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Query: UMLS:C0038454 (stroke)
 147,016 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The purposes of this article are to report a case with temporal arteritis (TA) and to summarize and reanalyze the cases of temporal arteritis associated with fever in published articles for understanding better the clinical features of TA. A case with biopsy-proven TA is reported. The publications with TA and fever were searched by using MEDLINE in English from 1966 to 1999. Three hundred sixty cases of temporal arteritis associated with fever were reanalyzed. The results showed that a case of biopsy-proven TA with typically clinical manifestation was initially misdiagnosed and that the reanalysis of 360 cases revealed that the common clinical findings at presentation were abnormal temporal arteries, headache, low fever, loss of weight, polymyalgia rheumatica, jaw claudication, vision disorder, arthralgis or myalyias, and ear pain and that the uncommon clinical findings at presentation were high fever, malaise, anorexia, breast pain, transient ischemic attack/stroke, cough, mental disorder, diarrhea, and uterine prolapse, etc. Laboratory findings were the range of erythrocyte sedimentation rate (ESR) 14 to 149 with a mean of 97.0 mm/hr, white blood cells being normal or increased in the range of 10.9 to 22.9 x 10(9)/L, hemoglobin level 7 to 16 g/dL, the platelets count increased to 785 x 10(9)/L, and microscopic hematuria. The diagnosis was made by a combination of clinical features, an increased ESR, a response to steroids, and, most specifically, temporal artery biopsy. The initial diagnosis was misdiagnosed in 38.2% of patients. In conclusion, the features of TA associated with fever have not been widely appreciated yet. TA is a common cause of fever of unknown origin (FUO) in the elderly. TA should be considered when patients complain of common and uncommon manifestations. An elevated ESR will aid in the diagnosis of TA, and temporal artery biopsy will provide certainty.
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PMID:Temporal arteritis and fever: report of a case and a clinical reanalysis of 360 cases. 1110 64

Giant cell arteritis (GCA) is the commonest primary systemic vasculitis in the United States. Severe outcomes include blindness and stroke, and death may result from aortic dissection. Temporal artery biopsy remains the gold standard for diagnosis. Magnetic resonance imaging (MRI) of involved vessels shows promise as a useful noninvasive method for diagnosis and assessment of disease activity. Corticosteroid therapy is effective but is associated with considerable morbidity. Longitudinal studies with large numbers of patients are required to identify appropriate steroid-sparing agents. New insights into the immunopathogenesis of GCA have allowed us to identify heterogeneous subsets of patients with varying clinical presentations corresponding to specific cytokine profiles. The concept of the involved artery as an active participant in the events leading to luminal obstruction has been realized and provides the opportunity to evaluate novel therapies to modify the course of the disease.
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PMID:Spectrum of giant cell vasculitis. 1112 88

Temporal arteritis (TA) is a vasculitis involving mainly cranial branches of the aorta that can lead to ischemic complications such as amaurosis or ischemic stroke. Increment in the platelet count has been described in the acute period of the disease. We studied retrospectively the platelet count in patients with TA, its association with ischemic complications and quantified its response to therapy. We found thrombocytosis in 44% of 34 patients with TA, with a mean reduction in the platelet count of 25.1% after therapy. We were also able to quantify the increment in the platelet count at the onset of the disease and its response to prednisone in a group of 5 patients. We did not find any relation between platelet count and ischemic complications of the disease or the result of the temporal artery biopsy. In conclusion TA is associated with an increase in the platelet count, with a 25% reduction after prednisone therapy. These two determinations are not related to ischemic complications of the disease.
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PMID:Increment of the platelet count in temporal arteritis: response to therapy and ischemic complications. 1115 Aug 40

Diagnosis of rheumatologic disorders in the elderly is often complicated by the primary care clinician's inability to differentiate among similar manifestations of rheumatologic disorders, the presence of comorbid conditions, and symptoms attributed simply to aging. A major consequence of the aches and pains associated with rheumatologic disorders, including polymyalgia rheumatica (PMR), is the impedance of activities of daily living, potentially leading to a loss of independence. PMR is common in the elderly. Often coexisting with PMR, temporal arteritis can lead to complications, including blindness, stroke, or cardiac sequelae. Timely detection and appropriate treatment of PMR in the elderly may improve quality of life, as well as deter irreversible problems. Patient education also has an important role.
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PMID:Pain in the elderly: polymyalgia rheumatica. 1185 17

