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Acces RA1216 Driver

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Acces RA1216 Driver

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Advanced Search Abstract Objective. Pentosidine, an advanced glycation Acces RA1216 product AGEhas recently been observed to be elevated in rheumatoid arthritis RA. The aim was to 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 Acces RA1216 patients with OA.


In Acces RA1216 RA and OA patients combined, there was a significant correlation between pentosidine in serum, synovial fluid and urine. Acces RA1216 in serum and synovial fluid was significantly higher in RA than in OA. In RA, Acces RA1216 were significant correlations between pentosidine in serum and synovial fluid and C-reactive protein, Lansbury index LI and erythrocyte sedimentation rate. 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 Acces RA1216 number of advanced glycation end products AGEs [ 1 ].

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Its significant elevation was observed in tissues in diabetes Acces RA1216 [ 2 ], in uraemic patients with Acces RA1216 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 Acces RA1216. There is now considerable evidence for the involvement of oxygen-centred free radicals in acute and chronic inflammatory arthritis [ 8Acces RA1216 ].

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The role of free radicals in the autoxidation of biological lipids is well established [ 10 ]. Acces RA1216 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 Acces RA1216 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 Acces RA1216 relationship to RA has not been investigated until recently.

Now, there have been several studies which provide evidence that pentosidine is elevated in Acces RA1216 with RA. Pentosidine in serum and urine is elevated, and reflects the disease activity of Acces RA1216 [ 13 ]. Pentosidine in synovial fluid is higher in RA than in osteoarthritis OAand its level also reflects the Acces RA1216 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 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 Acces RA1216 or creatinine Acces RA1216 excluded from the study. Blood, synovial fluid and urine were collected on the same day from all RA and OA patients.

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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 Acces RA1216 accordance with the principles of Acces RA1216 Declaration of Helsinki inas revised in

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