Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0039483 (giant cell arteritis)
 3,204 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

An acute loss of vision accompanied by signs of optic nerve head ischemia in an elderly patient should alert the examiner to suspect the presence of temporal arteritis until it can be proven otherwise. The patient presented here had ischemic optic neuropathy that was initially thought to be due to temporal arteritis, but eventually was proven to be associated with pronounced atherosclerotic aortic arch disease. The diagnosis was complicated by the severe loss of vision and by an elevated erythrocyte sedimentation rate (ESR). A temporal artery biopsy was normal, and other findings implicated the pronounced diffuse atherosclerosis as the cause of the ischemia of the optic nerve head. Therapy was directed toward the vascular occlusive disease, and involved an aortoinnominate bypass graft.
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PMID:Complicated aortic arch syndrome and ischemic optic neuropathy presenting as giant cell (temporal) arteritis. 703 43

To test the hypothesis that a systemic immune response to dietary protein can influence the development of experimental arterial disease rabbits were given diets containing 20% soya protein and 20% fat for 11 months. The substantial levels of circulating antisoya antibody were positively correlated with the macroscopic extent of aortic atheroma. In some arterial changes reminiscent of giant cell arteritis were seen. In subsequent similar experiments the breeding stock had been exposed to a soya containing diet, which was also available to their offspring, the experimental animals, in the perinatal period. The lower antibody titres, and much reduced atheroma in this experiment suggested that the animals had been tolerated to soya protein. In further experiments rabbits, bred on a soya free diet showed much higher levels of antisoya antibody and a giant cell reaction was again identified. It is concluded that the magnitude of the antibody response to dietary protein is an important, and previously unrecognised, factor in the development of experimental atherosclerosis.
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PMID:Dietary antigens, immune tolerance and atherosclerosis. 719 26

We have reviewed the clinical records and histology of 135 patients who underwent temporal artery biopsy between 1973 and 1978. Biopsies were classified histologically as giant-cell arteritis (17%), atypical arteritis (6%), healed arteritis (2%), arteriosclerosis (67%), atherosclerosis (5%), or normal (3%). Most of the histological diagnoses made at the time of biopsy were confirmed but eight cases which had originally been reported as atypical or healed arteritis were classified as arteriosclerosis when reviewed. All 33 patients with histological evidence of arteritis were accepted as clinical cases of temporal arteritis (31) or polymyalgia rheumatica (2) and treated with steroids. A further 24 patients had negative biopsies (arteriosclerosis or atherosclerosis) but were considered on clinical grounds to have cranial arteritis. They too were treated and made a full recovery. In 43 cases, all of whom had negative biopsies, a final diagnosis was reached which was thought to account for the clinical symptoms (e.g., cerebrovascular accident, rheumatoid disease, migraine, etc.). As less than 60% of patients with clinical temporal arteritis had positive biopsies, we suggest that this procedure could be omitted and replaced by a trial of steroid therapy. Biopsy should be reserved for patients with a strong medical contraindication to steroid therapy, or who fail to respond to treatment promptly.
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PMID:Temporal artery biopsy in giant-cell arteritis. A reappraisal. 727 Jul 80

This study of cutaneous elastic tissue and serum fluorescence supports the hypothesis that widespread destruction and resorption of elastic tissue (elastolysis) occurs in the temporal arteritis/polymyalgia rheumatica syndrome. A systemic elastolysis of this nature may be provoked by actinic (radiant) damage to the "exposed" elastic tissues in the skin and superficial arteries, the archetype of such injury being seen in temporal arteritis. Scattered giant cells are the usual agents of elastolysis but tuberculoid ("sarcoid") infiltrates often take over in the later stages. In acute polymyalgia, the phenomenon probably becomes diffuse and humoral. Elastolysis may be a direct pathogenetic link between polymyalgia and other vascular diseases such as idiopathic aneurysm and atherosclerosis.
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PMID:The role of actinically provoked systemic elastolysis in polymyalgic vascular disease. A study based on serum fluorescence and haptoglobin. 732 40