Stroke has enormous clinical, social, and economic implications, and demands a significant effort from both basic and clinical science in the search for successful therapies. Atherosclerosis, the pathologic process underlying most coronary artery disease and the majority of ischemic stroke in humans, is an inflammatory process. Complex interactions occur between the classic risk factors for atherosclerosis and its clinical consequences. These interactions appear to involve inflammatory mechanisms both in the periphery and in the CNS. Central nervous system inflammation is important in the pathophysiologic processes occurring after the onset of cerebral ischemia in ischemic stroke, subarachnoid hemorrhage, and head injury. In addition, inflammation in the CNS or in the periphery may be a risk factor for the initial development of cerebral ischemia. Peripheral infection and inflammatory processes are likely to be important in this respect. Thus, it appears that inflammation may be important both before, in predisposing to a stroke, and afterwards, where it is important in the mechanisms of cerebral injury and repair. Inflammation is mediated by both molecular components, including cytokines, and cellular components, such as leukocytes and microglia, many of which possess pro- and/or antiinflammatory properties, with harmful or beneficial effects. Classic acute-phase reactants and body temperature are also modified in stroke, and may be useful in the prediction of events, outcome, and as therapeutic targets. New imaging techniques are important clinically because they facilitate dynamic evaluation of tissue damage in relation to outcome. Inflammatory conditions such as giant cell arteritis and systemic lupus erythematosus predispose to stroke, as do a range of acute and chronic infections, principally respiratory. Diverse mechanisms have been proposed to account for inflammation and infection-associated stroke, ranging from classic risk factors to disturbances of the immune and coagulation systems. Considerable opportunities therefore exist for the development of novel therapies. It seems likely that drugs currently used in the treatment of stroke, such as aspirin, statins, and modulators of the renin-angiotensin-aldosterone system, act at least partly via antiinflammatory mechanisms. Newer approaches have included antimicrobial and antileukocyte strategies. One of the most promising avenues may be the use of cytokine antagonism, for example, interleukin-1 receptor antagonist.
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PMID:Inflammation and infection in clinical stroke. 1246 86

We report on the case of a 69-year-old man admitted with a transient ischemic attack preceded by a two months history of severe headache. Giant cell arteritis was diagnosed by means of temporal artery biopsy. Angiography showed an intra- and extracranial stenosis of the left internal carotid artery. The possible relationship between this stenosis and vasculitis is discussed and stroke as a clinical manifestation of the giant cell arteritis is reviewed.
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PMID:[Internal carotid stenosis and giant cell arteritis]. 1450 52

Giant cell arteritis (GCA) is a granulomatous and occlusive vasculitis that causes blindness, stroke, and aortic aneurysm. CD4(+) T cells are selectively activated in the adventitia of affected arteries. In human GCA artery-severe combined immunodeficiency (SCID) mouse chimeras, depletion of CD83(+) dendritic cells (DCs) abrogated vasculitis, suggesting that DCs are critical antigen-presenting cells in GCA. Healthy medium-size arteries possessed an indigenous population of DCs at the adventitia-media border. Adoptive T cell transfer into temporal artery-SCID mouse chimeras demonstrated that DCs in healthy arteries were functionally immature, but gained T cell stimulatory capacity after injection of lipopolysaccharide. In patients with polymyalgia rheumatica (PMR), a subclinical variant of GCA, adventitial DCs were mature and produced the chemokines CCL19 and CCL21, but vasculitic infiltrates were lacking. Human histocompatibility leukocyte antigen class II-matched healthy arteries, PMR arteries, and GCA arteries were coimplanted into SCID mice. Immature DCs in healthy arteries failed to stimulate T cells, but DCs in PMR arteries could attract, retain, and activate T cells that originated from the GCA lesions. We propose that in situ maturation of DCs in the adventitia is an early event in the pathogenesis of GCA. Activation of adventitial DCs initiates and maintains T cell responses in the artery and breaks tissue tolerance in the perivascular space.
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PMID:Activation of arterial wall dendritic cells and breakdown of self-tolerance in giant cell arteritis. 1473 23

