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[Biochemistry](https://durgical.com/en/biochemistry/) · Topic

# C-reactive protein (CRP) as a lab test

CRP is a liver protein that rises within hours with inflammation or infection; it does not say where the problem is.

Updated 2026-11-01

## Key facts

- A pentameric acute-phase protein made by the liver, mainly under interleukin 6.
- It binds phosphocholine on bacteria and damaged cells and activates complement (classical pathway): it aids opsonisation.
- It rises in 6–8 hours, peaks at about 48 h and falls quickly (half-life about 19 h) once the stimulus ends: better than ESR for following progress.
- It is non-specific: bacterial infection, trauma, surgery, infarction, autoimmune disease and cancer raise it.
- High-sensitivity CRP measures low values and has been used as a cardiovascular risk marker; cut-offs depend on the laboratory.

## In detail

- What it measures: serum CRP concentration by immunoassay.
- Where it comes from: hepatocytes raise its synthesis hundreds of times under IL-6, IL-1 and TNF-α during the acute-phase response.
- Why it rises: bacterial infections (more than viral ones, in general), sepsis, pneumonia, complicated appendicitis, pancreatitis, active rheumatoid arthritis, vasculitis, active Crohn disease, trauma, burns, recent surgery.
- Pitfalls: in active lupus CRP usually rises little unless there is infection or serositis; severe liver failure and some biologics (anti-IL-6) block its rise; obesity and smoking raise baseline levels.
- It belongs to the acute-phase response with fibrinogen, ferritin and serum amyloid A (positive) and albumin and transferrin (negative).

**Also called**
CRP, High-sensitivity CRP, hs-CRP, Acute-phase reactants

## Clinical notes

- A normal CRP does not exclude infection in the first hours; a CRP falling on treatment supports a good response.
- Ferritin rises as an acute-phase reactant: with a high CRP, a normal ferritin does not exclude iron deficiency.
- In acute pancreatitis a very high CRP at 48 hours is linked to greater severity.

## Related conditions

- [Sepsis and septic shock](https://durgical.com/en/conditions/sepsis-and-septic-shock/)
- [Community-acquired pneumonia](https://durgical.com/en/conditions/community-acquired-pneumonia/)
- [Rheumatoid arthritis](https://durgical.com/en/conditions/rheumatoid-arthritis/)
- [Acute appendicitis](https://durgical.com/en/conditions/acute-appendicitis/)
- [Atherosclerosis and dyslipidaemia](https://durgical.com/en/conditions/atherosclerosis-and-dyslipidaemia/)

## Related

- [Serum albumin as a lab test](https://durgical.com/en/biochemistry/topics/serum-albumin-as-a-lab-test/)
- [Iron metabolism](https://durgical.com/en/biochemistry/topics/iron-metabolism/)
- [Eicosanoids: prostaglandins, thromboxanes and leukotrienes](https://durgical.com/en/biochemistry/topics/eicosanoids-prostaglandins-thromboxanes-and-leukotrienes/)

## Test yourself

Think of the answer, then tap the question to see it.

## Which cytokine mainly drives hepatic CRP synthesis?

Interleukin 6, together with IL-1 and TNF-α.

## Why is CRP better than ESR for following an infection?

It rises and falls within hours (half-life about 19 h), while ESR changes slowly over days or weeks.

## What does CRP do in immune defence?

It binds phosphocholine on microbes and damaged cells and activates complement by the classical pathway, helping phagocytosis.

## Why does a normal ferritin not rule out iron deficiency when CRP is high?

Ferritin is also an acute-phase reactant: inflammation raises it and can hide the lack of iron.

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Educational information, not medical advice. For any symptom, see a health professional.

Sources: [C-Reactive Protein (CRP) Test: MedlinePlus Medical Test](https://medlineplus.gov/lab-tests/c-reactive-protein-crp-test/) (MedlinePlus, US National Library of Medicine, 2026); [C-reactive protein: MedlinePlus Medical Encyclopedia](https://medlineplus.gov/ency/article/003356.htm) (MedlinePlus, US National Library of Medicine, 2026); Textbook of Biochemistry for Medical Students, 6th ed. (Jaypee Brothers Medical Publishers (Vasudevan DM, Sreekumari S, Vaidyanathan K), 2011).

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