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)

Seven cases of inflammatory abdominal aortic aneurysms (IAs) were studied by light microscopy, transmission electron microscopy (TEM) and immunohistochemistry. Microscopically, atherosclerosis coexisted with adventitial fibrosis and inflammation. The inflammatory component showed a follicular and a diffuse pattern. Fibrous entrapment of fatty tissue, adventitial vasculitis, neuritis were also common findings. By TEM, sparse smooth muscle cells having dilated cisternae of rough endoplasmic reticulum, large bundles of collagen fibres and oedematous, amorphous fibrillary elastin were observed. By immunohistochemistry, the follicles mostly contained CD22+ B-cells. T4- (CD2+/CD4+/CD8-), T8-(CD2+/CD4-/CD8+) cells as well as macrophages (CD4+/CD11c+) and follicular dendritic reticulum cells (DRC1+) were also detected. The monoclonal antibody Ki-67 reacted with 2-48% of germinal center cells. In the fibrous extrafollicular adventitia, actively synthesizing plasma cells prevailed over T4-cells, and macrophages. Some of the macrophages were also activated (CD4+/CD11c+/CD25+/CD30-). IgM, IgG and C3c deposits were detected in the fibrous zone, in the germinal centers, within adventitial vessels and nerves. HLA-DR antigen was diffusely expressed in cells populating both the fibrous and the follicular zones as well as in endothelial and Schwann cells. These findings suggest that IAs could develop in some individuals affected by advanced atherosclerosis of the abdominal aorta through a pathogenic B-cell response to locally presented antigens.
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PMID:An immunohistochemical study of inflammatory abdominal aortic aneurysms. 809 31

We systematically investigated clinical, laboratory, radiologic, and pathologic features, including treatment and prognosis, of stroke syndromes in 30 patients, six from our institution and 24 from the literature, with systemic lupus erythematosus (SLE) and symptomatic large cerebral vessel occlusive disease, documented by angiography or autopsy. The average age at stroke onset was 35 years, and the diagnosis of SLE was made on average 4.4 years prior to that. At least 86% had active SLE at the time of their stroke. Headache was common at onset. We found major intracranial or extracranial vessel occlusive process by (1) thrombus, (2) dissection, (3) fibromuscular dysplasia or vasculitis, and (4) atherosclerosis. The presumed mechanisms were coagulopathy, cardiogenic embolism, large cerebral vessel vasculitis or occlusive vasculopathy, cervical arterial dissection, and premature atherosclerosis. The short-term death rate was 40% and the recurrent stroke rate was 13%. We conclude that symptomatic large cerebral vessel occlusive disease in SLE generally occurs several years after the diagnosis of SLE, usually during the active phase of the disease, is related to heterogeneous mechanisms, and carries a relatively poor short-term outcome.
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PMID:Large cerebral vessel occlusive disease in systemic lupus erythematosus. 814 3

Two 11-month-old 7-kg unrelated female Beagles had clinical signs referable to the cardiovascular system. Histologic studies in both dogs revealed strikingly similar findings of sclerosis of the arteries of the sinoatrial node. Histologic changes included intimal thickening and fibrosis, with marked luminal narrowing; medial hypertrophy, fibrosis, and smooth muscle cell proliferation; and elastic fiber disruption and reduplication. Possible differential diagnoses for this condition included systemic necrotizing vasculitis (canine pain syndrome), coronary polyarteritis, and atherosclerosis.
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PMID:Sinoatrial node arteriosclerosis in two young dogs. 817 70

von Willebrand factor (vWF), first described in a bleeding disorder, has numerous other roles, some of which can be viewed in terms of the pathogenesis of atherosclerosis and others in the formation of thrombus. As a marker of endothelial cell injury it provides a unique opportunity to observe the events involved in conditions where vasculitis may occur, e.g. inflammatory vascular disease and diabetes. Just as low levels predispose to disease, so excessively high levels may lead to adverse cardiovascular events such as myocardial infarction and femoral artery occlusion, which may both be precipitated by thrombus. It is possible that intervention (possibly with drugs, peptides or other agents) that reduces circulating vWF, perhaps by interfering with its activity in aggregating platelets and mediating their adhesion to the sub-endothelium, or reducing its release from the endothelium, may lead to a reduction in thrombotic disease.
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PMID:von Willebrand factor and the endothelium in vascular disease. 821 18

