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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 lesions in temporal arteritis (TA) are known to be often segmental and the pathologic study of involved temporal arteries may be falsely negative. Several reports suggest that direct immunofluorescence (IF) may be of value in the diagnosis of the disease. We have studied by IF 101 consecutive biopsies from 100 patients investigated during the last two years. Adjacent segments were processed for light and immunofluorescent microscopy. For the latter, tissues were immediately frozen in liquid nitrogen and stored at -- 70 degrees C. Cryostat sections were stained with anti-gamma, alpha, mu, C3, fibrinogen and albumin conjugates. A sister section was also stained with HE for light microscopy. Deposits of Ig and/or C were either granular (intra- or extra-cellular) or linear closely applied to internal elastic lamina. The 100 patients fall into 4 groups: Group I, (19 patients) with diagnosis ascertained upon typical clinical record and clear cut anatomic lesions by light microscopy; Group II (10 patients) with the clinical features of TA and a negative biopsy by light microscopy; Group III (29 patients) in whom the diagnostic criteria of polymyalgia rheumatica were fulfilled according to Forestier and Certonciny; Group IV (42 patients) affected with various diseases unrelated to T.A. (1 with polyarteritis nodosa, 5 with rheumatoid arthritis...). The following results were obtained by IF: in group I, deposits were found in 63% of the patients studied (linear in 11 and granular in 4 cases). They included Ig usually with C3 and fibrinogen. In group II, we observed linear deposits of IgG in one patient and granular C3 deposits in another case.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Does the direct immunofluorescence examination of superficial temporal artery biopsies have any value? Results of the study of 101 biopsies]. 637 88

Postulating an increased production of fibrin(ogen)olytic degradation products (FDP) and an abnormality of fibrinogen metabolism in polymyalgia rheumatica (PMR) and temporal arteritis (TA), we studied 16 PMR/TA patients and 10 control subjects using a sensitive radioimmunoassay for a specific type of FDP, namely, fibrin(ogen)-related D-antigen. Median serum D-antigen levels were increased five-fold in those 11 PMR/TA patients who were untreated compared with control subjects. In the five PMR/TA patients who were treated with prednisone the median D-antigen levels were not significantly different from those of the healthy controls. D-antigen concentration correlated significantly (r = 0.83) with ESR in the seven untreated PMR patients. In PMR patients prednisone therapy was followed by a reduction of serum D-antigen levels.
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PMID:Fibrin(ogen)olysis in polymyalgia rheumatica and temporal arteritis: preliminary findings on association with disease activity. 649 63

Until recent years, main biologic markers of inflammation used in current practice were limited to erythrocyte sedimentation rate, fibrinogen, and serum protein electrophoresis. A better understanding of inflammatory mechanisms and improvement of laboratories technologies helped in better understanding of the role and potential usefulness of inflammatory reaction proteins. Arrival of proteic profile and, more recently, the development of automation, still improved analysis of variations of different inflammatory reaction proteins. These proteins are then analyzed as an element of a "functional biological system", with known and so expected kinetics and ranges. The analyze of proteic profile combines the analyze of proteins variations, with elected but not exclusive associations, as Immunoglobulins and Complement, Orosomucoid and Haptoglobin, or Albumin and Transferrin. In Internal Medicine, proteic profile may help in solving daily problems. These problems may be so schematized: when the fundamental pathology is not yet known in an unraveling check-up, facing clinical symptoms, with a normal or fewly disrupted usual biologic panel, proteic profile may help to choose investigations necessary for the diagnosis; in the follow-up of patients treated for known inflammatory pathology facing new symptoms, part has to be done between complication of the disease and/or of the treatment, new pathology associated or unefficiency of the treatment. We report herein part of our experience of proteic profile in an Internal Medicine department, from some particularly demonstrative case reports: congenital or acquired abnormality of iron metabolism, with normal usual iron panel (iron deficiency, hemochromatosis); severe evolutive inflammatory or infectious disease with normal erythrocyte sedimentation rate (temporal arteritis, infectious endocarditis).
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PMID:[Importance of the protein profile in internal medicine]. 751 44

