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

Studies of autoimmune diseases have not yet elucidated why certain organs or vessels become the objects of injury while others are spared. This paper will explore the hypothesis that important differences exist in regions of the aorta that determine vulnerability to diseases, such as atherosclerosis, aortitis, giant cell arteritis and Takayasu's disease. The reader is invited to reassess; (1) whether the aorta is indeed a single homogeneous structure, and (2) whether the initial stage of aortitis (and indeed other diseases considered "autoimmune") may be primarily due to acquired alterations of substrate, that influence unique immune profiles, which by themselves may not be pathogenic. Disease susceptibility and patterns are influenced by many factors that are inborn and acquired. Examples include genetic background, gender, ethnicity, aging, prior and concomitant illnesses, habits, diet, toxin and environmental exposures. Studies of vascular diseases must assess how such variables may affect regional differences in endothelial cells, subendothelial matrix, vascular smooth muscle and the response of each to a variety of stimuli.
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PMID:Determinants of vessel targeting in vasculitis. 1555 74

Chlamydia pneumoniae has recently been implicated in the pathogenesis of several neurological diseases. As an intracellular parasite with its unusual life cycle it is able to circumvent the immune system and to persist in the organism. It has the ability to modify the function of the infected cell and supposedly induce autoimmune reactions. These properties can make it pathogenic in several chronic neurological diseases including multiple sclerosis, atherosclerosis, stroke, Alzheimer dementia and giant cell arteritis. The evaluation of the available, often contradictory, data that are based on various different methods is not easy. The importance of the issue is enhanced by the potential need for antibiotic treatment.
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PMID:[The significance of Chlamydia pneumoniae in selected neurologic disorders]. 1649 68

Tissue inhibitors of matrix metalloproteinases (TIMPs) comprise a family of four members, of which TIMP4 is characterized by being primarily restricted to cardiovascular structures. We demonstrate with immunohistochemical analysis of healthy human tissue that TIMP4 is present in medial smooth muscle cells and adventitial capillaries of arteries as well as in cardiomyocytes. Animal studies have suggested a role for TIMP4 in several inflammatory diseases and cardiovascular pathologies. We therefore examined whether TIMP4 is involved in human inflammatory cardiovascular disorders, specifically atherosclerosis, giant cell arteritis and chronic rejection of heart allografts. TIMP4 was most clearly visible in cardiovascular tissue areas populated by abundant inflammatory cells, mainly macrophages and CD3+ T cells. Using western blotting and immunocytochemistry, human blood derived lymphocytes, monocytes/macrophages and mast cells were shown to produce TIMP4. In advanced atherosclerotic lesions, TIMP4 was detected around necrotic lipid cores, whereas TIMP3 and caspase 3 resided within and around the core regions, indicating different roles for TIMP3 and TIMP4 in inflammation-induced apoptosis and in matrix turnover. In conclusion, the data demonstrate upregulation of TIMP4 in human cardiovascular disorders exhibiting inflammation, suggesting its future use as a novel systemic marker for vascular inflammation.
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PMID:Tissue inhibitor of metalloproteinases 4 (TIMP4) is involved in inflammatory processes of human cardiovascular pathology. 1652 Oct 2

A 73-year-old woman was referred to our hospital to investigate dilatation of an aortic arch which had been detected by a chest roentgenogram and severe aortic valve regurgitation detected by echocardiography. On admission, a computed tomography scan of the chest showed a large fusiform ascending aortic aneurysm. She had not shown any symptoms such as headache or polymyalgia rheumatica and had no significant coronary atherosclerosis. She underwent aneurysmectomy and reconstruction of the ascending aorta using cardiopulmonary bypass without aortic valve replacement, and pathological examination of the aneurismal wall revealed giant cell arteritis (GCA). Preoperatively, she did not have any temporal pain, and no signs of inflammation were detected serologically. Postoperatively, aortic valve regurgitation improved and she did well. However, three months after the surgery, she died suddenly due to the rupture or dissection of aorta. In the Japanese population, GCA is reportedly a rare cause of aortic aneurysm. However, retrospective studies show that GCA affects the aorta and that thoracic aortic aneurysm is a possible complication of GCA. In cases of the thoracic aortic aneurysms with unknown etiology, there is a possibility that GCA is the cause of the aortic aneurysm.
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PMID:Case of isolated thoracic aortic aneurysm as a manifestation of undiscovered giant cell arteritis. 1731 Aug 5

Emerging evidence implicating the participation of dendritic cells (DCs) and T cells in various vascular inflammatory diseases such as giant cell arteritis, Takayasu's arteritis, and atherosclerosis led us to hypothesize that they might also participate in the pathogenesis of coronary arteritis in Kawasaki disease (KD). Coronary artery specimens from 4 patients with KD and 6 control patients were obtained. Immunohistochemical and computer-assisted histomorphometric analyses were performed to detect all myeloid DCs (S-100(+), fascin(+)), all plasmacytoid DCs (CD123(+)) as well as specific DC subsets (mature myeloid DCs [CD83(+)], myeloid [BDCA-1(+)] and plasmacytoid DC precursors [BDCA-2(+)]), T cells (CD3(+)), and all antigen-presenting cells (HLA-DR(+)). Co-localization of DCs with T cells was assessed using double immunostaining. Significantly more myeloid DCs at a precursor, immature or mature stage were found in coronary lesions of KD patients than in controls. Myeloid DC precursors were distributed equally in the intima and adventitia. Mature myeloid DCs were particularly abundant in the adventitia. There was a significant correlation between mature DCs and HLA-DR expression. Double immunostaining demonstrated frequent contacts between myeloid DCs and T cells in the outer media and adventitia. Plasmacytoid DC precursors were rarely found in the adventitia. In conclusion, coronary artery lesions of KD patients contain increased numbers of mature myeloid DCs with high HLA-DR expression and frequent T cell contacts detected immunohistochemically. This suggests that mature arterial myeloid DCs might be activating T cells in situ and may be a significant factor in the pathogenesis of coronary arteritis in KD.
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PMID:Activated myeloid dendritic cells accumulate and co-localize with CD3+ T cells in coronary artery lesions in patients with Kawasaki disease. 1733 4

