“Stay in till tomorrow to recheck the CRP. If it goes down to less than 100 he goes home.”
“It’s day 2 post op. The CRP is 167 from 67 the day before. Is that normal or do we look for a possible infection?”
“Giant cell arteritis? Use ESR, CRP is useless.”
I decided to read up on the CRP, focusing on bits that would help make sense of the clinical situations above.
1. The half life of CRP is 18-19 hours.
“Stay in till tomorrow to recheck the CRP. If it goes down to less than 100 he goes home.”
This half life is remarkably constant no matter what else is going on, be it renal failure, liver failure, sepsis, polypharmacy etc. This means that the plasma level of CRP is dependent on how much was made and when. It is only dependent on factors affecting its production, not its elimination.
Once the insult is removed, CRP should drop toward baseline. It should be normal within two or three days (which corresponds to 3-4 half lives i.e. 7/8th or 15/16th eliminated).
The CRP can therefore lag behind the clinical picture. If the patient is clinically well and has an identifiable insult that has recovered in the last 48 hours, you do not necessarily need to wait for the CRP to come down to ‘prove’ the patient has recovered.
2. CRP levels usually peaks at about 48 hours after the insult.
“It’s day 2 post op. The CRP is 167 from 67 the day before. Is that normal or do we look for a possible infection?”
CRP production does not happen instantly at the time of the insult; it is delayed by at least 2 hours, and really kicks in at around 6 hours. This means that the CRP would normally rise between day 1 and day 2 post op for example.
3. The CRP goes up with most causes of inflammation.
“Giant cell arteritis? Use ESR, CRP is useless”
CRP is made pretty much exclusively by the liver as part of the acute phase response. The acute phase response includes a protein synthesis strategy change by the liver following activation of the innate immune system by something nasty – an infection, autoimmune disease, burns, trauma or maybe a neoplasm. A raised CRP is very sensitive for ‘some inflammation somewhere’ but very unhelpful for determining the aetiology.
The most famous exception is SLE, where CRP often stays normal whilst the disease flares. Interestingly, the SLE patient still mounts a CRP rise in response to infection. This means that measuring CRP during a suspected flare can help distinguish between an autoimmune flare or an infection.
A normal ESR is seen in 8-22.5% of cases of giant cell arteritis. In contrast, an elevated CRP is thought to be near 100% sensitive for the condition. You can have an elevated CRP with a normal ESR in GCA. However, it is ESR rather than CRP that is used in the diagnostic criteria for GCA.