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Query: UMLS:C0039483 (giant cell arteritis)
 3,204 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Staining technique is paramount for detecting and assessing the severe degeneration that occurs in the elastic tissues of the skin and its arteries in response to prolonged exposure to actinic radiation. With a selective "controlled" hematoxylin-and-eosin stain, actinically damaged ("elastotic") elastic tissue stains blue, as Unna described, and contrasts with normal and simply hyperplastic elastic tissue, which stains red. "Special" elastic stains such as Orcein and Verhoeff do not demonstrate this difference. When resorptive (elastolytic) giant cell reactions develop in relation to actinically degenerate elastic tissue of the skin, the papules that arise tend to form expanding, annular rings. A previously used and appropriate name for these autoimmune lesions in the skin is actinic granuloma because this name highlights the likely actinic origin and pathogenesis of many such lesions. Granulomatous inflammation in connection with actinically degenerate internal elastic lamina appears to be the basis of temporal arteritis. Actinic granulomas may occur in the skin concurrently with temporal arteritis. A recent study of temporal arteritis strongly relates its elastic tissue changes to those of "accelerated" atherosclerosis.
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PMID:Actinically degenerate elastic tissue is the likely antigenic basis of actinic granuloma of the skin and of temporal arteritis. 1002 48

A 77-year-old woman was admitted because of progressive vertigo, nausea and a dysarthric speech disorder. The patient's history of diabetes mellitus, hypertension and hypercholesterolaemia, and the finding of murmurs over peripheral arteries at physical examination led to a presumptive diagnosis of cerebellar ischaemia in the context of generalized atherosclerosis. However, the diagnosis was revised when bilateral cerebellar infarction was demonstrated radiologically, and a biopsy of a temporal artery revealed giant cell arteritis. Despite treatment with prednisone (60 mg daily) the patient's neurological condition deteriorated, and she succumbed several months later to pneumonia. The case illustrates the pitfalls in the diagnostic approach of elderly patients with multiple pathology and it also emphasizes that in an elderly person with high erythrocyte sedimentation rate (> 100 mm in the first hour) temporal arteritis should be ruled out as soon as possible to prevent further neurological damage.
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PMID:[Clinical thinking and decision making in practice. An elderly patient with vertigo and high sedimentation rate]. 1066 48

We examined the usefulness of color duplex ultrasonography in patients suspected of having temporal arteritis. Five patients, who were all aged 70 or older, developed a new onset of localized headache with temporal artery abnormalities, and had an elevated erythrocyte sedimentation rate of > 100 mm/hour. The final diagnoses were temporal arteritis in three patients, polymyalgia rheumatica in one, and probable healed temporal arteritis in one. Color duplex ultrasonography showed stenoses, which were confirmed histologically as well, in the superficial temporal artery of all patients. The characteristic findings of active temporal arteritis were, however, demonstrated in only three biopsy specimens, and in the remaining two the stenoses were thought to be related to previous arteritis. The hypoechoic halo, which has been reported to be a characteristic finding of color duplex ultrasonography in active temporal arteritis, was detected in only one patient with active temporal arteritis and another one with probable healed temporal arteritis. No stenoses were demonstrated in the superficial temporal arteries of 30 control subjects (20 with at least one risk factor of atherosclerosis and 10 without it). Color duplex ultrasonography can therefore be considered a powerful method for detecting stenoses in the superficial temporal artery. Its ability to identify their etiology is, however, unsatisfactory, so that temporal artery biopsy remains undoubtedly the most reliable test for etiological evaluation. We thus recommend color duplex ultrasonography as a supplementary method for the diagnosis of temporal arteritis, because it can provide useful information concerning the appropriate site of temporal artery biopsy.
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PMID:[The significance of color duplex ultrasonography for the diagnosis of temporal arteritis]. 1065 58

Extracranial carotid and vertebral arterial disease is most often attributable to underlying atherosclerosis. However, several other diseases may mimic atherosclerosis clinically. These include Takayasu's arteritis, giant cell arteritis, fibromuscular dysplasia, dissections, and aneurysms. It is important to recognize distinguishing characteristics of each condition to determine the appropriate course of treatment and long-term prognosis.
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PMID:Nonatherosclerotic arterial disease of the extracranial cerebrovasculature. 1087 56

Takayasu arteritis, Buerger's diseases, temporal arteritis, vascular Behcet disease and inflammatory abdominal aortic aneurysm are classified in Japan as intractable vasculitides involving mainly large vessels, because their etiologies are not yet elucidated and, therefore, treatments for them were not yet established. Recent experimental and vascular biological studies, however, have focussed on the roles of virus infection in vasa vasorum (vasa vasoritis) and on the subsequent inflammatory vascular changes through HLA and/or other autoimmune mechanisms. Several studies including ours have demonstrated that these vascular inflammatory changes progress from the adventitial side to the intimal side of the vessel, finally complicating atherosclerotic changes in the intima. These vascular inflammatory changes are also recognized during progression of atherosclerosis and these observations strongly suggest that inflammation is a serious risk factor of atherosclerosis.
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PMID:Vasa vasoritis, vasculitis and atherosclerosis. 1098 Mar 30

