CRP and COVID-19

Coronavirus (SARS-CoV-2) seems to increase C-reactive protein (CRP) levels significantly, due to inflammatory reaction and related tissue destruction was also seen in the SARS epidemic in 2002.

  • CRP concentrations on average 30–50 mg/L1-3
  • Higher concentrations indicate more severe disease - linked to lung damage and worse prognosis.3-5
  • Concentrations respond to the disease course: Is the patient getting better or worse?3-5

Practical use of CRP in COVID-19

  • IFCC guidance: One of the markers to evaluate the severity of infection, prognostics, and therapeutic monitoring
  • Chinese guideline: CRP test together with other clinical parameters for initial evaluation and follow-up of coronavirus infection. Cut-off for CRP: 40–50 mg/L

Why CRP increases in COVID-19

One possible explanation for this phenomenon is the overproduction of inflammatory cytokines. Cytokines fight against the pathogen but when the system hyperactivates, it can damage lung tissue. CRP production is induced by cytokines – and by tissue destruction.6-8

Additionally, secondary (also bacterial) infections have been reported in severe cases9.

CRP supports the clinical picture

  • CRP is non-specific marker of infection, inflammation and tissue injury.10.
  • Concentration tells about the severity of the illness11.
  • Peaks in 48 hours from the disease onset2 → Consider time when symptom started
  • Half-life is 19 hours12-13 → Concentration decreases when patient’s inflammatory stimulus ends, and patient is healing.

CRP products

The portable QuikRead go® instrument and easy-to-use QuikRead go CRP tests enable flexible and fast quantitative CRP measurement in various healthcare settings.

Read more on the product pages


  1. Chen et al. 2020. Lancet 2020; 395:P507-513.
  2. Mo et al. 2020. doi: 10.1093/cid/ciaa270.
  3. Gao et al. 2020 doi: 10.1002/jmv.25770.
  4. Wang et al. doi: 10.1093/cid/ciaa272.
  5. Deng et al. 2020. doi: 10.1097/CM9.0000000000000824
  6. Gabay C, Kushner I. Acute-phase proteins and other systemic responses to inflammation. N Engl J Med 1999; 340(6): 448-454.
  7. Vasileva & Badawi. C-reactive protein as a biomarker of severe H1N1 influenza. Inflamm Res 2019; 68:39-46.
  8. Huang et al. An interferon‐γ‐related cytokine storm in SARS patients. J Med Virol 2005; 75:185-194.
  9. Zhou et al. Clinical course and risk factors for mortality of adult inpatients with COVID-19 in Wuhan, China: a retrospective cohort study. Lancet 2020;395(10229):1054-1062
  10. Gabay C, Kushner I. N Engl J Med 1999; 340(6): 448-454.
  11. Shine B, de Beer FC, Pepys MB. Clin Chim Acta 1981; 117(1): 13-23.
  12. Pepys MB, Hirschfield GM. J Clin Invest 2003; 111(12): 1805-1812.
  13. Vigushin DM, Pepys MB, Hawkins PN. J Clin Invest 1993; 91(4): 1351-1357