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)

Interleukin 1 (IL-1) alters several potentially pathogenic endothelial cell (EC) functions. The authors report here that recombinant human IL-1 (rIL-1) alpha (0.1 to 10 ng/ml) or IL-1-beta (1 to 100 ng/ml) induce concentration- and time-dependent increases in IL-1-beta mRNA levels in EC derived from adult human saphenous vein. rIL-1 induced IL-1-alpha mRNA only in EC treated concomitantly with cycloheximide (2 micrograms/ml). IL-1-beta mRNA production began within 1 hr of exposure to rIL-1, peaked after 24 hr, and declined thereafter. Actinomycin D prevented the appearance of IL-1 mRNA in rIL-1-treated EC. rIL-1 also induced the release of biologically active IL-1 from EC, which was inhibited by cycloheximide (1 microgram/ml). When compared on the basis of their activity in the thymocyte costimulation assay, rIL-1-alpha and rIL-1-beta were equipotent as inducers of IL-1 production by EC. EC stimulated with rIL-1 produced prostaglandin E2, which inhibits IL-1 production by other cell types and also decreases the responsiveness of thymocytes to IL-1. When EC were exposed to rIL-1 in the presence of indomethacin (1 microgram/ml), which blocked prostaglandin E2 production, greater amounts of rIL-1-induced IL-1 release were detected, although the inhibitor did not affect IL-1-beta mRNA levels. IL-1-induced IL-1 production was unlikely to be caused by endotoxin contamination of tissue culture media or IL-1 preparations, because the lipopolysaccharide (LPS) antagonist polymyxin B (10 micrograms/ml) blocked LPS-induced IL-1 production by EC but did not affect IL-1 release in response to rIL-1-beta (100 ng/ml). The IL-1-inducing property of rIL-1-beta was heat-labile, whereas heated LPS stimulated EC IL-1 production. The source of IL-1 in our cultures was not monocyte/macrophages, as treatment of EC with monoclonal antibody to the monocyte antigen Mo2 under conditions that lysed adherent peripheral blood monocytes did not affect production of IL-1 by EC in response to LPS (1 microgram/ml) or rIL-1-beta (100 ng/ml). IL-1 elicits a coordinated program of altered endothelial function that increases adhesiveness for leukocytes and coagulability. IL-1-induced IL-1 gene expression in human adult EC could thus provide a positive feedback mechanism in the pathogenesis of vascular disease including atherosclerosis, vasculitis, and allograft rejection.
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PMID:Interleukin 1 induces interleukin 1. II. Recombinant human interleukin 1 induces interleukin 1 production by adult human vascular endothelial cells. 349 83

The chemistry, industrial usage, general toxicity, and experimental use of allylamine are briefly reviewed. This highly reactive unsaturated alkylamine has had industrial applications in a variety of organic processes, and continues to be utilized, although accurate data concerning production is not readily available. The general toxic effects of the freebase form are primarily related to irritation of the mucous membranes, whereas the relatively long history of experimental use of this chemical has emphasized its' extraordinarily deleterious effects on heart and vascular tissue. Allylamine has been given by a variety of routes to many species in attempts to cause lesions which mimic human acute vasculitis, acute myocardial necrosis, and atherosclerosis; examples of typical lesions are illustrated. More recent in vivo and in vitro experimental work concerning the cellular toxicity of allylamine are summarized, and possible mechanisms of this chemicals' toxic action are discussed.
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PMID:Allylamine cardiovascular toxicity. 355 Nov 96

Histo-morphological changes of the coronary vessels in cases of rheumatic heart disease (RHD) have been studied in 60 cases. Involvement of intramyocardial branches of coronary vessels in the form of active rheumatic vasculitis or inactive lesions characterized by medial hypertrophy and replacement fibrosis was seen in 15 of 60 cases. These lesions may affect myocardial function. Atherosclerosis of the pulmonary trunk and its branches was frequently seen in these hearts, indicating that this may be an important index of pulmonary hypertension. An unusual association of bicuspid aortic stenosis and RHD was seen in one case. Another case showed acute myocardial infarction due to coronary embolism from bacterial vegetation of bacterial endocarditis.
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PMID:An autopsy study of rheumatic heart disease. Part II. Associated findings. 359 4

