C-reactive protein Part II

C-reactive protein (CRP) values can be increased for multiple reasons. A major increase in CRP values is seen with infections (e.g. Bacterial, viral, fungal, or parastic infection), hypersensitive complications of infections (e.g. Rheumatic fever), acquired and inherited inflammatory diseases (e.g. Rheumatoid arthritis, Ankylosing spondylitis), tissue necrosis (e.g. Myocardial infection, Tumor embolization), trauma ( e.g. burns, surgery), neoplasia ( e.g.carcinoma, sarcoma), and also moderate increase in systemic lupus erthematousus, scleroderma, and graft vs.- host disease.

However the relation between CRP values and cardiovascular diseases (CVD) is the major area of focus, reason being the high prevalence of this disease in the developed and developing countries alike.

If you consider the number of studies coming out of the literature trying to link the high CRP levels and the occurrence of cardiovascular events, the relations seems to grow stronger.

Possible hypothesis for occurrence of CVD:
CRP is regulated by interleukin -6 (IL6), interleukin 1, tumor necrosis factor alpha, and other cytokines. CRP is thought to stimulate tissue factor production and activate complement when aggregated. Tissue factor may be the main stimulus to initiating coagulation, which could be crucial in CVD development. Also its shown that CRP binds to low density lipoprotein, which in turn activates complement, tissue factor production by macrophages leading to coagulation.

Another hypothesis based on findings, that an infection, possibly a bacterial or a viral (e.g. Helicobacter pylori, Chlamydia pneumoniae, Herpes simplex virus and cytomegalovirus) might contribute to atherosclerosis. Having known that CRP levels are increased in bacterial and viral infections this is quite possible.

A third theory suggests that CRP is a pro coagulant, increases opsonization and artherogenesis. CRP not only correlates with the increase in the other inflammatory markers but also is know to bind selectively to low and very low density lipoprotein (LDL and VLDL), found in the atheromatous plaque. CRP is also known to be deposited in these plaques, and along with its range of pro-inflammatory properties it could potentially contribute to the pathogenesis, progression and complications of atheroma. Data suggest that CRP is involved in foam cell formation by mediating the LDL uptake by the macrophages, and also its known presence in the plaques with pro inflammatory properties, may play a role in destabilizing the plaque.

During myocardial infraction (MI) the tissue necrosis occurring is a stimulus for CRP response. The CRP is deposited in and around infract not only reflects the extent of myocardial necrosis but also contributes significantly to the severity of ischaemic myocardial injury.

The higher CRP levels are been strongly associated with increased body mass index and metabolic syndrome. Adipocytes are the source of substantial portion of baseline IL6 production. Weight loss leads to reduction in baseline CRP concentration. CRP production predicts the development of type 2 diabetes independently of traditional risk factors. Low-insulin response diets may decrease plasma CRP by influencing adipocyte function. The elevated CRP levels may provide an additional marker for risk of progression to type 1 diabetes. Oral contraceptive use and systemic hormone replacement therapy are associated with significantly raised baseline CRP levels. Other associations with elevated baseline CRP values include periodontal disease, smoking, consumption of coffee, and stress.

With this little knowledge of CRP it would be certainly interesting to see the relation between CRP, periodontal disease and other systemic diseases, and that is what you would read in the third and final part.

References for Part I and II:
3) Saran de Ferranti, Nadir Rifai, C-reactive protein and cardiovascular disease: a review of risk prediction and interventions. Clinical Chimica Acta 2000; 317: 1-15
4) G.M. Hirschfield and M.B. Pepys, C-reactive protein and cardiovascular disease: new insights from an old molecule. Q J Med 2003; 96: 793 – 807.

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