YKL-40 in giant cells and macrophages from patients with giant cell arteritis.
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OBJECTIVE: YKL-40, a mammalian member of the family 18 glycosyl hydrolases, is secreted by activated macrophages at a late stage of differentiation. Macrophages are present in inflammation of the arterial wall and are thought to participate in the pathogenesis of giant cell arteritis (GCA). The aim of this study was to evaluate whether macrophages and giant cells of patients with GCA produce YKL-40, and whether serum YKL-40 concentrations are elevated in these patients. METHODS: Serum YKL-40 was determined by radioimmunoassay in 19 patients with GCA and 8 patients with polymyalgia rheumatica (PMR) who were followed up prospectively during 1 year of treatment with prednisolone. Immunohistochemical staining for YKL-40 was performed in temporal artery biopsy samples that were obtained before treatment. RESULTS: In the arteritic vessels of patients with GCA, positive staining for the YKL-40 antigen was found in CD68+ giant cells and mononuclear cells located in the media. Macrophages located in the adventitia and intima were negative for YKL-40. At the time of diagnosis, patients with GCA had an increased median serum level of YKL-40 (256 microg/liter; P<0.01) compared with healthy age-matched controls (median 118 microg/liter), and the serum level of YKL-40 decreased to normal levels during prednisolone treatment (-38% after 1 month; P<0.001). Most patients with PMR had normal serum YKL-40 levels (median 158 microg/liter) and had no changes in the serum YKL-40 levels during prednisolone treatment. The observed changes in serum YKL-40 did not always parallel the changes in serum C-reactive protein levels and erythrocyte sedimentation rate during the 1-year study period. CONCLUSION: YKL-40 is found in CD68+ giant cells and mononuclear cells in the media of arteritic vessels of patients with GCA, and the concentration of serum YKL-40 may reflect the local activity of these cells in the inflamed artery. (+info)
Temporal artery biopsy: a diagnostic tool for systemic necrotizing vasculitis. French Vasculitis Study Group.
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OBJECTIVE: To describe the clinical, biologic, and histologic features of temporal artery biopsy (TAB)-localized systemic necrotizing vasculitides (SNV), and to assess their frequency among elderly patients undergoing TAB for suspected giant cell (temporal) arteritis (GCA). METHODS: The frequency of a TAB localization of SNV was prospectively assessed in a multicenter study of elderly patients undergoing TAB for suspected GCA. All patients with SNV fulfilling the American College of Rheumatology criteria for a specific vasculitic syndrome and with evidence of vasculitis on TAB were included in a retrospective, descriptive study. RESULTS: SNV was diagnosed based on the TAB in 1.4% of the patients with suspected GCA and in 4.5% of the positive (inflamed) TAB specimens. We retrospectively selected 27 patients (18 female, 9 male; mean +/- SD age 62+/-15 years, range 22-79 years) with SNV and TAB-localized vasculitis. Only 2 of these patients were known to have SNV before TAB localization. Twenty-two patients (81%) had cephalic symptoms, including jaw claudication in 33%, clinically abnormal temporal arteries in 33%, and neuro-ophthalmologic symptoms in 11%. All patients had systemic symptoms suggestive of SNV and histologically proven NV in the TAB specimens (70%) or elsewhere in other biopsy sites (74%). Abnormal biologic results suggestive of SNV were present in 17 patients (63%). For 4 patients, the TAB-documented involvement led to initial misdiagnoses of GCA, and systemic manifestations that developed under steroid therapy revealed the correct diagnosis. The final diagnoses of the patients were polyarteritis nodosa (PAN) (n = 11), Churg-Strauss syndrome (n = 6), micropoly-angiitis (n = 3), Wegener's granulomatosis (n = 3), hepatitis B virus-related PAN (n = 2), hepatitis C virus-related cryoglobulinemic vasculitis (n = 1), and rheumatoid vasculitis (n = 1). CONCLUSION: TAB-localized SNV presents a major diagnostic dilemma because it can mimic GCA. Careful analysis of clinical, biologic, and histologic data should lead to the correct diagnosis and help guide the clinician's choice of appropriate therapy. (+info)
Cell adhesion molecules in the development of inflammatory infiltrates in giant cell arteritis: inflammation-induced angiogenesis as the preferential site of leukocyte-endothelial cell interactions.
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OBJECTIVE: To investigate the expression pattern of adhesion molecules involved in leukocyte-endothelial cell interactions in giant cell arteritis (GCA). METHODS: Immunohistochemical analysis was performed on frozen temporal artery sections from 32 patients with biopsy-proven GCA and from 12 control patients with other diseases. Adhesion molecules identified were intercellular adhesion molecule 1 (ICAM-1), ICAM-2, ICAM-3, vascular cell adhesion molecule 1 (VCAM-1), platelet endothelial cell adhesion molecule 1 (PECAM-1), E-selectin, P-selectin, L-selectin, lymphocyte function-associated antigen 1 (LFA-1), very late activation antigen 4 (VLA-4), Mac-1 (CD18/CD11b), and gp 150,95 (CD18/CD11c). Clinical and biochemical parameters of inflammation in the patients, as well as the duration of previous corticosteroid treatment, were prospectively recorded. RESULTS: Constitutive (PECAM-1, ICAM-1, ICAM-2, and P-selectin) and inducible (E-selectin and VCAM-1) endothelial adhesion molecules for leukocytes were mainly expressed by adventitial microvessels and neovessels within inflammatory infiltrates. Concurrent analysis of leukocyte receptors indicated a preferential use of VLA-4/VCAM-1 and LFA-1/ICAM-1 at the adventitia and Mac-1/ICAM-1 at the intima-media junction. The intensity of inducible endothelial adhesion molecule expression (E-selectin and VCAM-1) correlated with the intensity of the systemic inflammatory response. Previous corticosteroid treatment reduced, but did not completely abrogate, the expression of the inducible endothelial adhesion molecules E-selectin and VCAM-1. CONCLUSION: Inflammation-induced angiogenesis is the main site of leukocyte-endothelial cell interactions leading to the development of inflammatory infiltrates in GCA. The distribution of leukocyte-endothelial cell ligand pairs suggests a heterogeneity in leukocyte-endothelial cell interactions used by different functional cell subsets at distinct areas of the temporal artery. (+info)
Temporal artery biopsy: is there any value in examining biopsies at multiple levels?
