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The effect of chemonucleolysis on serum keratan sulfate levels in humans

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TLDR
It is demonstrated that serum KS levels rise predictably after CN, in a manner that reflects major catabolic events of cartilage.
Abstract
Sensitive measurements of serum keratan sulfate (KS), a glycosaminoglycan found in large quantities in the proteoglycans of human cartilage, can be obtained using an enzyme-linked immunosorbent-inhibition assay. Patients who are undergoing chemonucleolysis (CN) provide a clinical opportunity to monitor the large-scale proteolytic degradation of cartilage. By measuring serum KS levels both pre- and post-CN, we have demonstrated that serum KS levels rise predictably after CN, in a manner that reflects major catabolic events of cartilage.

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Citations
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The health assessment questionnaire 1992. Status and review

TL;DR: A brief overview of the HAQ is presented along with a guide to the accumulated literature and a few comments regarding future directions for research are also presented.
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Cytokines in osteoarthritis: mediators or markers of joint destruction?

TL;DR: Experimental evidence is emerging that catabolic cytokines are mediators of joint damage in OA, although their usefulness as markers of disease activity is limited because of the need to monitor a wide range of ligands and their inhibitors simultaneously.
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Synovial fluid chondroitin and keratan sulphate epitopes, glycosaminoglycans, and hyaluronan in arthritic and normal knees

TL;DR: Changed concentrations of SF CS and KS can be detected in OA with a profile that differs from that seen in RA, supporting different pathogenesis within OA subgroups and requirement for careful patient characterisation in SF studies.
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Levels of circulating tumor necrosis factor alpha and interleukin-6 in patients with rheumatoid arthritis. Relationship to serum levels of hyaluronan and antigenic keratan sulfate.

TL;DR: In vivo data support in vitro studies which have shown that TNF alpha is a potent stimulator of HA synthesis by synovial lining cells and strengthen the contention that serum HA may be a unique marker ofsynovial involvement and inflammation, rather than of only inflammation, in RA.
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Markers of cartilage matrix metabolism in human joint fluid and serum: the effect of exercise*

TL;DR: In serum from runners before exercise the concentration of keratan sulfate was significantly higher than in both the soccer and reference groups and further increased after exercise, suggesting an effect of mechanical loading in combination with a possible high turnover rate of body cartilage matrix in these individuals.
References
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Journal ArticleDOI

Identification of a monoclonal antibody that specifically recognizes corneal and skeletal keratan sulfate. Monoclonal antibodies to cartilage proteoglycan

TL;DR: The 1/20/5-D-4 monoclonal antibody appears to recognize a common determinant in their polysaccharide moieties, consistent with several biochemical analyses showing the absence of keratan sulfate in proteoglycan synthesised by this tissue.
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Plasma clearance, tissue distribution and metabolism of hyaluronic acid injected intravenously in the rabbit

TL;DR: It is concluded that hyaluronic acid is removed from the plasma and degraded quickly by an efficient extrarenal system with a high reserve capacity, sited mainly in the liver.
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Quantification of keratan sulfate in blood as a marker of cartilage catabolism.

TL;DR: If the appearance of elevated levels of serumKS do indeed correlate with the extent of cartilage erosion or destruction in individuals with OA, measurements of serum KS levels will prove extremely useful in the assessment and diagnosis of this joint disease.
Journal ArticleDOI

Circulating hyaluronate in rheumatoid arthritis: relationship to inflammatory activity and the effect of corticosteroid therapy.

TL;DR: The data obtained suggested an increased production of hyaluronate in rheumatoid arthritis, and the increase seems to be related to the activity of the inflammatory process.
Journal ArticleDOI

The glycosaminoglycans of human plasma

TL;DR: The hypothesis has been advanced that as a result of the action of tissue proteases, part of the "bound" G AG may be transformed into "free" GAG, the latter being immediately extruded from the tissues into the circulatory system.
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