Ho K M, Lipman J
Department of Intensive Care, Royal Perth Hospital, Perth, Western Australia, Australia.
Anaesth Intensive Care. 2009 Mar;37(2):234-41. doi: 10.1177/0310057X0903700217.
This review aims to summarise the physiology of C-reactive protein (CRP), its possible roles and limitations as an inflammatory and infective marker in intensive care medicine, and also the emerging roles of CRP in the pathogenesis of cardiovascular and autoimmune diseases. Observational and animal studies on uses of CRP were retrieved from the PubMed database without any language restrictions. Quantitative data were not pooled because of the heterogeneity of patient characteristics and disparate ways in which CRP was studied. Serum CRP concentrations are determined by the synthetic rate of its production in the liver regulated predominantly by interleukin-6. It has a half-life of 19 hours and is relatively slow in its onset and offset in response to an acute inflammatory process when compared to procalcitonin. It has some favourable properties and limitations as an inflammatory marker An elevated CRP concentration is not specific to infections and the absolute CRP concentrations cannot be used to differentiate between bacterial, fungal and severe viral infections. The dynamic response of CRP to therapy that aims to modify the underlying inflammatory process and the clinical context of a patient are of pivotal importance when CRP concentrations are interpreted. CRP is found to be a significant partaker and prognostic factor in a wide range of cardiovascular and chronic diseases. In summary, CRP concentration is an important prognostic factor of many acute and chronic diseases. Serial CRP measurements may be useful to reflect a patient's response to therapy that aims to modify the underlying inflammatory process.
