Aim of the Study
Acute-phase proteins are a class of proteins responsible for the increase and decrease of plasma concentration in the blood in response to inflammatory stimuli. One of the proteins under this class is the C-reactive protein or (CRP), which modifies the effect of invading pathogens (Boon and Davidson 77). The plasma levels of CRP are said to be autonomously related to the high risk of blockage of the coronary arteries, though it has been a question whether CRP is one of the causes or only an indicator of it.
Thus, the study aims to identify whether the plasma levels of C-reactive protein have any relation with the risk of coronary heart disease or merely a marker of the development of atherosclerosis (Elliott et al. 37). This experiment, focuses on whether there is a relationship between the danger of having a coronary ailment and the CPR levels through the genetic loci.
A genome-wide association (GWA) and replication study are done to identify which genetic loci are related to plasma CPR levels, while a mendelian randomization method is used to the most similarly related single-nucleotide polymorphism or (SNP) in the locus of the CRP. Published data is used on the rest of the CRP variants. This includes a total of 28,122 investigated cases on the association of CRP variants having coronary disease, in addition to the 100,823 controls. A meta-analysis of observed studies between CRP plasma levels and the danger of coronary heart disease is used as the predicted outcome. This is compared to the findings in order to determine whether there is a significant relationship between the two. The other loci related to CRP levels and with the most similar SNP are subjected to testing against cardiovascular disease. This includes 14,365 cases with 32,069 controls.
There is incongruity between the effect on the CRP plasma levels and the risk of coronary disease of CRP genotypes; thereby it is concluded that there is no causal relationship between CRP and coronary heart disease. The GWA study confirms the association of 5 genetic loci that are largely related to CRP levels. In the mendelian randomized study, there are significant relationships between CRP levels and CRP variants, and CRP levels and coronary heart disease. On the other hand, there is no significant relationship between CRP variants and coronary heart disease. This is because the predicted odd ratio (0.94) did not reach the estimated effect on coronary heart disease, with the odd ratio of 1.00.
This study proves that the C-reaction protein levels do not affect the risk of having coronary heart disease. Although increase in CRP levels is an indicator of inflammation, it is not the cause that increases the risk of coronary heart disease. This is in contrast to the belief that CRP may be a causative agent for the progress of atherosclerosis. Medical doctors and other health practitioners would use this information to prevent errors and misconceptions on patients’ results.
Furthermore, the study discourages scientists and researchers from involving themselves in studies revolving on the reduction of plasma levels of CRP as this would most likely become unfruitful.
On the other hand, it is known that through the investigation of genetic variants, there is now a means of determining loci susceptible to new kinds of diseases. During the study, two of these loci found to have potential susceptibility loci are LEPR and IL6R, which still need further studies to be confirmed. Through identifying new disease susceptibility loci, scientists may begin research on these loci to discover their possible effects, prevention of the diseases they may cause, and new therapeutic remedies.
Boon, Nicholas, and Stanley Davidson. Davidson’s Principles and Practice of Medicine. 20th ed. 2009. India: Elsevier Health Sciences. Print.
Elliott, Paul, et al. 2009, Genetic Loci Associated With C-Reactive Protein Levels and Risk of Coronary Heart Disease. PDF file. Web.