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)

To explore the role of adhesion molecules in mediating mononuclear cell localisation, development of the granulomatous reaction, and cell mediated damage to the arterial wall in giant cell arteritis, 17 temporal artery biopsy specimens were examined. Eleven showed the histological features of giant cell arteritis and six showed no evidence of arteritis. All were examined for the expression of LFA-3, ICAM-1 and its receptor LFA-1, and HLA-DR. Temporal arteries with early features of arteritis, as well as histologically unaffected skip areas, showed a regional induction of ICAM-1 expression, but not HLA-DR, on smooth muscle cells of the media. ICAM-1 expression was detected in areas where a clinically important mononuclear cell infiltrate had not yet developed. In more florid cases of giant cell arteritis there was an additional widespread induction of ICAM-1 expression on intimal myofibroblasts. Strong expression of ICAM-1, HLA-DR, and LFA-3 was found on macrophages, epithelioid cells, and giant cells comprising the granulomatous lesion. The pattern of expression of these adhesion molecules suggests that they have a role in leucocyte traffic into the vascular lesion as well as in mediating the intercellular interactions which constitute the granulomatous response.
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PMID:Analysis of adhesion molecules in the immunopathogenesis of giant cell arteritis. 181 93

Giant cell arteritis (GCA) (temporal arteritis) and polymyalgia rheumatica (PMR) are common, frequently related conditions in people generally over 50 years of age. Most studies have shown an association of GCA with HLA-DRB1 *04 alleles. As regards isolated PMR, however, the HLA class II genetic susceptibility varies from one population to another. Besides associations with HLA, tumor necrosis factor appears to influence susceptibility to both conditions. Genetic polymorphisms have also been considered to be important candidates as factors of susceptibility to GCA and PMR. In this regard, gene polymorphisms for ICAM-1 (intercellular adhesion molecule 1), RANTES (regulated upon activation, normal T cell expressed, and presumably secreted), and interleukin (IL)-1 receptor antagonist seem to play a role in the pathogenesis of GCA and PMR in some populations. However, additional studies are required to clarify the genetic influence on susceptibility to these conditions.
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PMID:Genetic epidemiology. Giant cell arteritis and polymyalgia rheumatica. 1129 56

Polymyalgia rheumatica (PMR) and giant cell arteritis (GCA) are closely related chronic inflammatory diseases. Glucocorticoids (GCs) are first-choice drugs for PMR and GCA, although some patients show poor responsiveness to the initial GC regimen or experience flares after GC tapering. To date, no valid biomarkers have been found to predict which patients are at most risk for developing GC resistance. In this review, we summarize PMR- and GCA-related gene polymorphisms and we associate these gene variants with GC resistance and therapeutic outcomes. A limited number of GC resistance associated-polymorphisms have been published so far, mostly related to HLA-DRB1*04 allele. Other genes such ICAM-1, TLR4 and 9, VEGF, and INFG may play a role, although discrepancies are often found among different populations. We conclude that more studies are required to identify reliable biomarkers of GC resistance. Such biomarkers could help distinguish non-responders from responders to GC treatment, with concomitant consequences for therapeutic strategy.
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PMID:Genetic Predispositions of Glucocorticoid Resistance and Therapeutic Outcomes in Polymyalgia Rheumatica and Giant Cell Arteritis. 3103 18