Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0042384 (vasculitis)
 20,525 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The presentation deals with the enzymatic spectrum of the blood serum (aminotransferase-glutamino-pyruvic and glutamino-oxaloacetic acid, sera cholinesterase, histidase, acid alkaline phosphatase) in 100 patients with transient disorders of cerebral circulation in the form of ischemic and hemorrhagic strokes. These disorders of circulation appeared on the background [corrected] of atherosclerosis and hypertensive disease or in other combination along with vasculitis of a different etiology. The most significant were changes of histidase and acid phosphatase activity and an inhibition of cholinesterase activity in ischemic and hemorrhagic strokes with expressed focal disorders of cerebral circulation. In an improvement of the clinical state following medicative therapy there was a normalization of these indices. The only exclusion was histidase the content of which in some cases remained cunhanged.
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PMID:[Blood serum enzymatic spectrum in vascular diseases of the brain]. 62 45

An unusual case of systemic lupus erythematosus (SLE) in a young child is reported with sudden death from myocardial infarction. The diagnosis of lupus erythematosus in this patient was made by renal biopsy at the age of 3 years. Atherosclerosis of the coronary arteries and aorta was found at autopsy with occlusion of the anterior descending branch of the left coronary artery. It is suggested that the vascular changes in this case were related to hypertriglyceridemia and prolonged prednisone therapy superimposed on a hypersensitivity vasculitis related to SLE.
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PMID:Myocardial infarct in a child with systemic lupus erythematosus. 66 98

The authors conducted a study of tolerance to glucose with the aid of a prednisolone-glucose-tolerance test in 2 groups of patients with brain strokes. The first group consisted of 63 patients younger than 45 years, the second-of 5 cases-older than 55 years of age. In both groups a positive prednisolone-glucose-tolerance test was found in patients with atherosclerosis or hypertensive disease and was not ever seen in strokes of other etiology (rheumatism, nonspecific vasculitis, cerebral vascular aneurysms, blood diseases, etc.). Irrespective of the age, latent diabetus was somewhat more frequently depicted in severe, generalized forms of atherosclerosis. The authors are of the opinion that larvated abnormalities of the carbohydrate metabolism are one of the significant "risk" factors facilitating earlier onset of atherosclerosis and hypertensive disease, as well as their different complications, including cerebral stokes. The report contains facts according to which dysglycemia seen in older patients should be considered not as a physiological aging sysmptoms, but as a sign of latent diabetus.
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PMID:[Role of latent anomalies in carbohydrate metabolism in the pathogenesis of vascular lesions of the brain]. 84 23

About 15% of patients with cancer have cerebrovascular lesions, resulting from 4 kinds of disorders sometimes intermingled in advanced disseminated cancer: coagulation disorders, direct effects of the tumor, infections and therapeutic measures. Infarction, hardly less frequent than hemorrhage, mostly complicates lymphoma and carcinoma. Hypercoagulation states, such as chronic disseminated intravascular coagulation, nonbacterial thrombotic endocarditis, and nonmetastatic cerebral venous thrombosis account for about 50% of cases. Tumor emboli, as seen in intravascular malignant lymphomatosis, arteritis related to aspergillus, granulomatous angiitis with or without herpes zoster and radiation-induced atherosclerosis are rarer. Cerebral hemorrhages, excluding bleeding from the metastases of choriocarcinoma and melanoma are mainly associated with leukemia by acute disseminated intravascular coagulation as in promyelocytic leukemia, by leukostasis or by pancytopenia. Both infarction and hemorrhage rarely reveal the neoplasia. Lesions are often small and disseminated, and therefore produce a picture of diffuse acute or subacute encephalopathy rather than acute focal deficits. Finally, there may be no relationship between the cerebrovascular event and the neoplasia, and atherosclerosis or traumatic subdural hematoma may well be the causal factor.
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PMID:[Cerebrovascular complications of cancers]. 130 55

The importance of inflammatory phenomena in atherosclerosis is now appreciated. Here, a clinical trial to be conducted using anti-inflammatory drugs (sulfasalazine, griseofulvin and colchicine) in angina pectoris, myocardial infarction and coronary restenosis after angioplasty and bypass grafting is proposed. Patients who have both atherosclerosis and a disease responsive to anti-inflammatory drugs (ulcerative colitis or Crohn's disease, dermatomycosis, necrotizing vasculitis, Behcet's disease, gout or other colchicine-sensitive diseases), are desirable targets of the present proposal.
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PMID:Proposal for clinical trials using anti-inflammatory drugs in the therapy of angina pectoris, myocardial infarction and coronary restenosis after angioplasty and bypass grafting. 135 49

Several studies during recent years have demonstrated the potential for vascular smooth muscle cells (SMC) and dermal fibroblasts to participate in immune interactions such as antigen presentation and alloreactivity. The molecular interactions mediating lymphocyte adhesion to these mesenchymal cells have, however, not previously been characterized in detail. In the present study we demonstrate ICAM-1 (CD54) expression by cultured human SMC and its up-regulation by IL-1, IFN-gamma, and bacterial lipopolysaccharide. Monoclonal antibodies were used to define the molecular interactions in the adhesion of 51Cr-labelled T lymphoblasts to adherent SMC and fibroblasts. ICAM-1 appeared to mediate adhesion of T lymphocytes by binding to the beta 2-integrin CD11a/CD18 (LFA-1) expressed by the lymphoblasts. We present evidence for the involvement of at least three different mechanisms in the adhesion of activated T lymphocytes to cultured fibroblasts. It was found that beta 2-integrin-mediated interaction could only account for less than half of the binding activity. The remaining adhesion was partly mediated by beta 1-integrins, presumably via VLA-5 since an anti-VLA-5 antibody and an RGD-containing peptide blocked adhesion to the same degree. However, antibodies to beta 1-, beta 2-, and beta 3-integrin subunits added together only inhibited adhesion by approximately 50%. The residual adhesion could be blocked by inhibition of cell metabolism and was increased by stimulation of the lymphocytes with phorbol ester, suggesting involvement of other, as yet undefined, adhesion molecules. The molecular interactions between lymphocytes and mesenchymal cells demonstrated in this study may have implications in several inflammatory conditions such as vasculitis, atherosclerosis, and connective tissue diseases.
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PMID:Adhesion of activated T lymphocytes to vascular smooth muscle cells and dermal fibroblasts is mediated by beta 1- and beta 2-integrins. 138 Jan 79

