By reducing inflammatory activity in rheumatoid arthritis, tumor necrosis factor α (TNFα) inhibitors likely decrease, rather than increase, the risk of heart failure, according to an article published in the March issue of Arthritis & Rheumatism.
Joachim Listing, Ph.D., of the German Rheumatism Research Centre in Berlin, Germany, and colleagues investigated the effect of TNFα inhibitors on the incidence or worsening of heart failure by comparing data from 2,757 rheumatoid arthritis patients treated with infliximab, etanercept or adalimumab, and 1,491 rheumatoid arthritis patients treated with conventional disease-modifying antirheumatic drugs enrolled in a German biologics register.
The three-year incidence rate of heart failure was 2.2 percent in patients with pre-existing cardiovascular disease and 0.4 percent in those without a history of cardiovascular disease. After controlling for traditional cardiovascular risk factors, higher 28-joint Disease Activity Scores at follow-up were associated with an increased risk of developing heart failure (hazard ratio 1.47). TNFα inhibitors were associated with a non-significant elevated risk of heart failure, but this risk was balanced by the efficacy of anti-TNF treatments.
"The findings of this study indicate that TNFα inhibitor treatment that effectively reduces the inflammatory activity of rheumatoid arthritis is more likely to be beneficial than harmful with regard to the risk of heart failure, especially if there is no concomitant therapy with glucocorticoids or cyclooxygenase 2 inhibitors," the authors conclude.
One co-author disclosed financial ties to pharmaceutical companies.
Abstract
http://www3.interscience.wiley.com/cgi-bin/abstract/117926534/ABSTRACT
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Prepared jointly by the editors of RN and HealthDay's Physicians' Briefing (www.physiciansbriefing.com).
would it be plausable to say that any dmrd that reduced inflamation
for a person whithout steroids reduces the risk of heart failiure..
studies on mtx show the same findings .. reading your article it would appeare
heart failiure may be expected
quote.... more likely to be beneficial than harmful with regard to the risk of heart failure,
Boney
CRP is a member of the class of acute phase reactants as its levels rise dramatically during inflammatory processes occurring in the body. This increment is due to a rise in the plasma concentration of IL-6, which is produced predominantly by macrophages[1] as well as adipocytes.[2] CRP binds to phosphorylcholine on microbes. It is thought to assist in complement binding to foreign and damaged cells and enhances phagocytosis by macrophages, which express a receptor for CRP. It is also believed to play an important role in innate immunity, as an early defense system against infections.
CRP rises up to 50,000 fold in acute inflammation, such as infection. It rises above normal limits within 6 hours, and peaks at 48 hours. Its half-life is constant, and therefore its level is mainly determined by the rate of production (and hence the severity of the precipitating cause). Serum amyloid A is a related acute phase marker that responds rapidly in similar circumstances.[1]
CRP is used mainly as a marker of inflammation. Apart from liver failure, there are few known factors that interfere with CRP production.[1]
Measuring and charting C-reactive protein values can prove useful in determining disease progress or the effectiveness of treatments. Blood, usually collected in a serum-separating tube, is analysed in a medical laboratory or at the point of testing.
Various analytical methods are available for CRP determination, such as ELISA, immunoturbidimetry, rapid immunodiffusion and visual agglutination.
Viral infections tend to give a lower CRP level than bacterial infection.
Arterial damage is thought to result from inflammation due to chemical insults. CRP is a general marker for inflammation and infection, so it can be used as a very rough proxy for heart disease risk. Since many things can cause elevated CRP, this is not a very specific prognostic indicator. A level above 2.4 mg/l reflects a doubled risk of a coronary event compared to levels below 1 mg/l.[1]
CRP may have sugars—sialic acid, glucose, galactose and mannose—attached to it (i.e. it gets glycosylated.) In different disease states, one or two amino-acids get lopped off CRP. It retains its activity, but these losses open it up to glycosylation. Different diseases (each of which raise CRP) will add sugars to it in different patterns. The patterns are different across diseases, but similar amongst patients who had the same disease. A 2003 study looked at patients with lupus, leukemia, tuberculosis, leishmaniasis, Cushing's syndrome and bone cancer. (Healthy subjects did not have enough CRP to successfully characterize "normal" CRP.)
Previous work had shown that CRP increased the rate at which a particular parasite could invade blood cells. The study showed that the different CRPs had very different potencies in this regard. The authors speculate that subtyping CRP may give us more insight into heart attack mechanisms. Although this did not demonstrate whether this glycation of CRP was a 'good thing' or a 'bad thing', it offered circumstantial evidence that the differing glycation is part of CRPs mode-of-action.[5]
Recent research suggests that patients with elevated basal levels of CRP are at an increased risk for diabetes,[6][7] hypertension and cardiovascular disease. A study of over 700 nurses showed that those in the highest quartile of trans fat consumption had blood levels of C-reactive protein (CRP, a pro-inflammatory cytokine which is a cardiovascular disease risk factor) that were 73% higher than those in the lowest quartile.[8] Although one group of researchers indicated that CRP may only be a moderate risk factor for cardiovascular disease,[9] this study (known as the Reykjavik Study) was found to have some problems for this type of analysis related to the characteristics of the population studied, and there was an extremely long follow-up time which may have attenuated the association between CRP and future outcomes.[10] Others have shown that CRP can exacerbate ischemic necrosis in a complement-dependent fashion and that CRP inhibition can be a safe and effective therapy for myocardial and cerebral infarcts; so far, this has only been demonstrated in animal models.[11]
To measure the CRP level, a "high-sensitivity" CRP or hs-CRP test needs to be performed and analyzed by a laboratory. This is an automated blood test designed for greater accuracy in measuring low levels of CRP, which allows the physician to assess cardiovascular risk. If a result in the low-risk range is found ( < 1 mg/L), it does not need repeating. Higher levels need repeating, and clinical evaluation as necessary.
The role of inflammation in cancer is not well known. Some organs of the body show greater risk of cancer when they are chronically inflamed.
Blood samples of persons with colon cancer have an average CRP concentration of 2.69 milligrams per liter. Persons without colon cancer average 1.97 milligrams per liter. The difference was statistically significant.[12] These findings concur with previous studies that indicate that anti-inflammatory drugs could lower colon cancer risk.[