunction may also present as part of multisystem disease, often involving vascular insufficiency or autoimmune disease. By far the most important of the multisystem and autoimmune diseases are seen as subclasses of the inflammatory disorders. 

ADM may evolve over several years, the extent of fiber atrophy provides an important indication of the chronicity of muscle degeneration. Acute muscle necrosis and phagocytosis give some indication as to how active the disease is at the time of biopsy. In most biopsies from ADM patients, the inflammatory cell foci are perivascular and perimysial rather than endomysial and are dominated by B-lymphocytes. The ratio of T4 lymphocytes (helper cells) to T8 lymphocytes (cytotoxic) generally indicates a predominance of the former. As in JDM, this is consistent with humoral mechanisms of cell damage, and vascular involvement is also apparent in the form of capillary endothelial cell abnormalities (tubular arrays) and duplication of basal lamina. Loss of myofibrillar ATPase from the central portions of fibers is a common prelude to muscle necrosis. 

---