Editing C-reactive protein (section)

=== Fibrosis and inflammation ===

[[Scleroderma]], [[polymyositis]], and [[dermatomyositis]] elicit little or no CRP response.{{citation needed|date=June 2022}} CRP levels also tend to remain low despite inflammatory activity in [[systemic lupus erythematosus]] (SLE) unless [[serositis]] or [[synovitis]] is present. This may be explained by increased levels of type I IFN in SLE, since type I IFN (i.e IFN alpha) inhibits hepatic CRP production.<ref>{{cite journal | vauthors = Enocsson H, Karlsson J, Li HY, Wu Y, Kushner I, Wetterö J, Sjöwall C | title = The Complex Role of C-Reactive Protein in Systemic Lupus Erythematosus | journal = Journal of Clinical Medicine | volume = 10 | issue = 24 | pages = 5837 | date = December 2021 | pmid = 34945133 | pmc = 8708507 | doi = 10.3390/jcm10245837 | doi-access = free }}</ref> A polymorphisms of the CRP gene which cause lower CRP levels is also more frequent in SLE patients compared with controls.<ref>{{cite journal | vauthors = Enocsson H, Gullstrand B, Eloranta ML, Wetterö J, Leonard D, Rönnblom L, Bengtsson AA, Sjöwall C | title = C-Reactive Protein Levels in Systemic Lupus Erythematosus Are Modulated by the Interferon Gene Signature and CRP Gene Polymorphism rs1205 | journal = Frontiers in Immunology | volume = 11 | pages = 622326 | date = 2021-01-28 | pmid = 33584722 | pmc = 7876312 | doi = 10.3389/fimmu.2020.622326 | doi-access = free }}</ref><ref>{{cite journal | vauthors = Enocsson H, Sjöwall C, Kastbom A, Skogh T, Eloranta ML, Rönnblom L, Wetterö J | title = Association of serum C-reactive protein levels with lupus disease activity in the absence of measurable interferon-α and a C-reactive protein gene variant | journal = Arthritis & Rheumatology | volume = 66 | issue = 6 | pages = 1568–1573 | date = June 2014 | pmid = 24574329 | doi = 10.1002/art.38408 }}</ref> Elevations of CRP in the absence of clinically significant inflammation can occur in [[kidney failure]]. CRP level is an independent risk factor for atherosclerotic disease. Patients with high CRP concentrations are more likely to develop [[stroke]], [[myocardial infarction]], and severe [[Peripheral artery disease|peripheral vascular disease]].<ref name="Risk">{{cite journal | vauthors = Clearfield MB | title = C-reactive protein: a new risk assessment tool for cardiovascular disease | journal = The Journal of the American Osteopathic Association | volume = 105 | issue = 9 | pages = 409–416 | date = September 2005 | pmid = 16239491 | url = http://www.jaoa.org/content/105/9/409.full | access-date = 2013-02-10 | url-status = dead | archive-url = https://web.archive.org/web/20120110071000/http://www.jaoa.org/content/105/9/409.full | archive-date = 2012-01-10 }}</ref> Elevated level of CRP can also be observed in [[inflammatory bowel disease]] (IBD), including [[Crohn's disease]] and [[ulcerative colitis]].<ref name="pmid23689052">{{cite journal | vauthors = Liu S, Ren J, Xia Q, Wu X, Han G, Ren H, Yan D, Wang G, Gu G, Li J | title = Preliminary case-control study to evaluate diagnostic values of C-reactive protein and erythrocyte sedimentation rate in differentiating active Crohn's disease from intestinal lymphoma, intestinal tuberculosis and Behcet's syndrome | journal = The American Journal of the Medical Sciences | volume = 346 | issue = 6 | pages = 467–472 | date = December 2013 | pmid = 23689052 | doi = 10.1097/MAJ.0b013e3182959a18 | s2cid = 5173681 }}</ref><ref name="Vermeire 661–665">{{cite journal | vauthors = Vermeire S, Van Assche G, Rutgeerts P | title = C-reactive protein as a marker for inflammatory bowel disease | journal = Inflammatory Bowel Diseases | volume = 10 | issue = 5 | pages = 661–665 | date = September 2004 | pmid = 15472532 | doi = 10.1097/00054725-200409000-00026 | s2cid = 11984165 }}</ref>

High levels of CRP has been associated to point mutation Cys130Arg in the ''APOE'' gene, coding for [[apolipoprotein E]], establishing a link between [[lipid]] values and inflammatory markers modulation.<ref>{{cite journal | vauthors = Sidore C, Busonero F, Maschio A, Porcu E, Naitza S, Zoledziewska M, Mulas A, Pistis G, Steri M, Danjou F, Kwong A, Ortega Del Vecchyo VD, Chiang CW, Bragg-Gresham J, Pitzalis M, Nagaraja R, Tarrier B, Brennan C, Uzzau S, Fuchsberger C, Atzeni R, Reinier F, Berutti R, Huang J, Timpson NJ, Toniolo D, Gasparini P, Malerba G, Dedoussis G, Zeggini E, Soranzo N, Jones C, Lyons R, Angius A, Kang HM, Novembre J, Sanna S, Schlessinger D, Cucca F, Abecasis GR | title = Genome sequencing elucidates Sardinian genetic architecture and augments association analyses for lipid and blood inflammatory markers | journal = Nature Genetics | volume = 47 | issue = 11 | pages = 1272–1281 | date = November 2015 | pmid = 26366554 | pmc = 4627508 | doi = 10.1038/ng.3368 }}</ref>{{MEDRS|date=November 2019}}<ref name="Vermeire 661–665"/>