Two elderly patients with polymyalgia rheumatica (PMR), one with and the other without temporal arteritis (TA), are presented. Immunofluorescence study of muscle biopsy specimens showed IgG, IgA, and fibrinogen deposits in the perifascicular area in the perimysium. This finding suggests that immune complexes play a role in the pathogenesis of this condition and that the pathophysiology of PMR involves an interstitial inflammatory process.
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PMID:Immunofluorescence study of immune complexes in polymyalgia rheumatica. 772 27

The clinical, laboratorial perimetric and fluorescein angiographic features of the arteritic type of the anterior ischemic optic neuropathy (A-AION) was studied in 25 patients (40 eyes) in order to characterize the profile of the disease and to allow the differential diagnosis with the non-arteritic anterior ischemic optic neuropathy (NA-AION) and other disorders of the optic nerve. The A-AION occurred in patients 60 to 88 years old (mean 74 years) and was highly predominant in females (64 per cent). Fifteen patients had both eyes involved, either simultaneously or usually within few days or weeks after the initial involvement. Headache and eye pain were the most commonly observed prodromic complaints whereas systemic symptoms of giant cell arteritis (GCA) were seen in all patients. The laboratorial abnormalities most commonly found were high values of reactive C protein, plasmatic fibrinogen and erythrocyte sedimentation rate. In the great majority of the patients visual acuity was severely affected. The optic disc was always abnormal, usually showing a pale edema. In addition to that retinal changes were commonly found. Goldmann perimetry disclosed a wide variety of visual fields abnormalities, the most common of them being inferior altitudinal defects. Fluorescein fundus angiography revealed delayed or absent disc fluorescence, or sectorial or diffuse hypofluorescence or hyperfluorescence of the optic disc. Choroidal filling delay was the most characteristic and frequent angiographic finding in the arteritc type of the disease.
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PMID:[The arteritic type of anterior ischemic optic neuropathy. Study of 25 cases]. 789 8

Thirty one patients with giant cell arteritis (GCA) receiving standardised prednisolone treatment were followed up for one year with analyses of plasma viscosity, erythrocyte sedimentation rate (ESR), C reactive protein (CRP), and fibrinogen concentration. On the day of diagnosis all patients had an increased plasma viscosity and ESR, whereas the concentration of CRP was normal in three patients and fibrinogen concentration and haptoglobin values were normal in one patient. IgG levels were increased in two patients. Plasma viscosity correlated significantly with the ESR, IgG level, and fibrinogen concentration. Laboratory variables in subgroups of patients with GCA proved by biopsy were not different from the whole group of patients with GCA. The follow up showed that CRP normalised faster than the ESR, plasma viscosity, and fibrinogen concentration. Plasma viscosity and the ESR paralleled clinical findings more closely and predicted flare ups better than the other variables. Plasma viscosity had advantages over the ESR for predicting flare ups and in the clinical monitoring of treatment with glucocorticoids.
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PMID:Plasma viscosity in giant cell arteritis as a predictor of disease activity. 750 12

