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

Temporal arteritis (TA) is a common idiopathic vasculitis of the elderly. It is controversial whether, in the absence of an active inflammatory process, vessel damage secondary to temporal arteritis is distinguishable from changes secondary to arteriosclerosis. The primary goal of this study was to attempt to differentiate microscopically between healed temporal arteritis and arteriosclerosis, in the absence of active vasculitis. This was a retrospective study in which 47 temporal artery biopsy specimens, done between 1981 and 1997 at University of British Columbia Hospital, were reviewed. As well, temporal arteries harvested from 10 autopsy cases with no clinical evidence of vasculitis were used as controls. Haematoxylin and Eosin and Movat's pentachrome stains were used to assess the degree of intimal thickening, presence or absence of inflammation, type of inflammatory cell(s), the degree of reduplication of elastic lamina, calcification, fibrosis, neovascularisation and gaps or losses in the internal and external elastic lamina. No histological findings were specific for temporal arteritis except the presence of mural inflammation. A high degree of variability existed for all other features assessed, within all groups studied. These results indicate that, in the absence of active inflammation, structural changes in the vessel wall do not allow reliable differentiation between healed or quiescent temporal arteritis and arteriosclerosis. The common practice of performing special stains in all temporal artery biopsy cases does not contribute to the ability to recognise temporal arteritis.
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PMID:Healed or quiescent temporal arteritis versus senescent changes in temporal artery biopsy specimens. 1135 48

Giant cell arteritis (GCA) is a chronic immune-mediated disease of medium-to-large sized arteries that affects older adults. GCA manifests with arthritis and occlusive symptoms of headaches, stroke or vision loss. Macrophages and T-helper lymphocytes infiltrate the vascular wall and produce a pro-inflammatory response that lead to vessel damage and ischemia. To date, there is no GCA biomarker that can monitor disease activity and guide therapeutic response. Folate receptor beta (FRB) is a glycosylphosphatidylinositol protein that is anchored on cell membranes and normally expressed in the myelomonocytic lineage and in the majority of myeloid leukemia cells as well as in tumor and rheumatoid synovial macrophages, where its expression correlates with disease severity. The ability of FRB to bind folate compounds, folic acid-conjugates and antifolate drugs has made it a druggable target in cancer and inflammatory disease research. This report describes the histopathologic and immunohistochemical methods used to assess expression and distribution of FRB in relation to GCAimmunopathology. Formalin-fixed and paraffin-embedded temporal artery biopsies from GCA and normal controls were stained with Hematoxylin and Eosin to review tissue histology and identify pathognomonic features.Immunohistochemistry was used to detect FRB, CD68 and CD3 expression. A microscopic analysis was performed to quantify the number of positively stained cells on 10 selected high-power-field sections and their respective locations in the arterial wall. Lymphohistiocytic (LH) inflammation accompanied by intimal hyperplasia and disrupted elastic lamina was seen in GCA with none found in controls. The LH infiltrate was composed of approximately 60% lymphocytes and 40% macrophages. FRB expression was restricted to macrophages, comprising 31% of the total CD68+ macrophage population and localized to the media and adventitia. No FRB was seen in controls. This protocol demonstrated a distinct numerical and spatial pattern of the FRB macrophage relative to the vascular immune microenvironment in GCA.
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PMID:An Immunohistopathologic Study to Profile the Folate Receptor Beta Macrophage and Vascular Immune Microenvironment in Giant Cell Arteritis. 3079 40