Please use this identifier to cite or link to this item:
標題: 糖化終產物及其可溶性接受器在成人型史迪兒氏症致病機轉之角色
Advanced glycation end products and its soluble receptor in AOSD pathogenic role
作者: 吳燕晴
Wu, Yen- Ching
關鍵字: 成人型史迪兒氏症;Adult onset Still’s disease;全身性紅斑狼瘡;糖化終產物;可溶性糖化終產物接受器;致病機轉;systemic lupus erythematosus;advanced glycation end products;soluble receptor for advanced glycation end products;pathogenesis
出版社: 生命科學院碩士在職專班
引用: 1 Maillard-Lefebvre H, Boulanger E, Daroux M, Gaxatte C, Hudson BI, Lambert M. Soluble receptor for advanced glycation end products: a new biomarker in diagnosis and prognosis of chronic inflammatory diseases. Rheumatology (Oxford) 2009;48(10):1190-6. 2 Thorpe SR, Baynes JW. Maillard reaction products in tissue proteins: new products and new perspectives. Amino acids 2003;25(3-4):275-81. 3 Wendt T, Tanji N, Guo J, et al. Glucose, glycation, and RAGE: implications for amplification of cellular dysfunction in diabetic nephropathy. Journal of the American Society of Nephrology : JASN 2003;14(5):1383-95. 4 Mosquera JA. [Role of the receptor for advanced glycation end products (RAGE) in inflammation]. Investigacion clinica 2010;51(2):257-68. 5 Kislinger T FC, Huber B, Qu W, Taguchi A, Du Yan S, Hofmann M, Yan SF, Pischetsrieder M, Stern D, Schmidt AM. N(epsilon)-(carbo- xymethyl)lysine modifications of proteins are ligands for RAGE that activate cell signalling pathways and modulate gene expression. . J Biol Chem. 1999;274(44):31740-9. 6 Hofmann MA, Drury S, Fu C, et al. RAGE mediates a novel proinflammatory axis: a central cell surface receptor for S100/calgranulin polypeptides. Cell 1999;97(7):889-901. 7 Sakaguchi T, Yan SF, Yan SD, et al. Central role of RAGE-dependent neointimal expansion in arterial restenosis. J Clin Invest 2003;111(7):959-72. 8 Wendt TM, Tanji N, Guo J, et al. RAGE drives the development of glomerulosclerosis and implicates podocyte activation in the pathogenesis of diabetic nephropathy. The American journal of pathology 2003;162(4):1123-37. 9 Lin L, Park S, Lakatta EG. RAGE signaling in inflammation and arterial aging. Front Biosci 2009;14:1403-13. 10 Bywaters EG. Still''s disease in the adult. Ann Rheum Dis. 1971;30(2):121-33. 11 Ohta A YM, Kaneoka H, Nagayoshi T, Hiida M. Adult Still''s disease: review of 228 cases from the literature. J Rheumatol. 1987;14(6):1139-46. 12 Masson C, Le Loet X, Liote F, et al. Adult Still''s disease: part I. Manifestations and complications in sixty-five cases in France. Rev Rhum Engl Ed 1995;62(11):748-57. 13 Efthimiou P PP, Bielory L. Diagnosis and management of adult onset Still''s disease. Ann Rheum Dis. 2006;65(5):564-72. 14 Kontzias A, Efthimiou P. Adult-onset Still''s disease: pathogenesis, clinical manifestations and therapeutic advances. Drugs 2008;68(3):319-37. 15 Lim E, Chng HH. Adult-onset Still''s disease in an oriental population: manifestations, course and outcome in 16 patients. Annals of the Academy of Medicine, Singapore 1998;27(1):11-5. 16 Zrour-Hassen S, Korbaa W, Mnif H, et al. [Adult-onset of Still''s disease with atypical articular and skin manifestations]. La Tunisie medicale 2010;88(12):937-41. 17 Yamaguchi M OA, Tsunematsu T, Kasukawa R, Mizushima Y, Kashiwagi H, Kashiwazaki S, Tanimoto K, Matsumoto Y, Ota T, et al. Preliminary criteria for classification of adult Still''s disease. J Rheumatol. 1992;19(3):424-30. 18 Pouchot J, Sampalis JS, Beaudet F, et al. Adult Still''s disease: manifestations, disease course, and outcome in 62 patients. Medicine 1991;70(2):118-36. 19 Chen D-Y. Recent advances in the treatment of adult-onset Still’s disease. . Expert Opinion on Orphan Drugs 2013. 20 Wouters JMGW, van der Veen J, van de Putte LBA, de Rooij DJRAM. Adult Still’s disease and viral infection. Ann Rheum Dis 1988;47:764-7. . 21 Pouchot J, Quakil H, Debin ML, et al. Adult Still’s disease associated with acute human parvovirus B19 infection. Lancet 1993;341:1280-1. 