Giant cell arteritis (GCA) is closely identified with the temporal arteritis-polymyalgia rheumatica syndrome of the elderly. It is also a systemic disease that can cripple and kill. Up to 15% of patients with temporal arteritis may have angiographic evidence of extracranial GCA, and aortic insufficiency, ruptured aortic aneurysm, aortic dissection, stroke, or myocardial infarction may be the initial manifestation of systemic GCA. A review of 72 cases of aortic and extracranial GCA, all with histopathologic verification of the disease, revealed that 25% of patients with aortic and extracranial large-vessel GCA had asymptomatic temporal arteritis; the ascending aorta and aortic arch were most frequently involved (39%), followed by the subclavian and axillary arteries (26%), and the femoropopliteal arteries (18%). Nine patients (12.5%) underwent an upper or lower limb amputation. Of the 18 patients whose death was directly attributable to extracranial GCA the causes were ruptured aortic aneurysm (6), aortic dissection (6), stroke (3), and myocardial infarction (3). The findings of these 72 cases caution against attributing all aortic and large-vessel arterial disease in the elderly to atherosclerosis and emphasize that timely surgical intervention may be necessary for life-saving and limb-salvage in patients with aortic and extracranial GCA.
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PMID:Aortic and extracranial large vessel giant cell arteritis: a review of 72 cases with histopathologic documentation. 766 46

Lingual necrosis is a rarely observed pathology. The authors report a case of a lingual necrosis in the follow up of an irradiation. Horton's disease is the first diagnosis to evoke facing a lingual necrosis. This pathology is also one of the radiotherapy's complication, irradiation accelerates atherosclerosis process. An early treatment of this arterial complication can be proposed by a good prepossession and a doppler-pulse supervision of neck vessels.
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PMID:[Lingual necrosis after neck irradiation]. 821 97

Giant cell arteritis (GCA) and polymyalgia rheumatica (PMR) are common diseases in the elderly. The arteritis usually affects medium sized vessels, but large vessel involvement can also occur leading to arm claudication, bruits, loss of pulses and pallor of the upper extremities. The differential diagnosis of large vessel arteritis includes atherosclerosis and Takayasu's disease. Atherosclerosis, which affects patients of similar age to GCA is usually confined to the lower limbs and can be differentiated on the basis of the clinical setting and investigations such as the ESR, arteriography and temporal artery biopsy. Takayasu's arteritis' although histologically and arteriographically indistinguishable from GCA, is predominantly a disease of young women. A patient is described who presented with upper limb ischemia. A clinical examination revealed absence of right radial pulses and presence of murmurs at level of the carotids. The blood pressure was unrecordable in the upper right limb. The ESR was 102 mm/hr and the C-reactive protein was 11.66 mg/dl. A selective arteriography of the aortic arch and its branches revealed a right subclavian artery obstruction with good collateral circulation and a left subclavian artery stenosis. The biopsy of left temporal artery showed a typical GCA in acute stage. Treatment with prednisolone 30 mg/day was started and four weeks later, the ESR had fallen to normal. In addition this case confirms that PMR implies a systemic arteritis.
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PMID:[Giant cell arteritis and polymyalgia rheumatica presenting as subclavian artery obstruction]. 823 15

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

The elastin peptide level (EP) and elastase-type activity (EA) were investigated in 89 patients with different types of systemic vasculitis (polyarteritis nodosa-14, non-specific aortoarteritis-33, temporal arteritis-23 and thromboangiitis obliterans-18) and compared to the controls: 31 patients with leg atherosclerosis and 12 aged subjects with no evident vascular pathology. EP and EA levels in patients with thromboangiitis obliterans were significantly lower as compared to leg atherosclerosis and the aged control group (p < 0.02 for EA, p < 0.05 for EP). The increase of EP predominated in giant-cell arteritis as compared to the other vasculitic groups (18/56 vs. 5/32, p < 0.05); EA in these patients was the lowest. The activation of elastin degradation after corticosteroid treatment was demonstrated by an increase of EP in temporal arteritis (p < 0.05) and of EA in thromboangiitis obliterans (p < 0.03). We suggest that the determination of the above parameters of elastin degradation may be helpful in the search for differences in mechanisms of vascular damage between atherosclerosis and inflammatory vascular diseases.
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PMID:Elastin degradation in systemic vasculitis. 876 87

A recent view of atherosclerosis indicates vascular smooth muscle cell proliferation not only as a response-to-injury but also as an essential reparative process leading to plaque stabilization. To assess the role of vascular smooth muscle cell in vasculitides we studied, as a model, 10 cases of Horton's arteritis. In particular, we investigated by immunohistochemical analysis cellular population and proliferation rate in the intimal layer. As in atherosclerotic plaques, intimal thickening in arteritis is essentially due to proliferation and migration of vascular smooth muscle cells. We suppose that, whatever the vascular disease, intimal hyperplasia contributes to stability of the vessel's wall; however the reactive/reparative process is extremely slow in spontaneous atherosclerosis, accelerated in arteritis.
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PMID:[The reactive and/or repair role of the smooth muscle cells in Horton's arteritis]. 948 94


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