In young patients episodes of amaurosis fugax usually correspond to processes not related with atherosclerosis of the extracranial vessels such as migraine, cardiac embolism, vasospasm, vasculitis, oral contraceptives or hematologic disease. In 11% of the cases, however, no cause can be found. These idiopathic cases generally have a benign course and their frequency decreases spontaneously allowing them to be described as benign amaurosis fugax. We describe four cases of amaurosis fugax in which no responsible cause was found despite extensive clinical, laboratory ultrasonographic and angiographic studies. The episodes progressively remitted. In these cases of benign amaurosis fugax the risk of a permanent deficit is exceptional and treatment is not necessary.
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PMID:[Benign amaurosis fugax]. 820 61

We report a 37-year-old man with cerebral infarction due to meningovascular neurosyphilis. He developed right hemiplegia and motor aphasia preceded by left retroorbital pain lasting a month. Bilateral tonic pupils were also observed. Magnetic resonance imaging (MRI) disclosed cerebral infarction in the distribution of perforating branches of the left middle cerebral artery. Abnormal enhancement was absent in the meninges on T1-weighted MRI examination. SPECT study with I-123 iodoamphetamine showed decreased perfusion in the area of the left middle cerebral artery on early phase. A delayed SPECT 4 hour later demonstrated redistribution of the cerebral blood flow in the area of its cortical branches. On cerebral angiograms, marked stenoses were disclosed at the supraclinoid segments of the bilateral internal carotid arteries as well as the M1 segment of the left middle cerebral artery. These stenoses were associated with increased collateral circulations on the left side. Atherosclerosis was not apparent, on angiography. The cerebrospinal fluid (CSF) showed pleocytosis and positive TPHA. The CSF/serum ratio of TPHA was 1/16. Oligoclonal IgG band was present in the CSF. CSF IgG index was elevated. These findings were consistent with meningovascular neurosyphilis. Causes of angiitis other than syphilis were excluded. A test for antibodies against human immunodeficiency virus was negative. The clinical course of his recovery was similar to that in patients with atherosclerotic thrombosis. The stenosis of the right internal carotid artery demonstrated by angiography could not be expected from the clinical manifestations and SPECT study.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Bilateral internal carotid artery stenoses in a patient with meningovascular neurosyphilis]. 826

Atherosclerotic lesions usually occur in the proximal and middle portion of the coronary arteries. Multiple obstructive lesions appearing only in the peripheral branches without lesions in the proximal or distal portion have not been reported. We encountered a patient with ischemic heart disease showing multiple obstruction in the peripheral branches of the right and left coronary arteries without significant stenotic lesions in the proximal or middle portion. This 49-year-old male was admitted to Yamada Red Cross Hospital due to angina pectoris. Coronary risk factors for him included hypertension, abnormal glucose tolerance, smoking habit, and obesity. Laboratory studies showed a complete blood count and normal blood chemistries, as well as thromboplastin and prothrombin times. Coronary angiography showed multiple obstruction or marked stenosis in the distal portion and peripheral branches; there was no stenosis in the proximal and middle portions. Left ventriculography showed severe hypokinesis in the diaphragmatic segment. Biopsy of the left ventricular endocardium showed interstitial fibrosis but showed no abnormalities in the myocardial fibers or cell infiltration to perivascular areas and vascular walls. Coronary angiography after two months showed multiple lesions, as previously observed. Although ischemic heart disease is caused by various types of vasculitis, embolism, coronary spasm, and fibromuscular dysplasia, in this patient, there were no findings suggestive of causes other than atherosclerosis. This case is interesting in terms of rare angiographic findings and its cause.
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PMID:Ischemic heart disease showing unusual angiographic findings. 834 Oct 3