Systemic lupus erythematosus (SLE) is a well-known acute and/or chronic multisystem disease of complex autoimmune nature, having predilection for cardiovascular system. While its cardiac manifestations have been adequately studied, there is paucity of information on its vascular manifestations. Accordingly, we studied the incidence of vascular manifestations in 50 consecutive SLE patients seen at our institutions and in private practice during the past 12 years. Systemic hypertension (44%) was the most common vascular manifestation followed by vasculitis (30%), Raynaud's phenomenon (26%), telangiectasis (20%), premature coronary atherosclerosis (6%), digital ulceration (6%), thrombophlebitis (6%), pulmonary hypertension (4%) and portal hypertension (4%). Diffuse systemic vasculitis similar to polyarteritis nodosa was rare (2%). Often more than one lesion was found in the same patient. The clinical diagnosis of these vascular manifestations in the context of the primary disease (SLE) usually does not pose any difficulty except when they antedate it. We also studied the pathology and pathogenesis of some of these vascular lesions in both autopsy and biopsy specimens by both light microscopy and immunofluorescent techniques. Our results as well as those of others who also studied these lesions indicate that immune complex deposition and subsequent complement activation play an important role in the pathogenesis of vasculitis, coronary arteritis and premature coronary atherosclerosis. Corticosteroids and vasodilators remain the drugs of choice for the management of the majority of the symptoms arising from the vascular lesions of SLE.
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PMID:Vascular manifestations of systemic lupus erythematosus. 372 68

Dissecting aneurysm and stroke are a rare complication of polymyositis. The present report describes an autopsy case of a 53-year-old woman, who suffered from polymyositis accompanied by dissecting aneurysms of right external iliac and right renal arteries, and furthermore, intracerebral hemorrhage. The latter was caused by necrotizing angiitis. The patient had no abnormal anatomical changes such as coarctation of aorta, aortic stenosis, bicuspid aortic valve or Marfan's syndrome. Atherosclerosis in the patient was mild, and cystic medial necrosis of aorta and arteries was not found. Since the patient was attacked by dissections of arteries following long-term steroid therapy, a possibility can be raised that arterial dissection was attributable to steroid treatment besides necrotizing angiitis complicating in polymyositis.
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PMID:Polymyositis associated with dissecting aneurysm of arteries and intracerebral hemorrhage. 377 35

The role of mononuclear cells in antibody-mediated endothelial cell damage and vascular diseases is not well understood when compared to our understanding of the role of neutrophil-mediated endothelial injury in vascular diseases. Thus we initiated these in-vitro studies to investigate the interactions of leukocytes (neutrophils and mononuclear cells) with vascular endothelial cells in the presence and absence of antiendothelial cell antibodies (anti-red blood cell antiserum-anti-RBC). Cultured endothelial cells were isolated from bovine pulmonary artery. The effects of unfractionated and fractionated human leukocytes (neutrophils, mononuclear cells, or lymphocytes) on endothelial cell viability was examined both quantitatively (51Cr release) and qualitatively (electron microscopy). Results from these studies indicated that the interactions of mononuclear cells and lymphocytes with antibody-coated endothelial cells resulted in a significant endothelial cell lysis within 1 to 6 hours of reactions. Neutrophils, on the other hand, failed to induce significant endothelial cell damage compared to mononuclear cells and lymphocytes when tested under similar conditions. In the absence of anti-RBC antibodies, all cell types (neutrophils, mononuclear cells, or lymphocytes) did not produce detectable endothelial damage. Additionally, the effectiveness of mononuclear cells to injure antibody-labeled endothelial cells was confirmed by ultrastructural examination. Similar studies, utilizing leukocytes obtained from patients with atherosclerosis disease, were also undertaken. In these studies we found that, again, only mononuclear cells and lymphocytes wer capable of inducing damage to endothelial cells precoated with antibodies. In summary, our results demonstrate the ability of mononuclear cells and lymphocytes to induce significant damage to antibody-coated endothelial cells. This finding suggests a major role of mononuclear leukocytes in vascular endothelial destruction in diseases that are characterized by the presence of circulating autoantibodies in serum and the adhesion of mononuclear cells to the vascular wall. Such diseases include vasculitis, allograft rejection, serum sickness, and perhaps atherosclerosis particularly in patients with autoimmune diseases.
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PMID:Influence of anti-endothelial cell antibodies on the interactions of leukocytes with vascular endothelial cells in vitro. 391 99

