The acute-phase response includes a wide variety of mediators, such as C-reactive protein (CRP), IL-6, and many others, and is known to have diverse effects. Metabolic pathways and coagulation are also affected by the acute-phase response. These acute-phase proteins have an important role, which has not yet been elucidated completely, in the body’s response to infection and injury.19–
On the other hand, statins significantly decrease CRP production.20–
The implications of such a reduction are not completely clear. Septic shock is a consequence of a maladaptive deregulated immune response. It follows that the attenuation of this exaggerated response, as reflected by the acute-phase reactants, could contribute to the restoration of homeostasis. By analogy, in a case-control analysis from the Physicians’ Health Study, 21–
higher CRP levels predicted future cardiovascular events in healthy middle-aged men, and aspirin reduced events more in those persons with higher, rather than lower, levels of this inflammatory marker. In a more recent retrospective analysis of data from the Air Force/Texas Coronary Atherosclerosis Prevention Study,22
lovastatin therapy prevented the occurrence of coronary events in participants with high-normal CRP values whose baseline levels of low-density lipoprotein (LDL) cholesterol were < 149.1 mg/dL. However, in participants whose levels of both CRP and LDL were below the median levels of the population, statin therapy did not significantly reduce the risk of coronary events. These findings implicate inflammation, reflected by elevated CRP levels, as an important contributor to atherosclerosis. We suggest a similar mechanism whereby statin therapy may create a nonfavorable milieu for the development of systemic inflammatory response by virtue of its ability to blunt the acute-phase response.