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

The clinical syndrome of polymyalgia rheumatica is reviewed. The relationship of this disease with temporal arteritis is discussed, and I consider both syndromes have a pathological basis of generalised giant cell arteritis.Seven cases of polymyalgia and four cases of temporal arteritis were recorded during the six-year period (1969-1975) in one general practice.The outlines of management are discussed, with a plea for earlier recognition of the syndromes of polymyalgia rheumatica and temporal arteritis in general practice.
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PMID:Giant cell arteritis in general practice. 0 44

Personal observations have confirmed the frequent association of HB-infection with certain forms of vasculitis. 4 of 11 patients with polyarteritis nodosa were repeatedly found to be HBs-Ag positive and had chronic hepatitis of varying severity. In patients with giant cell arteritis (polymyalgia rheumatica and temporal arteritis) anti-HBs was found more frequently than in controls, especially when examined within 6 months after onset of symptoms (7 of 20 equal 35% had anti-HBs, versus 6% of controls). Several lines of evidence point to the important role played by circulating HBs-Ag/anti-HBs complexes in the development of HB-associated vasculitis.
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PMID:[Vasculitis in hepatitis B infection]. 1 40

Giant cell arteritis, which is probably due to disturbed immune mechanisms, has a spectrum of clinical symptoms in elderly people. In nearly all cases such general signs as loss of appetite, loss of weight and fever are present. The sedimentation rate is almost without exception about 100 mm in the first hour. The two most frequent and typical clinical syndromes are polymyalgia rheumatica and cranial arteritis. The polymyalgia rheumatica is characterized by periarticular pain which is mostly symmetrical and accentuated in the shoulder girdle. Increasingly severe temporal headache and ocular distrubances are found with cranial arteritis in more than 50% of cases. A combination of both diseases is frequent. Other arterial branches are rarely involved. The course of the disease is over a period of 1 1/2 to 2 years. Treatment with corticosteroids is indicated mainly because of the severe ocular complications with blindness. It should begin immediately, be intensive and last over a long period. Regular followup is necessary over several years in order to avoid relapses.
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PMID:Giant cell arteritis (cranial arteritis, polymyalgia rheumatica). 8 Dec 71

Nineteen patients with polymyalgia rheumatica and/or temporal arteritis were classified by degree of clinical and arteriographic abnormality, biopsy grade of arteriosclerosis, and giant cell arteritis (GCA). Temporal arteriograms were very sensitive in detecting abnormal arteries. However, the assumption of some previous studies, that certain angiographic abnormalities are synonymous with GCA, was not supported, since biopsies from distal sites in a Class I and a Class II arteriogram revealed only arteriosclerosis. Class III arteriograms correlated with proximal biopsies of GCA. Immunofluorescent staining was negative in all cases.
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PMID:Temporal arteriography and immunofluorescence as diagnostic tools in temporal arteritis. 32 79

Sixty-four temporal arteries were studied. 36 were from patients with clinically active temporal arteritis or polymyalgia rheumatica; 22 showed histological changes of temporal arteritis, 12 of which were in an active stage. 28 arteries, none of which showed histological changes, were taken at necropsy or from patients with unrelated disease. Extracellular immunoglobulin and complement deposition was seen in the artery biopsies showing active arteries and in 1 of the 10 biopsies with inactive arteritis. There was no immunoglobulin or complement deposition in the 14 patients with clinically active temporal arteritis and/or polymyalgia rheumatica, but with a normal artery biopsy. Patients with clinically active temporal arteritis were more likely to have a positive biopsy. Our results support the suggestion that the immune deposition is concurrent with an active histologically proven arteritis. Immunofluorescent examination does not appear to be a better diagnostic test than histological examination.
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PMID:Immunological and histological study of temporal arteries. 35 59

