No announcement yet.

High sensitivity C-reactive protein

  • Filter
  • Time
  • Show
Clear All
new posts

  • #16
    The levels of CRP we are talking about are low (in the rheumatology world) somewheres between 0.05 and 0.99. The authors devided these into quartiles and those with the higherest quartiles had the the highest CV events. Keep in mind that the "normal" for CRP is about 1.0 in most assays. This is measured in mg/gL. hsCRP is now being reported in mg/L and that spreads the numbers out, but still we are not talking high grade inflammation.
    Now as to what lowers these already low CRPs: Aspirin, Statins both do. So even for the lowish LDL patient with high CRP: statin and ASA.
    The FDA has not evaluated my safety or efficacy...


    • #17
      How much asprin?


      • #18
        Primary prevention?
        Secondary prevention/treatment?
        ASA risk/benefit analysis?
        EBCT plus CRP in 30 year old?

        Its all too early to tell but everyone is calling today. They all also think that every pain is related to statins, Crestor will kill everyone. ASA is not necessarily benign given potential for GI bleeding (+ alcohol + NSAIDs+GERD(which all fat patients have)).

        I see more and more tools being offered that increase the potential patient pool for treatment but little work on nonpharm treatments, NNT numbers and rational treatment guidelines.


        • #19
          This week's NEJM has data from the PROVEIT study published by Ridker and colleagues that shows clearly that LDL reduction and CRP reduction with statins were both independently associated with better outcomes, with the best outcomes in those who's CRP fell below 2 and LDL below 70 mg/dl. This suggests that we should now be looking at dual targets in patietn with CAD

          Fahim Jafary


          • #20
            I think 81mg is fine. I don't remember how much better the drop with 325. Ridker is the guru in this area.
            The FDA has not evaluated my safety or efficacy...


            • #21

              You indicate that these are very low level CRPs considered normal in the rhematologic world. Do you know if there is a gradual rise in the CRP as people age? Obviously humans develop more illnesses beside CAD as they age, perhaps that is the reason for the relative increase. Inflammation seems to be a rather common response to multiple insults. I really wonder how specific it is to the illness of atherosclerosis.


              • #22
                Interesting question. These initial studies were done on frozen sera from earlier cohort studies. Using the outcome data from the cohort, the looked at whether the CRP level from 10 years ago was predictive and compared it to the LDL et cetera. They didn't follow levels over time. I don't think anybody has done that.
                There is some thought that low grade inflammation/infection such as gingivitis leads to low grade elevations in CRP and that's how you get CAD (remember the Chalymdia fad about chronic infection and CAD).
                C-RP is able to bind to C1q of the complement system and when stimulated it can lead to activation of complement and endothelial damage. It binds to phospholipids on bacterial and fungal cell walls, but may also bind some altered lipids in CAD. So it may not be just a marker, but also an effector of damage.
                It is under fairly tight synthetic control in the liver (via IL-6) and its levels flutuate based on that, so I don't know what role age plays.
                I don't know if that directly answers your question.

                BTW, celebrex lowers CRP levels! (Chenevard, Circulation 2003;107:r15-19)
                The FDA has not evaluated my safety or efficacy...


                • #23
                  It seems to me that the cardiologists are so focused on "their" system that they fail to take into account the many things that assail the aging body. I remember those concerns about gingivitis (not yet resovled?), chlamydia, chlamydia in aortic aneurysms. For awhile because generally women have less CAD prior to menopause and their in vitro studies suggested cardioprotection they pushed estrogen in spite of prior studies which suggested concern. Maybe there is just more drug and procedural money there. A strange turn since the rate of CAD and CAD morbidity has declined despite an aging population, and one with increasing girth and poor health habits to boot.

                  Scroggie thank you for your reply.


                  • #24
                    LOL. Finally a website I like -

                    The International Network of Cholesterol Skeptics


                    • #25
                      CRP is a marker for inflammation.
                      Healing is a type of inflammation.
                      Lets say you have intima damaged by atheroma.
                      The RESPONSE to the damage may well involve a measurable increase in mediators of inflammation (eg. CRP).

                      The correlation of hsCRP and ischemic events may represent CRP being a marker for intimal damage rather than (one of) its causes.

                      Thus the recent NEJM article.. C-Reactive Protein Levels and Outcomes after Statin Therapy..Jan 6 2005.. (
                      might be interpreted as follows.
                      The article showed that everyone had some lowering of LDL from statin therapy but the only those folks that also has a concommitent lowering of CRP actually had a lower risk of clinical endpoints.
                      Sounds to me like not everyone whose LDL went down actually had a healthier intima
                      as a result.
                      However those that DID end up with a healthier intimae, demonstated that fact by having lower CRP levels (less need for healing when the intima is healthier) and of course, fewer ischemic events.