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)

Antibodies against double-stranded (ds) DNA were demonstrated by an immunofluorescence technique using Crithidia luciliae kinetoplast as antigen, and by means of the Farr technique. Both techniques were used simultaneously in 172 sera from patients with systemic lupus erythematosus (SLE), rheumatoid arthritis (RA), juvenile rheumatoid arthritis (JRA), temporal arteritis (TA) and from healthy controls. Comparable results were obtained with the two techniques. SLE patients with active disease had higher titres of IgA antibodies than patients with inactive disease. Of the patients with RA and JRA, 10% had significant titres of dsDNA antibodies. Patients with TA and normal controls had either no dsDNA antibodies in their sera or very low titres without complement-fixing properties.
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PMID:Antibodies against double-stranded DNA in patients with connective tissue diseases. Comparison between Crithidia luciliae kinetoplast immunofluorescence test and Farr technique. 7 59

Biopsies from the temporal arteries of 62 out of 80 patients presenting the clinical picture of temporal arteritis and/or polymyalgia rheumatica showed morphologically active or healed arteritis. Fifty-five of these biopsies revealed anti-IgG activity as measured by the mixed agglutination test. In 21 of the 27 cases which could be completely studied, the anti-IgG activity was connected with the presence of IgA, either alone, or together with IgG or IgM, or both, and complement. All of these 21 biopsies showed morphologically active granulomatous arteritis with signs of tissue destruction. In 6 biopsies, the active component appeared to be some type of Fc receptor in the tissue. Morphologically these biopsies showed either non-granulomatous mononuclear arteritis without definite necrosis or they represented various stages of healing arteritis with no or minor signs of tissue destruction. Weak anti-IgG activity was often found in a morphological type characterized by minimal inflammatory activity. These lesions are easily overlooked and the mixed agglutination test proved to be a good diagnostic tool in such cases. Arteries without anti-IgG activity showed no signs of active arteritis.
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PMID:Immunological and histological studies of temporal arteries from patients with temporal arteritis and/or polymyalgia rheumatica. 108 9

Immunopathologic studies are done routinely on biopsy specimens from tissues affected by many autoimmune diseases. To evaluate the role of direct immunofluorescence microscopy (DIFM) in identifying temporal arteritis, the authors reviewed all temporal artery biopsies done over a 30-month period (100 consecutive biopsies). The DIFM, using antibodies to IgG, IgM, IgA, complement, and fibrinogen, had a diagnostic sensitivity rate of 93% and a specificity rate of 87% compared with light microscopy. In biopsy specimens showing arteritis by light microscopy, IgG was demonstrated by DIFM in 85% of cases, IgM in 69%, and IgA in 15%. In one patient, a DIFM staining pattern highly suspicious of temporal arteritis identified a patient with features of clinical temporal arteritis despite negative findings by light microscopy. The demonstration of immunoglobulin by DIFM supports the possible role of humoral immunity in the pathogenesis of temporal arteritis.
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PMID:Temporal artery biopsies. Correlation of light microscopy and immunofluorescence microscopy. 267 48

An 84-year-old woman was admitted to Tokyo Metropolitan Tama Geriatric Hospital because of knee pain, anemia and hyperglobulinemia. On physical examination, evidence of arthritis was observed in both knees. Nodular temporal arteries were palpable with hypertrophy and weak pulsation. The urine was normal except that the sediment contained 20-30 with blood cells per high power view. Laboratory data showed raised erythrocyte sedimentation rate of 150 mm per hour, elevation of beta and gamma globulin and mild anemia. Although the levels of serum IgG, IgA were markedly increased, there was no monoclonal component on immunoelectrophoresis. Light microscopy examination of an aspirated specimen of bone marrow showed slight hypocellularity and mild plasmacytosis. However, atypical plasma cells were not observed. Radiographs of the knee showed narrowing of the joint space and calcification of articular cartilage and meniscus. Biopsy of the left temporal artery revealed typical findings of giant cell arteritis. The administration of prednisolone resulted in rapid normalization of laboratory findings. But her arthralgia, which had been relieved by analgesics after admission, was worsened if she took prednisolone without analgesic. Therefore, analgesics were given again with prednisolone for the control of the arthralgia.
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PMID:[A case of temporal arteritis associated with marked elevation of serum IgG, IgA levels]. 279 81

Serum samples were obtained from patients with polymyalgia rheumatica (PMR: n = 10) or giant cell arteritis (GCA; n = 7), or both. Samples were taken either before treatment or within one week of starting prednisolone. Immune complexes (IC) were concentrated by polyethylene glycol (PEG) precipitation then purified with either IgG anti-C1q-Sepharose or IgG anti-C3c-Sepharose. Complex components were separated by sodium dodecyl sulphate (SDS) gradient polyacrylamide gel electrophoresis then transferred to nitrocellulose by Western blotting. Identification of proteins was carried out using specific antisera. All the IC contained IgM (mu chain), some contained IgA (alpha chain), and IgG (gamma chain). C1r, C1s, C1q, C3, C4, and C reactive protein (CRP), where tested, were found in most but not all IC. The occurrence of properdin, factor B, alpha 2 macroglobulin (alpha 2M), factor H (beta 1H), C1 esterase inhibitor, and C4 binding protein was also investigated. Immune complexes in PMR and GCA differed from those previously characterized in rheumatoid arthritis (RA)1 purified by anti-C1q-Sepharose which contained immunoglobulins and C1q only. No properdin or factor B were detected in RA IC purified with either anti-C1q-Sepharose or anti-C3c-Sepharose.
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PMID:Isolation and analysis of immune complexes from sera of patients with polymyalgia rheumatica and giant cell arteritis. 282 Mar 20