It is important to establish the diagnosis of temporal arteritis because the disease is treatable; treatment may prevent blindness and even death. Temporal arteritis usually occurs in people older than 51 years of age, although very rarely, histologically documented disease occurs in younger people. The onset may be occult, so that there are few findings. A multitude of signs and symptoms may occur such as fever, headaches, malaise, weight loss, anemia, stroke, cranial nerve palsies, polymyalgia rheumatica, aortitis and other large vessel involvement. The eye may suffer from ischemic optic neuropathy (anterior or posterior), central or cilio-retinal arterial occlusion, ophthalmic artery ischemia, or extraocular muscle palsies. An arterial biopsy showing giant cell arteritis establishes the diagnosis. However, a negative biopsy does not rule out the disease because of the occasional presence of skip areas. Arteriography has only rarely yielded a positive temporal artery biopsy when the initial biopsy done elsewhere was negative. As a diagnostic parameter, the erythrocyte sedimentation rate is nonspecific, being elevated in diseases other than temporal arteritis and sometimes being falsely lowered by technical factors. Furthermore, the temporal artery biopsy is occasionally positive despite a normal erythrocyte sedimentation rate. Treatment is aimed at relieving the patient's symptoms and normalizing the erythrocyte sedimentation rate. Because of the wide spectrum of clinical and laboratory finding in temporal arteritis, no one specific treatment regimen with systemic corticosteroids works for all patients. Temporal arteritis is a well known disease of the elderly which ir rarely fatal but results in significant visual morbidity (Hinzpeter & Naumann, 1976; Spencer & Hoyt, 1960). Since Hutchinson's (1890) description, more than a thousand articles have been written on the subject (Cohen & Smith, 1974). Despite this, many unanswered questions and controversies remain concerning the diagnosis, prognosis and treatment of temporal arteritis. My goal is to review these questions and areas of controversy.
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PMID:Controversies regarding giant cell (temporal, cranial) arteritis. 39 20

A case of polymyalgia rheumatica (PMR) with biopsy-proven giant cell arteritis (GCA) is described in which there were marked abnormalities noted on electromyography (EMG). Spike potentials, positive waves, and fibrillation potentials were seen in the proximal musculature of the upper and lower extremities as well as in the erector spinae muscles. Investigation failed to reveal abnormalities in either creatinine phosphokinase (CPK), aldolase, or muscle obtained at biopsy. The presence of these EMG findings in the PMR-GCA syndrome is unusual. Response to therapy with systemic corticosteroids and normalization of the EMG are documented.
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PMID:Unusual electromyographic findings in a patient with polymyalgia rheumatica. 42 Jul 18

In a patient who had a hysterectomy and bilateral salpingo-oophorectomy for endometrial adenocarcinoma, a giant cell arteritis was found in many of the myometrial and tubal vessels and in a few of the small arteries of the cervix and ovaries. On subsequent questioning, a history of treatment for polymyalgia rheumatica during the preceding 12 months was elicited. Of the three previously reported patients with giant cell arteritis of the uterus, two were suffering from polymyalgia rheumatica whilst one possibly had disseminated visceral giant cell arteritis.
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PMID:Giant cell arteritis of the female genital tract. 42 54

Peripheral blood lymphocyte functions were evaluated in 20 patients with active polymyalgia rheumatica (PMR) and/or giant cell arteritis (GCA) by determining the percent of E-rosette-forming cells and by measuring the uptake of tritiated thymidine by peripheral blood lymphocytes after exposure to common infectious antigens and to homogenates of homologous and heterologous artery, muscle, and elastin. Although lymphocytes from patients with PMR and/or GCA were stimulated slightly by artery and muscle homogenates, no differences in lymphocyte responses were found when the results were compared with 22 normal controls and 16 patients with rheumatoid arthritis. The hypothesis that GCA results from a cellular immune reaction to normal or diseased arterial wall antigens is not supported by these studies.
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PMID:Cellular immunity in polymyalgia rheumatica and giant cell arteritis: lack of response to muscle or artery homogenates. 45 1

Reports of polymyalgia rheumatica and temporal arteritis in blacks are rare. We analyzed five cases of polymyalgia rheumatica and one case of temporal arteritis appearing in blacks. Polymyalgia rheumatica and temporal arteritis in blacks have the same presentation, course, and response to treatment as in Caucasians. A previously unrecorded case of polymyalgia rheumatica and biopsy-proven temporal arteritis in a black had a similar presentation and course as cases in whites. HLA typing of five cases of polymyalgia rheumatica in blacks revealed an increased incidence of AW30 and BW16 in comparison to whites and polymyalgia.
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PMID:Polymyalgia rheumatica and temporal arteritis in blacks--clinical features and HLA typing. 60 81


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