IgG antibodies to cardiolipin and beta 2-glycoprotein I were looked for using an enzyme-linked immunosorbent assay (ELISA) in 19 patients with giant cell arteritis (meeting 1990 American College of Rheumatology criteria), including 16 with concomitant polymyalgia rheumatica (meeting Bird's criteria) and in three patients with isolated polymyalgia rheumatica. IgG anti-cardiolipin antibodies were demonstrated in eight patients (36%) and IgG anti-beta 2-glycoprotein I antibodies in two patients (9%) including one without anti-cardiolipin antibodies. Titers of anti-cardiolipin antibodies ranged from 27 to 190 units of IgG antiphospholipid antibodies (UGPL) (mean 71 UGPL). Of the eight patients with anti-cardiolipin antibodies, two had giant cell arteritis without polymyalgia rheumatica and six had polymyalgia rheumatica with clinical (n = 2) or histologic (n = 4) evidence of giant cell arteritis. None of the three patients with polymyalgia rheumatica but no giant cell arteritis had anti-cardiolipin or anti-beta 2 glycoprotein I antibodies. The VDRL was negative in the 14 patients who had this test. Tests for lupus anticoagulant were performed routinely, always with negative results. Among giant cell arteritis patients, those who tested positive for anticardiolipin antibody had significantly higher values for the erythrocyte sedimentation rate (p < 0.006) and for serum C-reactive protein (p < 0.03) and fibrinogen values (p = 0.05), and a trend toward higher platelet counts, as compared to those who tested negative for anticardiolipin antibody. The mean daily prednisone dose at the time of sampling was significantly lower in giant cell arteritis patients with anti-cardiolipin antibodies (p < 0.05); this difference may account for the apparent correlation between anti-cardiolipin antibodies and laboratory markers for inflammation. These data, as well as findings from serial measurements, suggest that anti-cardiolipin antibodies are present early in the course of giant cell arteritis and disappear within a few weeks of initiation of corticosteroid therapy in a dose of more than 25 mg prednisone per day. In this study, only one patient without anticardiolipin antibodies developed a cerebrovascular accident. Positive tests for anti-cardiolipin antibody or anti-beta 2 glycoprotein I antibody in a patient with polymyalgia rheumatica suggest a diagnosis of concomitant giant cell arteritis, which is usually symptomatic.
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PMID:Antibodies to cardiolipin and beta 2 glycoprotein I in patients with polymyalgia rheumatica and giant cell arteritis. 873 42

The aim of this prospective study was to examine the role of coagulation factor XIII (FXIII) in relation to disease activity in inflammatory bowel disease (IBD) and in giant cell arteritis. Plasma FXIII activity was studied during active and inactive disease in newly diagnosed patients with Crohn's disease (CD; n = 20), ulcerative colitis (UC; n = 18) and giant cell arteritis (GCA; n = 19), in 3-month intervals (median follow-up 12 months). FXIII was also measured in two noninflammatory control groups, age and sex matched for IBD (n = 25) and GCA (n = 26). FXIII activity was significantly lower in active CD or UC than in active GCA or the noninflammatory controls. Both in CD and UC, FXIII activity correlated inversely with indices of clinical disease activity, the erythrocyte sedimentation rate, fibrinogen and C-reactive protein levels. Low FXIII activity is a characteristic feature of active IBD, and serial measurements may be useful to assess IBD activity.
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PMID:Differential behavior of coagulation factor XIII in patients with inflammatory bowel disease and in patients with giant cell arteritis. 1084 6

Giant cell arteritis (arteritis temporalis) is the most common form of systemic vasculitis in the elderly. A series of symptoms such as new-onset headache, jaw claudication, proximal myalgia, weight loss, and fever may lead to the diagnosis. However, there is also a silent or occult presentation with minor or no systemic symptoms, especially no headache. A number of laboratory values (erythrocyte sedimentation rate, CRP, fibrinogen, thrombocytes, and cardiolipin antibodies) indicate giant cell arteritis, but none of this proves the diagnosis. Temporal artery biopsy is the gold standard for diagnosis of giant cell arteritis. Due to skip lesions, a negative result does not exclude the diagnosis. The most important complication of giant cell arteritis is visual loss in one or both eyes due to AION or retinal artery occlusion. Usually, visual loss is irreversible even with therapy. Corticosteroids are the drug of choice to treat giant cell arteritis. Therapy is required for a long time, monitored by parameters of inflammation (ESR, CRP).
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PMID:[Temporal arteritis (giant cell arteritis). Clinical picture, histology, and treatment]. 1655 35

Case report of a 66-year-old woman with episodes of amaurosis fugax and hemicranic headache with otherwise normal ophthalmologic and neurological examinations and normal imaging. While ESR was in the normal range for patient's age, acute phase proteins (C-reactive protein and fibrinogen) were elevated. Giant cell arteritis was proved by temporal artery biopsy. Giant cell arteritis should be considered as an important differential diagnosis of amaurosis fugax even in patients with normal ESR. Acute phase protein testing can give relevant diagnostic information.
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PMID:[Amaurosis fugax with elevated acute phase proteins]. 1798 30


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