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

Of 248 patients with giant cell arteritis, 34 had evidence that the disease affected the aorta or its major branches. Symptoms suggestive of large artery involvement were intermittent claudication of an extremity, paresthesias, and Raynaud's phenomenon. Physical findings included absent or decreased large artery pulses and bruits over large arteries. Four patients presented with decreased upper extremity pulses as the initial manifestation of their arteritis. Nine other patients under treatment for temporal arteritis or polymyalgia rheumatica first developed evidence of large artery involvement as corticosteroid therapy was tapered or discontinued. Angiography, performed in 10 patients, was helpful in indicating arteritis rather than atherosclerosis as the cause of large artery disease. Three patients died with aortic rupture, and, at autopsy, widespread giant cell arteritis was found. However, when corticosteroids were given in adequate doses, the response was favorable in most patients; intermittent claudication decreased and the pulses improved.
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PMID:Large artery involvement in giant cell (temporal) arteritis. 120 May 25

Infarcts in the territory of cerebellar arteries, often involving both brainstem and cerebellum, have been well recognized in recent pathological and clinicoradiological studies. To evaluate the situation of pure cerebellar infarcts (PCI) we studied 30 consecutive cases of symptomatic PCI (22 men and 8 women, mean age 58 +/- 17 years) admitted over a 5-year period and selected on the basis of brain computed tomography completed by magnetic resonance in 20 cases and angiography in 15 cases. PCIs accounted for 53 percent of cerebellar infarcts, 10 percent of vertebrobasilar infarcts and 3.2 percent of all cerebral infarcts. The arterial territories involved were the superior cerebellar artery (SCA) in 13 cases (alone in 8 cases), the anterior inferior cerebellar artery in 2 cases, the posterior inferior cerebellar artery (PICA) in 17 cases (alone in 13 cases) and border areas in 5 cases (associated with SCA or PICA). The symptoms were the same in the arterial territories involved (SCA versus PICA), except for dysmetria and vestibular syndrome which were more frequent respectively in SCA territory infarction (P < 0.001) and in PICA territory infarction (P < 0.01). Certain or presumed causes were cardiogenic embolism (23 percent), atherosclerosis (43 percent) and other identified causes, such as oral contraceptives or temporal arteritis (10 percent). They remained undetermined in 24 percent of the cases. Although most patients were severely disabled in the acute stage (Barthel index < 60 in 21 cases), 90 percent recovered subsequently (Barthel index about 100 and 0-2 score on modified Rankin scale). Our findings indicate that symptomatic PCIs are rare; their main causes (cardioembolism and atherosclerosis) do not differ in frequency from those of all cerebral infarcts collected in stroke registries and their functional prognosis is good in almost all cases.
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PMID:[Pure cerebellar infarction. Thirty cases]. 147 Jun 12

An 80-year-old white man presented with gangrenous lesions involving several distal phalanges of his left hand and an elevated erythrocyte sedimentation rate (ESR). Temporal artery biopsy showed patchy destruction of the internal elastic lamina by mononuclear cell infiltration, consistent with the diagnosis of temporal arteritis. After amputation of gangrenous lesions, he was discharged taking prednisone (60 mg/day). Twelve months after discharge there was no recurrence of ischemic manifestations and ESR was normal. Association of digital gangrene and elevated ESR should alert the clinician toward this diagnosis once other diseases such as atherosclerosis, scleroderma, lupus erythematosus, periarteritis nodosa have been ruled out.
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PMID:Temporal arteritis revealed by upper limb gangrene. 271 2

Four patients with giant cell arteritis (GCA) involving the vessels of lower extremities (3 males and 1 female, the age range from 57 to 67 yr) are described. The maximal changes were revealed in the femoropopliteal segment of the arterial bed. The role of morphologic study for the differential diagnosis of GCA with obliterating atherosclerosis is stressed.
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PMID:[Giant-cell arteritis with involvement of the vessels of the lower extremities]. 360 20

Clinical and laboratory findings of 237 consecutive patients who had 250 temporal artery biopsies performed at the Wilmer Institute during a 15-year period were reviewed. Biopsies were reviewed independently on three separate occasions by four observers who, unaware of the clinical history, made one of the following histopathologic diagnoses: active arteritis, healed arteritis, arteriosclerosis, atherosclerosis, normal, or other. Biopsies were reviewed a fourth time by the observers together to establish a consensus diagnosis. The frequency of intraobserver disagreement in biopsy interpretation ranged from 4.4 to 25.6% of cases. The frequency with which observers disagreed with the consensus diagnosis (interobserver variation) ranged from 4.3 to 13.5% of cases. Pre-biopsy steroid therapy for seven to eight weeks or longer was associated with loss of the histopathologic features of active arteritis. We recommend biopsies for all patients with known contraindications to steroid therapy. In addition, multivariant regression analysis suggests that certain patients can be selected who are likely to have positive biopsies. For some patients, the clinical diagnosis of temporal arteritis can be based on the clinical signs and symptoms and their response to a therapeutic trial of steroids.
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PMID:Temporal arteritis. A clinicopathologic study. 370 28