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AIMS: To analyse the cost-effectiveness of three strategies for examining temporal artery biopsies based on data from cases examined over the past 10 years. METHODS: Of a total of 172 temporal artery biopsies, five were unsuitable for further analysis, 47 had already had levels cut, and 120 had levels cut as part of the study. All the biopsies were examined blind before and after levels. A tree with eventual diagnostic outcomes for different strategies was constructed and economic and sensitivity analyses performed. Welcan units were used to assess technical workload. RESULTS: Only one of the 132 initially normal cases and two of 14 diagnosed with periarterial lymphocytic infiltration (PALI) revealed giant cell arteritis after examining the tissue at multiple levels. Fifteen cases (8.9%) showed PALI not previously observed. The marginal cost for each extra case of giant cell arteritis detected was 83.5 Welcan units for a strategy of routine levels on all sections, and 21 Welcan units for a strategy of only cutting levels if PALI was present on the initial section. These costs were sensitive to the frequency of giant cell arteritis in cases with PALI and to the relative extra cost of moving from cutting single section to routine levels. CONCLUSIONS: Routinely examining a temporal artery biopsy at multiple levels does not increase the diagnostic yield of the test, although selective further examination may be indicated in some cases. The significance of PALI is uncertain. The cost-benefit of the different strategies in terms of clinical decision making revolve around the perceived risk inherent in not making a diagnosis of giant cell arteritis. (+info)
The importance of skip lesions in temporal arteritis.
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AIM: To determine the frequency of skip lesions in an unselected series of temporal artery biopsies and compare the results with other series. METHODS: The study was a retrospective review of 102 consecutive temporal artery biopsies taken in a five year period (1992-1997) in one large hospital. RESULTS: 35 cases (34.3%) showed evidence of active cranial vasculitis with pathological evidence of inflammation of the intima or media, with or without giant cells. Three of these cases (8.5%) showed apparent skip lesions: normal intima, media, and adventitia in one segment while in other segments there was clear evidence of active vasculitis. Immunocytochemical stains for leucocyte common antigen (LCA) and CD15 were helpful in identifying the absence of intimal or medial inflammatory cell infiltrates within skip lesions. Skip lesions have been described in up to 28.3% of cases in some series, while others have not found evidence of skip lesions or have identified them in a much smaller percentage of cases. CONCLUSIONS: In this series skip lesions were relatively rare, accounting for 8.5% of cases of active vasculitis. The degree of inflammation in temporal arteritis is discontinuous. Immunostaining for inflammatory cells, for example LCA and CD15, may be helpful in identifying the presence of an inflammatory cell infiltrate in skip lesion segments of the temporal artery. (+info)
Saphenous vein graft bypass in the treatment of giant cavernous sinus aneurysms: report of two cases.
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Two cases of giant intracavernous aneurysms treated by high flow bypass with saphenous vein graft between the external carotid artery (ECA) and branches of the middle cerebral artery (MCA) are presented. Very often these aneurysms are unclippable because they are fusiform or have a large neck. Occlusion of the internal carotid artery (ICA) is the treatment of choice in many cases. This procedure has however a high risk of brain infarction. Revascularization of the brain by extra-intracranial anastomosis between the superficial temporal artery (STA) and branches of the MCA is frequently performed. This procedure provides however a low flow bypass and brain infarction may occur. We report two cases of giant cavernous sinus aneurysms treated by high flow bypass and endovascular balloon occlusion of the ICA. Immediate high flow revascularization of MCA branches was achieved and the patients showed no ischemic events. Follow-up of 8 and 14 months after operation shows patency of the venous graft and no neurological deficits. Angiographic control examination showed complete aneurysm occlusion in both cases. (+info)
Superficial temporal artery dilatation in a patient with infectious temporal headache clinically mimicking temporal arteritis.
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A 57-year-old woman noticed a pulsatile shooting headache in her right temporal region 3 days after extraction of a tooth from the right mandible. The following day, a localized headache over the right superficial temporal artery (STA), low grade fever, and jaw claudication appeared and progressed subacutely. Seven days after the onset, magnetic resonance imaging and angiography (MRI/MRA) disclosed inflammatory swelling of the right temporal muscle and dilatation of the right STA. All the symptoms disappeared following antibiotic treatment, and neuroimaging findings were improved. In conclusion, MRA is thought to be useful to non-invasively identify reversible inflammatory dilatation of extracranial vessels. (+info)
Multiple arteriosclerotic fusiform aneurysms of the superficial temporal artery--case report.
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Superficial temporal artery (STA) aneurysms are very rare, and usually occur in young adult men due to blunt trauma as pseudoaneurysms. An 85-year-old male presented with two non-traumatic STA aneurysms. The aneurysms were ligated and resected. Histological examination showed arteriosclerotic fusiform aneurysm. The pathogenesis of non-traumatic aneurysm of the STA appears to be arteriosclerotic change and/or hemodynamic stress. (+info)