22 Bilidi M, Gatfosse M, Barjonet G. Adult onset Still disease associated with acute parvovirus B19 infection in pregnancy. . Ann Med Int 1996;147:518-9. 23 Correction: Acute-Phase Proteins and Other Systemic Responses to Inflammation. The New England journal of medicine 1999;340(17):1376. 24 Izumikawa K, Morinaga Y, Kondo A, et al. Adult Still’s disease associated with cytomegalovirus infection. . J Infect Chemother 2007;13:114-7. 25 Chen DY, Chen YM, Lan JL, Tzang BS, Lin CC, Hsu TC. Significant association of past parvovirus B19 Infection with cytopenia and arthritis in patients with adult-onset Still’s disease. . Clinica Chimica Acta 2012;413:855-60. 26 Pullerits R, Bokarewa M, Dahlberg L, Tarkowski A. Decreased levels of soluble receptor for advanced glycation end products in patients with rheumatoid arthritis indicating deficient inflammatory control. Arthritis Research & Therapy 2005;7(4):R817-24. 27 Foell D, Ichida F, Vogl T, et al. S100A12 (EN-RAGE) in monitoring Kawasaki disease. Lancet 2003;361(9365):1270-2. 28 Katz J, Stavropoulos F, Bhattacharyya I, Stewart C, Perez FM, Caudle RM. Receptor of advanced glycation end product (RAGE) expression in the minor salivary glands of patients with Sjogren''s syndrome: a preliminary study. Scandinavian journal of rheumatology 2004;33(3):174-8. 29 Nienhuis HL, de Leeuw K, Bijzet J, et al. Skin autofluorescence is increased in systemic lupus erythematosus but is not reflected by elevated plasma levels of advanced glycation endproducts. Rheumatology (Oxford, England) 2008;47:1554-8. 30 Koyama H, Shoji T, Yokoyama H, et al. Plasma level of endogenous secretory RAGE is associated with components of the metabolic syndrome and atherosclerosis. Arterioscler Thromb Vasc Biol 2005;25:2587-93. 31 Liu F-C, Hung L-F, Wu W-L, et al. Chondroprotective effects and mechanisms of resveratrol in advanced glycation end products-stimulated chondrocytes. Arthritis research & therapy 2010;12(5):R167. 32 Rubin LA, Urowitz MB, Gladman DD. Mortality in systemic lupus erythematosus: the bimodal pattern revisited. The Quarterly journal of medicine 1985;55(216):87-98. 33 Urowitz MB, Bookman AA, Koehler BE, Gordon DA, Smythe HA, Ogryzlo MA. The bimodal mortality pattern of systemic lupus erythematosus. The American journal of medicine 1976;60(2):221-5. 34 Romero-Diaz J, Isenberg D, Ramsey-Goldman R. Measures of adult systemic lupus erythematosus: updated version of British Isles Lupus Assessment Group (BILAG 2004), European Consensus Lupus Activity Measurements (ECLAM), Systemic Lupus Activity Measure, Revised (SLAM-R), Systemic Lupus Activity Questionnaire for Population Studies (SLAQ), Systemic Lupus Erythematosus Disease Activity Index 2000 (SLEDAI-2K), and Systemic Lupus International Collaborating Clinics/American College of Rheumatology Damage Index (SDI). Arthritis care & research 2011;63 Suppl 11:S37-46. 35 Tan EM, Cohen AS, Fries JF, Masi AT, McShane DJ, Rothfield NF, et al. The 1982 revised criteria for the classification of systemic lupus erythematosus. Arthritis Rheum 1982;25:1271-7. 36 Gladman DD, Ibanez D, Urowitz MB. Systemic lupus erythematosus disease activity index 2000. J Rheumatol 2002;29(2):288-91. 37 de Leeuw K, Graaff R, de Vries R, et al. Accumulation of advanced glycation endproducts in patients with systemic lupus erythematosus. Rheumatology (Oxford, England) 2007;46(10):1551-6. 38 Nienhuis HL, de Leeuw K, Bijzet J, et al. Skin autofluorescence is increased in systemic lupus erythematosus but is not reflected by elevated plasma levels of advanced glycation endproducts. Rheumatology (Oxford, England) 2008;47(10):1554-8. 39 Reddy Munagala VV, Misra R, Agarwal V, Lawrence A, Aggarwal A. Adult onset Still''s disease: experience from a tertiary care rheumatology unit. International journal of rheumatic diseases 2012;15(6):e136-41. 