Increased pentosidine, an advanced glycation end product, in serum and synovial fluid from patients with knee osteoarthritis and its relation with cartilage oligomeric matrix protein

. 2005 Jun ; 64 (6) : 886-90.

Jazyk angličtina Země Spojené státy americké Médium print

Typ dokumentu časopisecké články, práce podpořená grantem

Perzistentní odkaz   https://www.medvik.cz/link/pmid15897309
Odkazy

PubMed 15897309
PubMed Central PMC1755507
DOI 10.1136/ard.2004.029140
PII: S0003-4967(24)42979-8
Knihovny.cz E-zdroje

BACKGROUND: Pentosidine, an advanced glycation end product, increasingly accumulates in articular cartilage with age, and contributes to the pathogenesis of osteoarthritis (OA). Increased pentosidine concentrations are associated with inflammatory disorders-for example, rheumatoid arthritis. OBJECTIVE: To compare pentosidine serum concentrations in patients with knee OA and in healthy volunteers and to determine a relationship between pentosidine and cartilage oligomeric matrix protein (COMP)-a marker of articular cartilage destruction. METHODS: Paired serum and synovial fluid samples were obtained by arthrocentesis from 38 patients with knee OA and from 38 healthy volunteers. Pentosidine concentration was measured by reverse phase high performance liquid chromatography with fluorescent detection and COMP was determined by sandwich ELISA. RESULTS: Significantly increased serum pentosidine (p<0.01) and COMP (p<0.05) levels were detected in the patients with OA compared with the control group. Serum pentosidine correlated significantly with synovial fluid pentosidine (p<0.001). Pentosidine in synovial fluid (p<0.05) and in serum (p<0.05) correlated significantly with synovial fluid COMP. Pentosidine and COMP concentrations did not correlate significantly with the radiological stage of the disease. CONCLUSION: Increased pentosidine serum concentration in patients with OA and its correlation with the cartilage destruction marker COMP in synovial fluid suggests that pentosidine may be important in OA pathology and is a new potential OA marker.

Zobrazit více v PubMed

Br J Rheumatol. 1998 Jul;37(7):721-8 PubMed

J Am Soc Nephrol. 1998 Sep;9(9):1681-8 PubMed

J Rheumatol. 1998 Dec;25(12):2440-4 PubMed

Arthritis Rheum. 1999 May;42(5):1003-9 PubMed

Rheumatology (Oxford). 1999 Dec;38(12):1275-8 PubMed

Biochem J. 2000 Sep 1;350 Pt 2:381-7 PubMed

Osteoarthritis Cartilage. 2000 Sep;8(5):335-42 PubMed

Rheum Dis Clin North Am. 2000 Aug;26(3):547-67 PubMed

J Orthop Res. 2001 Jan;19(1):33-42 PubMed

Arthritis Rheum. 2001 Nov;44(11):2562-71 PubMed

Osteoarthritis Cartilage. 2002 Jan;10(1):1-4 PubMed

Arthritis Rheum. 2002 Jan;46(1):114-23 PubMed

Cell Mol Life Sci. 2002 Jan;59(1):5-18 PubMed

Osteoarthritis Cartilage. 2002 Sep;10(9):707-13 PubMed

Rheumatology (Oxford). 2002 Sep;41(9):996-1000 PubMed

Clin Chim Acta. 2003 Feb;328(1-2):59-69 PubMed

Aging Clin Exp Res. 2003 Oct;15(5):364-72 PubMed

Ann Rheum Dis. 2004 Feb;63(2):200-5 PubMed

Osteoarthritis Cartilage. 2004 Apr;12(4):277-83 PubMed

Arthritis Rheum. 2004 Apr;50(4):1207-15 PubMed

Arthritis Rheum. 1986 Aug;29(8):1039-49 PubMed

J Biol Chem. 1989 Dec 25;264(36):21597-602 PubMed

Br J Rheumatol. 1992 Sep;31(9):583-91 PubMed

Arthritis Rheum. 1994 May;37(5):724-8 PubMed

Br J Rheumatol. 1995 Apr;34(4):306-10 PubMed

Osteoarthritis Cartilage. 1995 Sep;3 Suppl A:3-70 PubMed

Nephrol Dial Transplant. 1996;11 Suppl 5:27-30 PubMed

Arthritis Rheum. 1997 Apr;40(4):723-7 PubMed

Br J Rheumatol. 1997 Nov;36(11):1151-60 PubMed

Biochem Biophys Res Commun. 1998 Mar 6;244(1):45-9 PubMed

Arthritis Rheum. 1998 May;41(5):778-99 PubMed

Najít záznam

Citační ukazatele

Nahrávání dat ...

Možnosti archivace

Nahrávání dat ...