Oxidant injury has been implicated in the pathogenesis of inflammatory, metabolic and toxic insults, in ischemic-reperfusion injury, and in carcinogenesis, aging and atherosclerosis. Oxidant injury is initiated by free radicals and reactive oxygen molecules which are generated by activated neutrophils, monocytes, and mesangial cells, during normal and abnormal metabolic processes, and from the metabolism of exogenous drugs and toxins. When cells and organs are exposed to oxidant stress, several different antioxidant defense mechanisms operate to prevent or limit oxidant injury. When antioxidant defense mechanisms are decreased, or when the generation of reactive oxygen molecules is increased, oxidant injury results from the shift in the oxidant/antioxidant balance. Oxidant-induced alterations of proteins, membranes, DNA, and basement membranes leads to cell and organ dysfunction. Several renal diseases including glomerulonephritis, vasculitis, toxic nephropathies, pyelonephritis, acute renal failure, and others are likely to be mediated at least in part by oxidant injury. In the future, mechanisms to decrease the generation of reactive oxygen molecules and/or antioxidant therapy may develop into new avenues of therapeutic intervention.
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PMID:Reactive oxygen molecules, oxidant injury and renal disease. 166 82

Most ischemic heart disease in associated with severe coronary atherosclerosis. A small subset of patients, however, had angina pectoris despite angiographically normal coronary arteries and absence of inducible coronary spasm. Coronary microcirculation (i.e. arteries too small to be visualized by current angiographic techniques) has been identified as the weak point of these patients. Small coronary vessel involvement may be due to organic conditions (such as diabetes, vasculitis, systemic collagen-vascular diseases, infectious processes) that act through coronary thrombosis or embolism and related alteration in coronary vasomotion; alternatively, the vascular abnormality appears to be entirely functional (no ultrastructural myocardial changes) such as the case of hypertension, hypertrophic cardiomyopathy and syndrome X. Whatever the cause(s) and mechanism(s) of the small coronary artery involvement, this leads to myocardial ischemia and to the related complications as in classic atherosclerotic heart disease. Syndrome X is characterized by effort-induced angina pectoris, ST-segment changes during exercise testing, negative ergonovine test and reduced coronary reserve. A pre-arteriolar hypersensitivity to vasoconstrictor influences (elicited by cold pressor test or ergonovine) and a reduced vasodilator capacity (unmasked by metabolic and pharmacological studies) have been proposed as potential pathogenetic substrate. This dynamic alteration in vasomotion would answer for both symptoms and signs of myocardial ischemia, that, however, appear to be contemporarily elicitable in a minority of patients. Treatment with beta-blockers and calcium-antagonists has been found to be effective. The long-term follow-up shows favorable outcome with a high survival rate and a low incidence of cardiovascular events.
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PMID:[Angina due to microvascular pathology]. 184 63

We describe a 48-year-old, previously healthy, anti-Ro/SS-A and anti-La/SS-B antibody positive black woman with negative risk factors for atherosclerosis, who developed mental status and personality changes over a 6-12-month period, and progressive cortical blindness over a 2-week period. Angiographic and computed axial tomographic studies of the brain demonstrated multiple large areas of infarction correlating with stenosis and occlusions of the internal carotid and posterior cerebral arteries. Moya moya-like findings were prominent radiographically. Results of angiographic, computed tomographic, and magnetic resonance imaging studies were interpreted as being compatible with large, medium, and small vessel disease, most likely a vasculitis.
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PMID:Cerebral vasculopathy associated with collateralization resembling moya moya phenomenon and with anti-Ro/SS-A and anti-La/SS-B antibodies. 185 80

The present study was designed to investigate the capacity of human vascular smooth muscle cells (SMCs) to produce a cytokine chemotactic for monocytes (monocyte chemotactic protein [MCP]) and by way of comparison, a related polypeptide activator of neutrophils (known as interleukin-8 [IL-8] or neutrophil activating protein-1 [NAP-1]. On exposure to IL-1, SMCs released high levels of chemotactic activity for monocytes, which could be removed by absorption with anti-MCP antibodies. MCP production by activated SMCs was comparable to that of IL-1-stimulated umbilical vein endothelial cells. Activated SMCs released appreciable levels of IL-8, as determined by a specific enzyme-linked immunosorbent assay, but little chemotactic activity for neutrophils. IL-1-treated SMCs expressed high levels of both MCP and IL-8 mRNA transcripts, as assessed by Northern blot analysis. Tumor necrosis factor and bacterial lipopolysaccharide but not IL-6 also induced MCP and IL-8 gene expression in SMCs. Nuclear runoff analysis revealed that IL-1 augmented transcription of the MCP and IL-8 genes. The capacity of SMCs to produce a cytokine (MCP) that recruits and activates circulating mononuclear phagocytes may be of considerable importance in the pathogenesis of vascular diseases (e.g., vasculitis and atherosclerosis) that are characterized by monocyte infiltration of the vessel wall.
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PMID:Expression of monocyte chemotactic protein and interleukin-8 by cytokine-activated human vascular smooth muscle cells. 191 3


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