40 Yan SF, Ramasamy R, Schmidt AM. Mechanisms of disease: advanced glycation end-products and their receptor in inflammation and diabetes complications. Nature clinical practice. Endocrinology & metabolism 2008;4(5):285-93. 41 Romero R, Espinoza J, Hassan S, et al. Soluble receptor for advanced glycation end products (sRAGE) and endogenous secretory RAGE (esRAGE) in amniotic fluid: modulation by infection and inflammation. Journal of perinatal medicine 2008;36(5):388-98. 42 Lalla E, Lamster IB, Stern DM, Schmidt AM. Receptor for advanced glycation end products, inflammation, and accelerated periodontal disease in diabetes: mechanisms and insights into therapeutic modalities. Annals of periodontology / the American Academy of Periodontology 2001;6(1):113-8. 43 Rodriguez-Garcia J, Requena JR, Rodriguez-Segade S. Increased concentrations of serum pentosidine in rheumatoid arthritis. Clinical chemistry 1998;44(2):250-5. 44 Drinda S, Franke S, Eidner T, et al. Decreased RAGE expression in peripheral blood mononuclear cells of patients with rheumatoid arthritis. Clinical and experimental rheumatology 2009;27(3):483-90. 45 Vytasek R, Sedova L, Vilim V. Increased concentration of two different advanced glycation end-products detected by enzyme immunoassays with new monoclonal antibodies in sera of patients with rheumatoid arthritis. BMC musculoskeletal disorders 2010;11:83. 46 Takahashi M, Suzuki M, Kushida K, Miyamoto S, Inoue T. Relationship between pentosidine levels in serum and urine and activity in rheumatoid arthritis. British journal of rheumatology 1997;36(6):637-42. 47 Chen DY, Lan JL, Hsieh TY, Chen YH. Clinical manifestations, disease course, and complications of adult-onset Still''s disease in Taiwan. Journal of the Formosan Medical Association = Taiwan yi zhi 2004;103(11):844-52. 48 Yamamoto T. Cutaneous manifestations associated with adult-onset Still''s disease: important diagnostic values. Rheumatology international 2012;32(8):2233-7. 49 Gabay C, Kushner I. Acute-phase proteins and other systemic responses to inflammation. The New England journal of medicine 1999;340(6):448-54. 50 Li J, Hou F, Guo Z, Shan Y, Zhang X, Liu Z. Advanced glycation end products upregulate C-reactive protein synthesis by human hepatocytes through stimulation of monocyte IL-6 and IL-1 beta production. Scandinavian journal of immunology 2007;66(5):555-62. 51 Zhong Y, Li SH, Liu SM, et al. C-Reactive protein upregulates receptor for advanced glycation end products expression in human endothelial cells. Hypertension 2006;48(3):504-11. 52 McNair ED, Wells CR, Mabood Qureshi A, et al. Modulation of high sensitivity C-reactive protein by soluble receptor for advanced glycation end products. Molecular and cellular biochemistry 2010;341(1-2):135-8. 53 McNair ED, Wells CR, Qureshi AM, et al. Low levels of soluble receptor for advanced glycation end products in non-ST elevation myocardial infarction patients. The International journal of angiology : official publication of the International College of Angiology, Inc 2009;18(4):187-92. 54 Qi Y, Gong F, Zhang Q, Xie C, Wang W, Fu S. Reverse regulation of soluble receptor for advanced glycation end products and proinflammatory factor resistin and S100A12 in Kawasaki disease. Arthritis Research & Therapy 2012;14(6):R251. 55 Tam LS, Shang Q, Li EK, et al. Serum Soluble Receptor for Advanced Glycation End Products Levels and Aortic Augmentation Index in Early Rheumatoid Arthritis-A Prospective Study. Seminars in arthritis and rheumatism 2012. 56 Ma CY, Ma JL, Jiao YL, et al. The plasma level of soluble receptor for advanced glycation end products is decreased in patients with systemic lupus erythematosus. Scandinavian journal of immunology 2012;75(6):614-22. 57 Meddeb N, Amira C, Elleuch M, et al. [Articular manifestations of adult Still''s disease]. La Tunisie medicale 2003;81(4):245-9.