Serologic studies and lymphocyte analysis were carried out in 29 patients with giant cell arteritis (GCA). IgA-containing circulating immune complexes (CIC) were detected in 16 GCA patients with or without polymyalgia rheumatica (55%). A significant difference was demonstrated in autologous rosette-forming cells between the patients as a whole, and matched controls (8.6 +/- 2.0 vs 11.6 +/- 2.4, p less than 0.001), and also between patients with and patients without CIC (7.9 +/- 1.6 vs 9.4 +/- 2.0, p less than 0.001).
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PMID:Immune complexes and autoantibodies in patients with giant cell arteritis and their relationship with autologous rosette-forming cells. 397 91

Immunohistochemical studies were performed on the temporal artery of 34 patients with clinically established polymyalgia rheumatica (PR) or temporal arteritis, 6 patients with vasculitis, and 25 patients with various diseases. The combined immunofluorescence and peroxidase-anti-Peroxidase Methode zeigte Immunoglobulin- und C3-Ablagerunin histologically affected and to some degree also in unaffected arteries of patients with PR and in all patients with temporal arteritis. The deposits were found both inter- and intracellularly, and contained IgA and to a lesser extend IgG, IgM, and C3. Linear deposits of leukocyte elastase were found along the fragmented internal lamina, and decaying polymorphonuclear (PMN) leukocytes surrounded by elastase-containing inclusions were found in the neighborhood of zones rich in elastic material. These findings suggest that immune complex deposition is a prominent feature of temporal arteritis and that the PMN elastase is probably involved in the destruction of elastic fibers. The combined immunohistochemical investigation appears to increase the diagnostic value of temporal artery biopsy.
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PMID:Temporal arteritis in polymyalgia rheumatica: immune complex deposits and the role of the leukocyte elastase in the pathogenesis. 655 32

Since immunological mechanisms may be involved in the pathogenesis of temporal arteritis, serum samples of 15 patients with ocular manifestations of temporal arteritis were investigated for the presence of circulating immune compleses (CICs) and antinuclear antibodies (ANAs). In addition, the serum levels of IgG, IgA, IgM, and the complement components C3 and C4 were determined. In none of our patients could CICs be detected. Serum samples of two of the patients were positive for ANA. The values for IgG, IgM, C3, and C4 were within normal limits. Our data indicate that circulating C1q-binding immune complexes and ANAs are not the cause of ocular manifestation of temporal arteritis. This does not exclude the possibility that other forms of circulating immune complexes or the local formation of immune complexes might play a role in the pathogenesis of this disease.
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PMID:Ocular manifestation of temporal arteritis. Immunological studies. 697 Oct 89

The levels of the immunoglobulins IgA, IgM, and IgG, as well as the complement components C3 and C4 were measured in the sera of patients with vascular pseudopapillitis. The ischemic papilledema was caused by either temporal or idiopathic arteritis. In the temporal arteritis group, the levels of IgG, IgM and C4 were significantly higher than in the idiopathic group. However, these facts are of little value for the differential diagnosis of vascular pseudopapillitis, because there is a considerable overlapping of values in the two groups.
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PMID:[Differential diagnosis of ischemic optic neuropathy (author' transl)]. 733 55

Malondialdehyde (MDA), a peroxidative end-product released during polyunsaturated fatty acid degradation, reacts strongly with lysine residues of cellular proteins. MDA-modified proteins become immunogenic and may elicit specific autoantibody formation. We hypothesized that systemic diseases in which inflammatory events occur, could be an interesting model for studying oxidative stress. A few studies have suggested that MDA-modified proteins may exist in systemic diseases, and that autoantibodies to MDA-modified structures might reflect this oxidative process. Autoantibodies to MDA-modified epitope(s) were therefore assayed in sera of patients with systemic lupus erythematosus (SLE, n = 29), scleroderma (SCL, n = 11), giant cell arteritis (GCA, n = 11), periarteritis nodosa (PAN, n = 10), rheumatoid arthritis (RA, n = 9), and healthy subjects (HS, n = 32). Significantly increased anti-MDA-modified epitope(s) autoantibodies were found in patients with SLE and also in other systemic diseases such as PAN and SCL. Autoantibodies to MDA-modified epitope(s) were predominantly of IgM isotype, with low levels of IgG and no IgA activity. In SLE, anti-MDA-modified epitope(s) autoantibody titres correlated strongly with systemic lupus activity measure (SLAM, r = 0.702, P = 0.0001), anti-nuclear antigen autoantibodies (ANA, r = 0.4, P = 0.029), IgG anti-cardiolipin (r = 0.558, P = 0.03) and the steroid drug regimen (r = 0.52, P = 0.004). Autoantibodies to MDA-modified epitope(s) may reflect oxidative modifications occurring in systemic diseases, and might be useful as clinical markers of SLE activity if further investigated.
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PMID:Autoantibodies to malondialdehyde-modified epitope in connective tissue diseases and vasculitides. 754 46


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