Calprotectin in diagnosis and monitoring of treatment response in RA

28. May 2020 | 4 min read

Calprotectin in diagnosis and monitoring of treatment response in RA

Calprotectin in rheumatoid arthritis (RA)

Calprotectin, a biomarker for neutrophil activation, has been shown to have clinical diagnostic and prognostic value in rheumatoid arthritis (RA), including the potential to monitor treatment response. During inflammation, neutrophils migrate to the inflammatory site and secrete large amounts of calprotectin which act as a soluble proinflammatory mediator [1].

Calprotectin is released locally at inflammation sites, including inflamed synovium, and enters the systemic circulation where it can be measured. Since calprotectin is released predominantly from locally activated leukocytes at the sites of joint inflammation, it directly reflects joint inflammatory activity [2].


The ability to monitor disease activity and relapse in RA

Since the concentration of calprotectin reflects the degree of inflammation, it can provide valuable monitoring of disease activity, treatment response and relapse. Circulating calprotectin is elevated in active disease and decreases after effective treatment and has been shown to be a more sensitive biomarker of disease activity in RA than conventionally used acute-phase proteins [3]. Calprotectin can be more effective than erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP) to gauge disease activity, as it has been demonstrated that more than 40% of RA patients have normal ESR or CRP [4-6]. In these patients, calprotectin can potentially be a useful inflammatory marker.

Calprotectin may also be used to more accurately predict relapse in patients in remission or with low disease activity receiving biological drugs, which potentially would guide therapeutic decisions towards safer and more cost-effective treatment strategies [7].



Monitoring treatment response whilst using TNF-alpha, IL-1 and IL-6 and other bDMARDs

RA patients are often treated with a wide range of medication. It is important to realise that some medication which moderates TNF-alpha, interleukin IL-1 or IL-6 might, in addition to a reduction of the inflammatory activity, also lower the circulating cytokines. Which further activates the acute phase proteins. Calprotectin can therefore represent a useful biomarker when for example CRP is normal or difficult to interpret, such as in patients treated with therapies that suppress IL-6 [8] . Calprotectin, however, is not influenced by these medications, and will only reflect the leucocyte activation during inflammation [9].

Calprotectin has also been seen to have the highest agreement with ultrasound synovitis and anticipated treatment response. Hence, it could be considered as a marker for assessing inflammation and responsiveness in patients with RA on bDMARD treatment [10]. Moreover, calprotectin may more accurately segregate the disease activity in RA patients receiving TNF-alpha treatment than other acute phase reactants, even in patients with low inflammatory activity [11].


Gentian's Calprotectin (GCAL®) Immunoassay in RA

GCAL® is an inflammation marker which can have the ability to diagnose and monitor disease activity, treatment response and relapse in RA. Since GCAL® is a novel Particle-Enhanced Turbidimetric Immunoassay (PETIA), the assay is rapidly performed in only 10 minutes. The GCAL® immunoassay can be applied on a wide range of automated clinical chemistry analysers. The GCAL® immunoassay is developed and manufactured by Gentian.

Contact us

For more details on Gentian Calprotectin Immunoassay products and prices please contact us at or fill out the form below:


Calprotectin for RA



  1. Ometto et al. (2017), Experimental Biology and Medicine; 242: 859–873
  2. Johne B et al. (1997) Mol Pathol. 1997; 50(3):113-23
  3. Andrés et al. Arthritis Res Ther. 2011;13:R122
  4. Pincus T, Sokka T (2009) Rheum Dis Clin N Am 35(4):731–734
  5. Sokka T, Pincus T (2009) J Rheumatol 36(7):1387–1390
  6. Pincus et al. (2014) Clin Exp Rheumatol 32(5 Suppl 85):S-23-28
  7. Inciarte-Mundo et al. (2018) Arthritis research and therapy 20:275
  8. Jarlborg et al. al. (2020) Arthritis Research & Therapy 22:105
  9. Berner Hammer et al. (2007) Ann Rheum Dis 2007; 66:1093-1097
  10. Nordal et al. Arthritis Research & Therapy (2017) 19:3
  11. Inciarte-Mundo et al. Arthritis Research & Therapy (2016) 18:160

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