[(18)F]fluorodeoxyglucose (FDG) PET is a noninvasive metabolic imaging modality based on the regional distribution of [18F]FDG that is highly effective in assessing the activity and extent of giant cell arteritis and Takayasu's arteritis, respectively. Metabolic imaging using [18F]FDG-PET has been shown to identify more affected vascular regions than morphologic imaging with MRI in both diseases. The visual grading of vascular [18F]FDG uptake helps to discriminate arteritis from atherosclerosis and therefore provides high specificity. High sensitivity is attained by scanning during the active inflammatory phase. Thus, [18F]FDG-PET has the potential to develop into a valuable tool in the diagnostic workup of giant cell arteritis and Takayasu's arteritis.
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PMID:[(18)F]fluorodeoxyglucose PET in large vessel vasculitis. 1770 37

A total of 338 surgical specimens of the thoracic aorta were studied morphologically. These were obtained from patients (238 males, 100 females) operated on for aortic aneurysm or dissection at the Careggi Hospital, Florence, Italy, between January 1999 and June 2005. Medial degeneration was diagnosed in 299 cases (138 aneurysms, 161 dissections), atherosclerosis with extensive medial destruction was seen in 32 cases (26 aneurysms, 6 dissections), and giant cell arteritis (GCA) was found in 7 cases (all aneurysms). These data show that medial degeneration was a common nonspecific histologic diagnosis in aortic resection after the occurrence of aneurysm or dissection. Considering that this diagnosis was made in as many as 118 patients over 70 years of age and in 175 patients over 65, normal advancing age would appear as the most frequent correlation with these aortic events. Ageing is also associated with the increasing number of cases of GCA with aortic involvement. Angiogenesis, always observed next to areas of medial damage whatever the underlying pathology, may contribute to the pathogenesis of aortic dissection and aneurysm.
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PMID:Pathology of the thoracic aorta: a morphologic review of 338 surgical specimens over a 7-year period. 1850 84

Though a myriad of vascular conditions affect the elderly, atherosclerosis remains the most common vascular disorder, followed by venous thromboembolism and varicose veins. In this article, the authors discuss the imaging of atherosclerosis affecting various vascular territories and pay special attention to the elderly population. The authors also discuss imaging findings of segmental arterial mediolysis, giant cell arteritis, and venous thromboembolism.
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PMID:Vascular imaging in the elderly. 1892 87

Premature atherosclerosis has been observed during the course of different systemic inflammatory diseases such as rheumatoid arthritis and sytemic lupus erythematosus. Remarkably, relatively few studies have been published on the occurrence of accelerated atherosclerosis in patients with vasculitis. In giant cell arteritis (GCA), mortality because of ischaemic heart disease is not increased. In addition, intima media thickness (IMT) is lower in patients with GCA than in age-matched controls. In contrast, IMT is increased significantly in Takayasu arteritis, another form of large vessel vasculitis occurring in younger patients. In Takayasu arteritis and in Kawasaki disease, a form of medium-sized vessel vasculitis, accelerated atherosclerosis has been well documented. In small vessel vasculitis because of anti-neutrophil cytoplasmic autoantibodies-associated vasculitis, cardiovascular diseases are a major cause of mortality. IMT measurements reveal conflicting results. During active disease these patients experience acceleration of the atherosclerotic process. However, when inflammation is controlled, these patients have atherosclerotic development as in healthy subjects. Several risk factors, such as diabetes and hypertension, are present more often in patients with vasculitis compared with healthy controls. In addition, steroids may be pro-atherogenic. Most importantly, many patients have impaired renal function, persistent proteinuria and increased levels of C-reactive protein, well-known risk factors for acceleration of atherosclerosis. Enhanced oxidation processes, persistently activated T cells and reduced numbers of regulatory T cells are among the many pathophysiological factors that play a role during acceleration of atherogenesis. Finally, autoantibodies that may be relevant for acceleration of atherosclerosis are found frequently in elevated titres in patients with vasculitis. Because patients have an increased risk for cardiovascular events, vasculitis should be treated with as much care as possible. In addition, treatment should be considered with angiotensin-converting-enzyme inhibitors and/or angiotensin receptor-1 blockers, statins and acetylsalicyl acid. Finally, classical risk factors for cardiovascular disease should be monitored and treated as much as possible.
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PMID:Translational mini-review series on immunology of vascular disease: accelerated atherosclerosis in vasculitis. 1930 50

Patients with polymyalgia rheumatica have been shown to have an increased risk of peripheral arterial disease on longitudinal follow-up. Possible explanations for this include premature atherosclerosis related to chronic inflammation, as with other inflammatory rheumatological conditions. Alternatively, polymyalgia rheumatica can be associated with vasculitis, even in the absence of clinical giant cell arteritis, and peripheral vascular disease may represent subclinical vasculitis. Further work is required to elucidate the reasons for this increased risk. Currently, it would remain reasonable to aggressively control modifiable atherosclerotic risk factors.
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PMID:Peripheral arterial disease in polymyalgia rheumatica. 1933 2


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