Giant cell arteritis (GCA) is a vasculitis of unknown etiology that affects medium-sized and large arteries, and is the most common form of vasculitis in populations of predominantly Northern European ancestry. If left untreated, GCA can lead to significant morbidity including blindness, stroke, aortic aneurysm and dissection, as well as large-artery stenosis. Glucocorticosteroids are in general very effective in the treatment of GCA. Treatment with high dose glucocorticosteroids is associated with considerable morbidity and for some, but not all patients is required for prolonged periods sometimes exceeding several years. Numerous efforts have been made over the decades to optimize therapeutic outcomes and reduce the side effects of glucocorticosteroids by enlisting adjuvant and alternative therapies. This review focuses primarily on evidence from randomized controlled trials with the objective of efficacy assessment of the respective drugs and dosing regimens in the treatment of GCA. Various glucocorticosteroid dosing regimens including alternate-day dosing, disease-modifying therapies including methotrexate and azathioprine, and the prospect of using monoclonal anti-cytokine or anti-cytokine receptor antibodies in the treatment of GCA are addressed. Thus far, no disease-modifying antirheumatic drug therapy or alternative to daily glucocorticosteroid therapy has been found to be unequivocally effective in the treatment of GCA.
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PMID:The role of disease-modifying antirheumatic drugs in the treatment of giant cell arteritis. 1474 Apr 25

Over a 5-year period, we investigated 77 consecutive patients (36 males, 41 females, mean age 40.9 years) referred to our hospital with the diagnosis of CNS vasculitis. Extensive workup including MRI, echocardiography, laboratory tests, angiography ( n=53), and biopsies at appropriate sites ( n=26) was performed based on individual history and symptoms. Prominent symptoms were stroke ( n=61), encephalopathy ( n=14), and headaches ( n=2). Vasculitis was finally diagnosed in 13 patients (17%) including isolated angiitis of the CNS ( n=3), giant cell arteritis ( n=4), and septic arteritis ( n=3). Thirty-two patients (42%) presented noninflammatory vasculopathies including moyamoya ( n=6), Sneddon's syndrome ( n=5), dissection ( n=4), CADASIL ( n=2), and collagen vascular disease ( n=9). Coagulopathy was found in 14 cases (18%) including antiphospholipid syndrome ( n=8) and APC resistance ( n=4). Other causes were cardiogenic embolism ( n=8), multiple sclerosis ( n=5), and migraine stroke ( n=3). Only a minority of patients referred for evaluation of suspected CNS vasculitis actually present with inflammatory vascular disease. Main differential diagnosis includes noninflammatory vasculopathies, coagulopathies, and cardiac disease. Since septic processes may be responsible for the symptoms, "blind" treatment with immunosuppressive agents should be strictly avoided.
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PMID:[Diagnosis and differential cerebral vasculitis diagnosis]. 1477 Feb 79

Giant cell arteritis (GCA), a vasculitis that targets medium- and large-size arteries, is ranked as a medical emergency because of its potential to cause blindness and stroke. The typical lesions, granulomas in the vessel wall, are formed by IFN-gamma-producing CD4+ T cells and macrophages. CD4+ T cells undergo in situ activation in the adventitia, where they interact with indigenous dendritic cells. Tissue injury is mediated by several distinct sets of macrophages that are committed to diverse effector functions. The dominant tissue injury in the media results from oxidative stress and leads to smooth muscle cell apoptosis and nitration of endothelial cells. Macrophage-derived growth factors are instrumental in driving the response-to-injury program of the artery that causes intimal hyperplasia and vessel occlusion. Clinical manifestations are those of tissue ischemia or a syndrome of exuberant systemic inflammation. The vascular and the systemic components of GCA contribute differentially to the disease, leading to distinct clinical phenotypes of this arteritis. Immunologically most interesting is polymyalgia rheumatica, in which the systemic component is combined with aborted vasculitis, suggesting a role for artery-specific tolerance mechanisms.
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PMID:Immunopathways in giant cell arteritis and polymyalgia rheumatica. 1487 49


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