Re: RESEARCH - Inhibition of antithrombin by hyaluronic acid may be involved in the pathogenesis of RA

[Guest guest]

So, if I read this correctly, it sounds like even if HA worked well

for people with OA, it would NOT be a good idea for people with RA.

Right?

>

> Research article

>

> Inhibition of antithrombin by hyaluronic acid may be involved in

the

> pathogenesis of rheumatoid arthritis

>

> Xiaotian Chang1 , Ryo Yamada1 and Kazuhiko Yamamoto1 ,2

> 1Laboratory for Rheumatic Diseases, SNP Research Center, The

Institute of

> Physical and Chemical Research (RIKEN), Kanagawa, Japan

> 2Department of Allergy and Rheumatology, Graduate School of

Medicine,

> University of Tokyo, Tokyo, Japan

>

> Arthritis Res Ther 2005, 7:R268-R273 doi:10.1186/ar1487

>

> The electronic version of this article is the complete one and can

be found

> online at: http://arthritis-research.com/content/7/2/R268

>

> Published 11 January 2005

>

>

> Thrombin is a key factor in the stimulation of fibrin deposition,

> angiogenesis, proinflammatory processes, and proliferation of

> fibroblast-like cells. Abnormalities in these processes are

primary features

> of rheumatoid arthritis (RA) in synovial tissues. Tissue

destruction in

> joints causes the accumulation of large quantities of free

hyaluronic acid

> (HA) in RA synovial fluid. The present study was conducted to

investigate

> the effects of HA and several other glycosaminoglycans on

antithrombin, a

> plasma inhibitor of thrombin. Various glycosaminoglycans,

including HA,

> chondroitin sulfate, keratan sulfate, heparin, and heparan, were

incubated

> with human antithrombin III in vitro. The residual activity of

antithrombin

> was determined using a thrombin-specific chromogenic assay. HA

> concentrations ranging from 250 to 1000 μg/ml significantly

blocked the

> ability of antithrombin to inhibit thrombin in the presence of

Ca2+ or Fe3+,

> and chondroitin A, B and C also reduced this ability under the same

> conditions but to a lesser extent. Our study suggests that the high

> concentration of free HA in RA synovium may block antithrombin

locally,

> thereby deregulating thrombin activity to drive the pathogenic

process of RA

> under physiological conditions. The study also helps to explain

why RA

> occurs and develops in joint tissue, because the inflamed RA

synovium is

> uniquely rich in free HA along with extracellular matrix

degeneration. Our

> findings are consistent with those of others regarding increased

coagulation

> activity in RA synovium.

>

>

> http://arthritis-research.com/content/7/2/R268

>

>

>

>

> Not an MD

>

> I'll tell you where to go!

>

> Mayo Clinic in Rochester

> http://www.mayoclinic.org/rochester

>

> s Hopkins Medicine

> http://www.hopkinsmedicine.org

>