In this review, the cardiac lesions which develop in association with the various collagen-vascular diseases are described. In rheumatoid arthritis, the most frequent lesions are: fibrous obliterative pericarditis, with pericardial deposits of calcium, fibrin, cholesterol, and rheumatoid granulomas; granulomatous or nonspecific myocarditis; valvulitis, vasculitis, and amyloid deposits. In ankylosing spondylitis, the lesions involve mainly the valves (aortic and mitral valves) and the aorta. In systemic lupus erythematosus, the predominant cardiovascular lesions are: pericarditis, Libman-Sacks endocarditis, nonspecific myocarditis, vasculitis with fibrinoid necrosis, and acceleration of atherosclerosis. In scleroderma, the main cardiac lesion is fibrosis with only scanty inflammatory cells; pericarditis and nonbacterial thrombotic endocarditis also occur. In dermatomyositis/polymyositis, fibrous or fibrinous pericarditis can occur, as well as myocarditis with infiltrates of lymphocytes and plasma cells and with degeneration and necrosis of myocytes; valvulitis is uncommon except when the disease is related to mucinous adenocarcinoma. In polyarteritis nodosa, various stages of necrotizing vasculitis involve all layers of the arterial walls; foci of myocardial necrosis of various sizes can occur in association with these lesions; cardiac hypertrophy related to hypertension and pericarditis related to uremia, may also be found. In Wegener's granulomatosis, pericarditis, inflammatory infiltrates, necrotizing granulomas, and vasculitis have been observed in the heart.
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PMID:Cardiovascular lesions in collagen-vascular diseases. 391 76

A 6-year-old, obese, spayed female Doberman pinscher dog was presented for clinical examination with a 1-day history of repeated seizures and a long-term history of periodic bouts of ataxia, circling, and head tilt. The seizures were controlled with phenobarbital, but the dog died 2 days after presentation. Necropsy revealed severe, diffuse, follicular atrophy of the thyroid gland (primary hypothyroidism), severe generalized atherosclerosis, severe pseudolaminar cortical necrosis and acute vasculitis in the cerebrum, and congestive heart failure. The neurologic signs were explained by the pseudolaminar necrosis and associated cerebrovascular atherosclerosis. The cerebrocortical necrosis was believed to be caused by tissue hypoxia secondary to progressive vascular occlusion. Cerebrovascular atherosclerosis, secondary to primary hypothyroidism, was considered the most important cause of the hypoxia.
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PMID:Neurologic manifestations of cerebrovascular atherosclerosis associated with primary hypothyroidism in a dog. 397 13

The case of a 34-year-old white male who died suddenly and unexpectedly of a thrombosed coronary artery aneurysm is presented. Coronary artery aneurysms have a prevalence of approximately 2%; over half of these are caused by atherosclerosis with the remainder due to syphilis, infections, trauma, congenital malformations, vasculitis, neoplasms, and connective tissue disorders (Ehlers-Danlos and Marfan's syndromes). Replacement of the media by atherosclerotic debris is the cause of atherosclerotic aneurysms. Complications include rupture and thrombosis. Sudden death has been reported in eight other cases of atherosclerotic aneurysms; sudden unexpected death as the presenting symptom of atherosclerotic coronary artery aneurysm, as in our case, is rare.
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PMID:Sudden unexpected death due to atherosclerotic coronary artery aneurysm. 402 68

One hundred consecutive female patients with active systemic lupus erythematosus (SLE) were studied from the cardiovascular point of view by means of non invasive methods. Seventy percent of the cases presented some type of cardiovascular anomaly. Seventy four percent of the resting electrocardiograms were abnormal as well as 72% of the M mode echocardiograms and 55% of the cardiac X ray series. The most frequent observed complications were: pericarditis and or pericardial effusion (39%), arterial hypertension (22%), ischemic heart disease (16%), myocarditis (14%), congestive heart failure (10%), pulmonary hypertension (9%), valvular heart disease (9%), pleural effusion (7%) and cerebro vascular accident (3%). We analyzed each one of these complications and found of special interest the high incidence of ischemic heart disease which is more frequent than has been hitherto reported. Ischemic heart disease was observed in two types of patients: a) Those with long term steroid therapy. In these, the mechanism seems to be an atherosclerotic disease probably induced by the chronic use of steroids. The management of these cases do not differ from other types of coronary heart disease due to atherosclerosis. b) Those with frank episodes of vasculitis in whom the basic mechanism is an inflammatory process of the coronary arteries and its treatment is fundamentally that of the vasculitis. We consider necessary to study routinely all patients with SLE through non invasive cardiological methods.
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PMID:Cardiovascular manifestations in systemic lupus erythematosus. Prospective study of 100 patients. 402 48


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