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ACCES RA1216 DRIVER
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Pentosidine, an advanced glycation end product AGEhas recently been observed to be elevated in rheumatoid arthritis RA. The aim was Acces RA1216 elucidate which pentosidine levels, i.
We measured levels of pentosidine in serum, synovial fluid or urine in RA compared with osteoarthritis OAand examined the relationship between pentosidine Acces RA1216 RA disease activity. Subjects were 20 patients with RA and 22 patients with OA.
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In total RA and OA patients combined, there was a significant correlation between pentosidine in serum, synovial fluid and urine. Pentosidine in serum and synovial fluid was significantly higher in RA than in OA. In RA, there were significant correlations between pentosidine in serum and synovial fluid and C-reactive protein, Lansbury index LI and erythrocyte sedimentation Acces RA1216. These results demonstrate that pentosidine levels in body fluids correlated with each other, and pentosidine in serum and in synovial fluid is associated with the systemic inflammatory activity of RA. Higher or similar concentrations of pentosidine in serum compared with synovial fluids indicate that the elevated pentosidine levels in serum in RA are not derived from the synovial fluid, but from an increase in the formation of pentosidine in the whole body in RA.
Among body fluids, serum pentosidine was the superior indicator for RA disease status. Rheumatoid arthritisOsteoarthritisPentosidineOxygen radicals Pentosidine is one of a number of advanced glycation end products AGEs [ 1 ]. Its significant elevation was observed in Acces RA1216 in diabetes mellitus [ 2 ], in uraemic patients with end-stage renal failure [ 2 — 4 ], and in accelerated aging [ 5 — 7 ]. Pentosidine is formed by sequential glycosylation and oxidation reactions. Therefore, it is hypothesized that pentosidine formation is accelerated in diseases related to oxidative stress. Rheumatoid arthritis RA is a chronic systemic disease, although its major clinical consequence is inflammation of the joints and contiguous structures.
There is now considerable evidence for the involvement of oxygen-centred free radicals in acute and chronic inflammatory arthritis [ 89 ]. The role of free radicals in the autoxidation of biological lipids is well established [ 10 ]. Patients with RA have depressed serum levels of the antioxidant, and a low antioxidant level is a risk factor for RA [ 11 ]. Because oxidative stress and oxygen free radicals play a significant role in tissue damage and inflammation in RA, pentosidine is supposed to be implicated in this disease [ 12 — 15 ]. Several years ago, pentosidine was reported to be elevated in the articular cartilage of RA [ 12 ].
However, its significant relationship to RA has not been investigated until recently. Now, there have been several studies which provide evidence that pentosidine is elevated in patients with Acces RA1216. Pentosidine in serum and urine is elevated, and reflects the disease activity of RA [ 13 ].
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Pentosidine in synovial fluid is higher Acces RA1216 RA than in osteoarthritis OAand its level also reflects the disease activity of RA [ 16 ]. Although all pentosidine levels in body fluids have been associated with RA disease activity, it has not been clear which pentosidine levels, i. In the present study, therefore, we investigated pentosidine levels in serum, synovial fluid and urine in OA and RA. OA of the knee joints was diagnosed on the basis of clinical symptoms, examination and radiographic findings.
Acces RA1216 There was no significant difference in age between RA and OA patients. Patients who had diabetes mellitus, steroid users and those with abnormal levels of serum blood urea nitrogen BUN or creatinine were excluded from the study. Blood, synovial fluid and urine were collected on the same day from all RA and OA patients. After collection, blood samples were centrifuged at r. Synovial fluid was obtained by knee aspiration.
Informed consent was obtained from all participants. The procedures followed were in accordance with the principles Acces RA1216 the Declaration of Helsinki inas revised in A Lansbury index LI was determined based on the duration of morning stiffness, ESR value at 1 hgrip strength mmHg and joint score [ 1819 ]. Urinary creatinine content was measured by a routine laboratory method. Measurements of pentosidine in serum, synovial fluid and urine The pre-treatment of samples before injection into the HPLC column was described previously [ 1316 ].
Pentosidine was measured by a direct HPLC method with column switching as described previously [ 13 ]. The urine sample was injected directly into the HPLC column without acid hydrolysis.
Standard pentosidine was synthesized [ 20 ] and the concentration was calibrated with pentosidine, which was a gift from Dr V. Statistical analysis The statistical significance of difference was determined with non-parametric statistics using Mann—Whitney U-tests between two groups. Simple regression was performed for univariate correlation and the statistical significance of correlation was Acces RA1216 with the Spearman rank correlation test. In urine, pentosidine levels tended to be higher in RA than in OA, but not significantly so. In either RA or OA, pentosidine levels tended to be higher in serum than in synovial fluid, but there was no Acces RA1216 significant difference. The correlations of pentosidine levels between serum, synovial fluid and urine were examined in total patients of RA and OA.
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