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Anaesth Intensive Care 2009; 37: 234-241

An update on C-reactive protein for intensivists
K. M. Ho*, J. LIPMAN†
Department of Intensive Care, Royal Perth Hospital, Perth, Western Australia, Australia

SUMMARy 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, andalso 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 thesynthetic 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 CRPconcentrations 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 cardiovascularand 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.
Key Words: inflammatory markers, inflammatory response, infection, prognostic factor, predictor, outcomes

C-reactive protein (CRP) wasfirst discovered in 1930 when a protein in the serum of patients with Streptococcus pneumoniae was found to precipitate and bind to the C-polysaccharide derived from the pneumococcal cell wall1. It has been known for a long time that CRP is one of many non-specific acute phase reactants that are elevated during an inflammatory process. Because the CRP response to an inflammatory process isnon-specific, many clinicians have not adopted its use as a predictive and prognostic test in intensive care medicine. Furthermore, the role of CRP as a predictor of infection, instead of inflammation, has become even more controversial since the introduction of procalcitonin as a test in this regard. Comparing CRP with other inflammatory markers such as

*M.B., B.S., M.P.H., Ph.D., F.R.C.P.(Glasg),F.A.N.Z.C.A., F.J.F.I.C.M., Staff Specialist, Department of Intensive Care, Royal Perth Hospital and Clinical Associate Professor, School of Population Health, University of Western Australia. †M.D., F.J.F.I.C.M., F.F.A.(Critical Care), Professor and Head, Anaesthesiology and Critical Care, University of Queensland and Director, Department of Intensive Care Medicine, Royal Brisbane and Women’sHospital, Brisbane, Queensland. Address for reprints: Clinical Associate Professor K. M. Ho, Intensive Care Unit, Royal Perth Hospital, Perth, WA 6000. Accepted for publication on September 18, 2008.

procalcitonin can be difficult because of their different kinetics and many studies have looked at different types of patients2. The overall evidence suggests that procalcitonin has much faster kinetics,both in its onset and offset, and may also be more specific than the CRP in diagnosing some infections3-5. Because the CRP test is widely available and relatively cheap, it is likely to be widely used in many institutions in the foreseeable future. It is not the intention of this brief review to compare the advantages and disadvantages of CRP with the procalcitonin because this subject has been...