The major cause of late death in cardiac transplant recipients is cardiac allograft vasculopathy also referred to as cardiac transplant atherosclerosis which occurs in 15% to 20% of transplant recipients. It differs from traditional atherosclerosis in that it is a concentric and diffuse intimal hyperplastic process, the internal elastic lamina remains intact, and calcification is rare. The distal portion of the coronary vessel is the earliest to occlude, with occlusion occurring rapidly. Sometimes a low grade vasculitis is also present. There is no definitive reason for cardiac allograft vasculopathy occurring though it has been suggested that it may actually be caused by immunologic and nonimmunologic damage to endothelial cells resulting in myointimal proliferation. Intravascular ultrasound and coronary angioscopy seem to be a more sensitive diagnostic measure of cardiac allograft vasculopathy than coronary angiography. To date, retransplantation seems to be the only definitive therapy for cardiac allograft vasculopathy. But only fair results are being seen with this procedure.
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PMID:Cardiac allograft vasculopathy: current concepts. 839 71

Iron-derived reactive oxygen species are implicated in the pathogenesis of various vascular disorders including atherosclerosis, vasculitis, and reperfusion injury. The present studies examine whether heme, when liganded to physiologically relevant proteins as in hemoglobin, can provide potentially damaging iron to intact endothelium. We demonstrate that reduced ferrohemoglobin, while relatively innocuous to cultured endothelial cells, when oxidized to ferrihemoglobin (methemoglobin), greatly amplifies oxidant (H2O2)-mediated endothelial-cell injury. Drawing upon our previous observation that free heme similarly primes endothelium for oxidant damage, we posited that methemoglobin, but not ferrohemoglobin, releases its hemes that can then be incorporated into endothelial cells. In support, cultured endothelial cells exposed to methemoglobin--in contrast to exposure to ferrohemoglobin, cytochrome c, or metmyoglobin--rapidly increased their heme oxygenase mRNA and enzyme activity, thereby supporting heme uptake; ferritin production was also markedly increased after such exposure, thus attesting to eventual incorporation of Fe. These cellular methemoglobin effects were inhibited by the heme-scavenging protein hemopexin and by haptoglobin or cyanide, agents that strengthen the liganding between heme and globin. If the endothelium is exposed to methemoglobin for a more prolonged period (16 hr), it accumulates large amounts of ferritin; concomitantly, and presumably associated with iron sequestration by this protein, the endothelium converts from hypersusceptible to hyperresistant to oxidative damage. We conclude that when oxidation of hemoglobin facilitates release of its heme groups, catalytically active iron is provided to neighboring tissue environments. The effect of this relinquished heme on the vasculature is determined both by extracellular factors--i.e., plasma proteins, such as haptoglobin and hemopexin--as well as intracellular factors, including heme oxygenase and ferritin. Acutely, if both extra- and intracellular defenses are overwhelmed, cellular toxicity arises; chronically, when ferritin is induced, resistance to oxidative injury may supervene.
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PMID:Endothelial-cell heme uptake from heme proteins: induction of sensitization and desensitization to oxidant damage. 841 93

It is generally accepted that myocardial ischemia, and its extreme consequence, acute myocardial infarction, can result from transient or permanent disproportion between myocardial oxygen demand and coronary artery blood supply. Insufficient coronary artery blood supply may have many reasons. The aim of the study is to point to the clinical features of the coronary vasculitides as well as to the diagnostic and therapeutic possibilities. Coronary artery involvement in infectious angiitis, in Takayasu's arteritis, in granulomatous giant cell arteritis, in thromboangiitis obliterans, in polyarteritis nodosa, in Wegener's granulomatosis and in Churg--Strauss syndrome is discussed. The diagnosis of coronary vasculitis must be supposed in every patient with primary or secondary vasculitis in whom chest pain or cardiac failure appear. In young patients with clinical, electrocardiographic or laboratory signs of coronary artery disease, especially in absence of risk factors for atherosclerosis, the diagnosis of coronary vasculitis must be considered in differential diagnosis. (Fig. 4, Tab. 1, Ref. 32.).
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PMID:[Vasculitides of the coronary arteries]. 862 Mar 25


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