Some arguments are in favor of the role of Chlamydia in the pathogenesis of atherosclerosis and some vasculitis. Illustrating this possible relation, we report the case of a patient developing consecutively a Chlamydia psittacci infection and a temporal arteritis. A 73-year-old woman, with no significant medical history, was hospitalized for constitutional symptoms. Three weeks before, she had described fever and sore throat of two days' duration. Since that time, she had remained exhausted and developed a mild intermittent claudication of the jaws. Clinical examination was poor. A biological inflammatory syndrome was noticed. Chest X-ray revealed bilateral interstitial opacities. The titer of anti-C. psittaci antibodies was significant (positive 1g G at 1/2048). Soon after initiation of doxycycline, a temporal arteritis biopsy was performed, due to the persistence of clinical symptoms and high inflammatory syndrome, conclusive for the diagnosis of temporal arteritis. Corticotherapy was added to antibiotic therapy, resulting in the decrease of inflammatory syndrome and an improvement in the general status of the patient. X-ray opacities decreased in three weeks. Serological control after three months showed a decrease of the titer of anti-C. psittacci antibodies to 1/256, confirming the initial diagnosis of Chlamydia pneumopathy. Our observation could provide one more argument for the role of bacteria-like Chlamydia in the pathogenesis of vascular diseases. Prospective seroepidemiological and molecular biology studies could allow us to clarify the association between Chlamydia infections and inflammatory vasculitis-like temporal arteritis.
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PMID:A possible association between Chlamydiae psittacci infection and temporal arteritis. 1119 20

T lymphocytes, encountering stimulatory signals in the adventitia of medium-size arteries, emerge as the key players in inflammation-associated injury pathways. In GCA, all injury mechanisms have been related to effector macrophages. Regulated by IFN-gamma-producing T cells, macrophages commit to distinct avenues of differentiation and acquire a spectrum of potentially harmful capabilities (Figure 1). Macrophages in the adventitia focus on production of pro-inflammatory cytokines. Macrophages in the media specialize in oxidative damage with lipid peroxidation attacking smooth muscle cells and matrix components. These macrophages also supply reactive oxygen intermediates that, in combination with nitrogen intermediates, cause protein nitration of endothelial cells. Production of oxygen radicals is complemented by the production of metalloproteinases, likely essential in the breakdown of elastic membranes. With the fragmentation of the internal elastic lamina, the intimal layer becomes accessible to migratory myofibroblasts that, driven by PDGF, form a hyperplastic intimal layer and cause occlusion of the vessel lumen. Expansion of the hyperplastic intima is accompanied by intense neoangiogenesis, supported by angiogenesis factors that again derive from specialized macrophages. Similarities in injury pathways between GCA and another arterial disease, atherosclerosis, are beginning to be recognized. Specifically, activated T cells and macrophages are increasingly appreciated as key players in the process of instability and rupture of atherosclerotic plaque. A specialized subset of CD4 T cells, CD4+ CD28- T cells, are suspected to participate in tissue injury in the plaque. These T cells are equipped with cytolytic capabilities and release large amounts of IFN-gamma. Comparative studies between patients with GCA and those with acute coronary syndromes should enhance our ability to define the principles of arterial wall inflammation, the specifics of injury in that microenvironment, and help in the identification of the eliciting signals.
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PMID:Pathogenic mechanisms in giant cell arteritis. 1208 61

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

The article presents diagnostic criteria for nonspecific aortic arteritis proposed by K. Ishikawa (1988), American Rheumatology Society (1990), algorithm of differential diagnosis with giant cell arteritis, obliterating thrombotic angiitis, Marfan's syndrome, atherosclerosis of major vessels, etc.
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PMID:[Differential diagnosis of nonspecific aortic arteritis]. 1263 16

Because the prognosis of giant cell arteritis (GCA) is related to the development of ischemic complications, we sought to assess the possible influence of traditional risk factors of atherosclerosis in the development of severe ischemic complications of GCA. We conducted a retrospective study of patients with biopsy-proven GCA diagnosed from 1981 to 2001 at the single hospital for a well-defined population of almost 250,000 people. Patients were considered to have severe ischemic manifestations if they suffered visual manifestations, cerebrovascular accidents, jaw claudication, or signs of occlusive changes in large arteries of the extremities. Patients were assessed for the presence of hypercholesterolemia, hypertension, diabetes mellitus, and heavy smoking at the time of GCA diagnosis. The presence of traditional risk factors of atherosclerosis at the time of GCA diagnosis in this series of 210 patients increased significantly the risk of developing at least 1 of the severe ischemic complications (odds ratio [OR], 1.79; 95% confidence intervals [CI], 1.03-3.11; p = 0.04). Patients with traditional atherosclerosis risk factors had fever less commonly than the rest of GCA patients (5.2% vs. 16.0%; p = 0.01). GCA patients with hypertension exhibited a significantly increased risk of developing severe ischemic complications (OR, 1.80; 95% CI, 1.00-3.25; p = 0.05). The current study suggests that the presence of atherosclerosis risk factors at the time of diagnosis of GCA may influence the development of severe ischemic manifestations of the disease.
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PMID:Influence of traditional risk factors of atherosclerosis in the development of severe ischemic complications in giant cell arteritis. 1552 46


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