Medicine Ave 2 1 Although he’s handled wild stallions, he just can’t seem to tame his phosphorus levels iFO S R EN O L (lanthanum carbonate) Erosion in rheumatoid arthritis Then, once IL-1 and TN F -a are present, other interleukin* flL-6. IL-S, and IL-10) stimulate local fihrohtas? proliferation and recruit leukocytes. Although inflamed vynovul cells express T N F -a , it is seemed to a far lewer extent than IL-1.4,1 Earl)'in the RA disease process, IL-1 causes cartilage dcgradarioo by inducing rapid chondrocytes.114 Since IL -1 aho stimulates OKeocbsd) bone resorption occurs.1* Higher levels of IL-1 seen with bone erosion ----- ------------------ •Wm v___ The critical role of I L - 1 damage and bone resorption, and suggest that TNF-a is more responsible for the In animal studies, joint swelling anti cartilage damage arc still present in T\F-a knockout mice (which cannot produce TNF-a), while there is an impressive reduction of cartilage damage, bone erosion, and chronic synovial infiltration in IL-1-deficient mice.* These findings arc supported by clinical evidence that patients with RA who have bone erosions also hase higher IL-1 lock in their synovial fluid than RA paoents who do not have lione erosions. Together, these findings point to the primary n>lc of IL-1 in the bone and cartilage erosion seen in RAT The IL-1 gene family consists of IL-1 a, IH p. anti IL-1 receptor antagonist (IL-1 Ra), which is the naturally occurring cytokine antagonist that normally balances the destructive effects of IL -la and IL -lfl in rheumatoid arthritis1' However, in RA. production of IL-1 cannot he suffioendy countcrcd by endogenous IL-1 Ra alone; this leads to the damaging hone and cartilage cfleets seen in rheumatoid joints1-* Amgen is conducting research in the area of rheumatology to develop new and important therapies. jcs^xDJice<f'wirFll RA.J'>7 low of proteoglycans and odraubting L i , ; •hem nf,!,.™ rKdx60" ■ * ” ilitease?»rocrs«. Pto-iftflammatnry cjtiAines *utn*pfc6K monocytes, and lyot- ■stirm igr*iero the jnuowuth. In i .l^^j46rTtstol<j|pc-wo<iics of macrophages i f in Chesynovial tissue, IL -T hkilKen ded**f»t»wd in the Animal studies, predinical research, and ^ • c tf^ - p u to * junctipn a>well asm the early dinkal studies all support the •*^3 fe it.g role dut IL-1 ploy* in cartilage Advancing the science of rheumatology / OjhS c^A*.'usw*a* cwow-s*sitewrt*w»»«<*» v- « B«R«tt X. yvnm M.ounlrvS.MM * * rod t«wouf **<**■ \ Uttor w * yrmrvwetefd«rtvO»- ontaoget 1m. amf tpunmeet, mg: 218
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