A 68 year-old woman presented with a two-week history of amaurosis fugax, ipsilateral fronto-temporal headache and jaw claudication suggesting carotid giant cell arteritis. However, this syndrome proved to be due to atherosclerosis causing complete occlusion of the external carotid artery at its origin and narrowing of the internal carotid artery. Combined external and internal carotid endarterectomy relieved the symptoms. The symptom complex of temporal arteritis may be rarely mimicked by carotid atherosclerotic occlusive disease.
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PMID:Temporal arteritis-like presentation of carotid atherosclerosis. 396 42

Destruction (elastolysis) of the internal elastic lamina is frequently observed near early atherosclerotic plaques. Elastolysis and plaque formation are also found together in the temporal arteritis/polymyalgia rheumatica syndrome. Could it be that atherosclerosis and the syndrome are more closely akin than usually thought, with elastolysis acting as the pathogenetic link between them? A kinship of this nature is in accord with the growing recognition that elastin-related autoimmunity prevails in both these forms of vascular disease. A case can also be made out for the belief that the autoimmune reactions in internal vessels may be provoked by events in the integument where a slow but ultimately massive turnover of dermal and vascular elastic tissue takes place under the harmful influence of solar and other forms of actinic radiation.
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PMID:Destruction of elastic tissue (elastolysis) as a link between atherosclerosis and the temporal arteritis/polymyalgia rheumatica syndrome. Observations on an actinic factor in vascular disease. 636 8

Two cases of strokes in the vertebrobasilar territory were observed in patients with Horton's disease during the first week of treatment when the inflammatory process seemed clinically and biologically under control. The mechanisms of arterial ischaemia are discussed: specific localisation of giant cell arteritis, associated atherosclerosis, failure of therapy or a possible inducing role of steroid therapy as the chronology of these cases would suggest.
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PMID:[Early cerebral vascular accidents in treated Horton's disease. Responsibility of the corticoid treatment?]. 651 24

We utilized a standardized in vitro method which employs transmission electron microscopy to monitor the degree of surface activation (cytoplasmic spreading) and amount of aggregation displayed by platelet populations from 314 patients with one of five distinct rheumatic diseases and from 72 normal subjects. The percentage of patients in each group whose platelet populations were hyperactive was as follows: polymyalgia rheumatica, 75 percent; scleroderma, 65 percent; primary gout, 61 percent; rheumatoid arthritis, 57 percent; and degenerative joint disease, 40 percent. Pair-wise contrasts performed after an analysis of variance suggest the following differences and similarities: (1) the mean differential platelet count of the normal subjects differed from that in each disease state; (2) the platelet responsivity in patients with degenerative joint disease most closely resembled that in normal subjects; (3) the platelet response in polymyalgia rheumatica plus temporal arteritis was the most abnormal; and (4) platelet response in scleroderma, rheumatoid arthritis, and gout closely resembled each other. The increased platelet response in vitro may reflect the in vivo presence of disease-related "risk factors" (hyperuricemia, immune complexes, and atherosclerosis). Those patients with "triggered" platelet populations may be appropriate candidates for antiplatelet therapy.
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PMID:A comparative study of platelet reactivity in arthritis. 694 59

Acquired lesions of the aorta are not confined to atherosclerosis alone, and diagnostic, etiological, pathogenic, and therapeutic problems may be raised when confronted with less frequent infective or inflammatory processes. Syphilitic aortitis was for a long time considered to be the only infective lesion involving the aorta, but bacterial (mycotic) aneurysms were now known to exist. Many pathogenic agents may be involved: staphylococcus, Salmonella, pneumococcus, Proteus, Klebsiella, Brucella, more rarely KB, Rickettsia, or nematodes. Inflammatory causes have been recognized more recently, epidemiological and histological studies confirming their presence and the multiple etiologies involved: Horton's disease, rheumatic disorders, connective tissue diseases.
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PMID:[Inflammatory lesions of the aorta and its branches, Introduction and etiological aspects (excluding Takayasu's disease)(author's transl)]. 697 20


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