成人型史迪兒氏症(adult onset Still’s disease,簡稱AOSD) 是一種慢性發炎疾病,患者會有不明原因的發燒、關節炎、皮膚紅疹或其他內臟器官之侵犯,致病機轉目前尚未明瞭。有研究顯示糖化終產物(advanced glycation end products,簡稱AGEs)與慢性發炎有關。在某些慢性發炎疾病,例如全身性紅斑狼瘡(systemic lupus erythematosus,簡稱SLE)等研究中發現AGEs的累積與病程發展有關,但在AOSD患者目前沒有相關的研究。為了探討AGEs及其可溶性RAGE接受器(soluble receptors for advanced glycation end products,簡稱sRAGE) 與AOSD致病機轉的關聯,我們收納52名AOSD患者、36名SLE患者及16名健康者的檢體,以酵素連結免疫吸附法( enzyme- linked immuno- sorbent assay ,簡稱ELISA) 檢測血漿(或血清)AGEs濃度,及可溶性RAGE接受器(能於循環血液中與AGEs接合,阻止AGEs接到細胞膜上RAGE)。由我們檢測的數據發現,活動期AOSD患者檢體的AGEs濃度明顯高於健康對照組( mean± SEM; 19.47± 1.84 µg/ ml比8.45± 0.97μg/ ml; p < 0.001),也明顯高於非活動期AOSD患者( mean± SEM; 7.52± 0.57μg/ ml; p < 0.001)。sRAGE於活動期AOSD患者檢體的濃度明顯低於健康對照組( mean± SEM; 650.7± 59.0 pg/ml比1129.7± 98.7 pg/ ml;p < 0.001),也明顯低於非活動期AOSD患者( mean± SEM; 985.3± 106.9 pg/ ml ; p <0.05),而SLE患者檢體的AGEs 和sRAGE的檢測結果也與AOSD相似。另外AOSD患者檢體的AGEs濃度與疾病活動度的指標activity score (r =0.836 ; p < 0.001)、ferritin ( r =0.372;p <0.05)、ESR(r =0.413;p <0.005)、CRP( r =0.396;p <0.005) 都呈正相關。我們的結果顯示AGEs 和sRAGE可能在AOSD的致病機轉扮演重要角色,且可以做為疾病活動度的監控指標。

Adult onset Still’s disease (AOSD) is a chronic inflammatory disease characterized by fever of unknown origin, arthritis, and skin rash. However the etiopathogenesis of AOSD remains unclear. Studies have shown that the levels of advanced glycation end products (AGEs) were associated with chronic inflammation, and were positively correlated with disease duration of systemic lupus erythematosus (SLE). Although AOSD is also an inflammatory disease, there is no any data regarding AGEs in this disease. In order to explore the relationship between AOSD and AGEs as well as their receptors, we enrolled 52 patients with AOSD, 36 patients with SLE, and 16 healthy volunteers, and used the enzyme-linked immunosorbent assay (ELISA) to detect plasma (or serum) levels of AGEs and their soluble receptors for advanced glycation end products (sRAGE). Our results showed plasma (or serum) AGEs levels were significantly higher in patients with active AOSD compared with healthy controls (mean± SEM; 19.47± 1.84 µg/ ml vs. 8.45± 0.97μg/ ml; p < 0.001). Plasma (or serum) AGEs levels were also significantly higher in patients with active AOSD compared with inactive AOSD (mean± SEM; 7.52± 0.57μg/ ml; p < 0.001). Whereas, plasma (or serum) sRAGE levels were significantly lower in patients with active AOSD compared with healthy controls (mean± SEM; 650.7± 59.0 pg/ml vs.1129.7± 98.7 pg/ ml; p< 0.001). Plasma (or serum) sRAGE levels were lower in patients with active AOSD compared with inactive AOSD (mean± SEM; 985.3± 106.9 pg/ ml; p < 0.05). Similarly, plasma (or serum) AGEs levels were higher and sRAGE levels were lower in patients with active SLE compared with inactive SLE or healthy control. Plasma (or serum) AGEs levels were also positively correlated with activity markers of AOSD including a activity score (r =0.836 ; p < 0.001)、ferritin ( r =0.372;p <0.05)、ESR(r =0.413;p <0.005)、CRP( r =0.396;p <0.005).In conclusion our results suggested that AGEs and sRAGE could be useful markers for clinical physician to monitor disease activity of AOSD.
其他識別: U0005-0102201310405500
Appears in Collections:生命科學院

Show full item record

Google ScholarTM


Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.