CRP was 1st described in 1930 by Tillet and Francis.
C-reactive protein plays a key role in the host's defence against infection by activating the complement system and acts as an opsonin for bacterial sequences and nuclear material which has been expressed from a cell during apoptosis, and thus enhances phagocytosis thereby helping to fight infections as well as protect against auto-immune disease.
It was so named because it reacts with the C-polysaccharide of Streptococcus pneumoniae.
C-reactive protein elevation is part of the acute-phase response to acute and chronic inflammation.
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the ESR reflects concentrations of fibrinogen and alpha-globulins. It is influenced by immunoglobulins that are not acute-phase proteins. These proteins all have half-lives of days to weeks, and there is a significant lag time between changes at the clinical level and variations in the ESR. This, plus the influence of various other factors on the ESR such as diurnal variation, anaemia, food intake and red cell morphology, makes it an imprecise guide to disease activity in most cases.
however, ESR remains helpful in certain clinical situations such as the detection of paraproteinaemias, which often do not elicit an acute phase response.
raised CRP is 90% sensitive for presence of significant inflammation (but does take some 12 hours to go up)
a raised CRP has sensitivity of around 75% and specificity of around 67% for sepsis but this depends on the cutoff used and the clinical setting
viral infections generally cause a mild or no rise in CRP, but some viruses will cause a high CRP such as the hepatitis viruses
burn injury causes a high CRP
various non-infective inflammatory conditions cause a high CRP such as
Crohn's disease activation of sympathetic nervous system may cause a raised CRP such as major trauma, severe haemorrhage, and this response appears to be able to be blocked by
beta adrenergic blockers procalcitonin generally has a higher sensitivity and specificity for sepsis (and in paediatrics as well as with
Covid-19 better differentiates viral vs bacterial infection), rising earlier than CRP and levels correlate with degree of severity and respond to treatment success (and a fall of 25% over 5 day period is a predictive survival indicator for septic shock patients), and is more predictive of late mortality from sepsis
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is predominantly made in the liver and is secreted in increased amounts within six hours of an acute inflammatory stimulus - primarily stimulated by IL-6, but response is enhanced by IL1-B and TNF-a.
The plasma concentration can double at least every eight hours, reaching a peak after about 50 hours. After effective treatment or removal of the inflammatory stimulus, concentrations can fall almost as rapidly as the 5-7 hour plasma half-life of labelled exogenous C-reactive protein.
C-reactive protein responses may be reduced by severe hepatocellular impairment, but renal dysfunction can elevate concentrations of C-reactive protein.
baseline concentrations for a normal individual is in part genetically determined.