Juvenile idiopathic arthritis (JIA) is the most common occurring paediatric chronic rheumatic disease, defined as arthritis of unknown origin that starts before the age of 16.1 Systemic juvenile idiopathic arthritis (sJIA) on the other hand is the paediatric form of Still’s disease, a systemic autoinflammatory disease characterised by prominent symptoms of systemic inflammation such as spiking fever. Adult form of Still’s is called adult-onset Still’s disease (AOSD).1-3 The neutrophilic protein calprotectin has been described as valuable biomarker in several rheumatic conditions, including rheumatoid arthritis (RA)4-7 and JIA,8,9 where the highest levels have been reported in sJIA,8 as well as AOSD.10
Calprotectin serum and plasma levels are strongly correlated with the degree of inflammation,8,9,11 hence it can provide important assessment of disease activity, treatment response and relapse. Rheumatic patients are often treated with a wide range of medications, some of which indirectly lower downstream levels of C-reactive protein (CRP). Calprotectin can therefore be a useful biomarker when CRP is normal or difficult to interpret, reported in RA patients treated with therapies that suppress interleukin-6 (IL-6) or tumour necrosis factor (TNF),12-15 as well as methotrexate (MTX).16
In patient management of JIA, circulating calprotectin has proven great value in assessment and prediction of treatment response, remission and flares.
High calprotectin concentrations at baseline has been shown as good predictor of positive response to several treatment forms (biological DMARDs (Disease-modifying antirheumatic drugs), MTX, anti-TNF),11,17-19 and notably the patient groups do not differ in regards to any other clinical or laboratory parameters.11,17 After the discontinuation of treatment and in stable clinically inactive remission, low levels of calprotectin were associated with decreased risk of subsequent flares.18,20,21
In a long-term follow up study of MTX treated JIA patients in a routine clinical setting, clinicians reported that calprotectin was ordered for assessment and guidance of medication. Low calprotectin levels were interpreted favourably for stopping, notably no patients with a low calprotectin result flared within 12 months. In clinical routine, high calprotectin levels can therefore guide decision towards the continuation of treatment even in clinical inactive disease.22
The innate immune system plays a pivotal role in Still’s pathogenesis and immunocytes are heavily activated, including neutrophils. As neutrophil activation marker, plasma and serum calprotectin has been implicated in diagnosis, prediction of relapse, and evaluation of disease activity in both paediatric and adult Still's disease.1-3
Diagnosis of sJIA and AOSD is heavily depended on exclusion due to the non-specificity of clinical presentation. Differentiating from other inflammatory conditions, infections and fever of unknown origin (FUO) is particularly challenging, where calprotectin can allow the crucial early differentiation. Circulating calprotectin has been shown to differentiate sJIA of FUO more effectively than CRP,23-25 as well as distinguishing both sJIA and AOSD from other rheumatic diseases.8,10,26-28
In patient monitoring, calprotectin has been described as a predictive biomarker for relapse in sJIA, surpassing the performance of erythrocytes sedimentation rate (ESR) and CRP.29 Furthermore, it correlates with treatment response in both sJIA23,29 and AOSD,26 providing clinicians with the ability to track the progression of the disease.
Gentian’s calprotectin immunoassay GCAL® is the first turbidimetric assay for the quantitative measurement of calprotectin in plasma and serum intended as an aid in the detection and assessment of inflammation and inflammatory response to infection.
The assay can be applied on a wide range of automated clinical chemistry analysers. GCAL® is CE-marked and IVDR certified. It is not cleared for use in the USA (Research Use Only).
For more details on GCAL® products and prices please contact us at email@example.com
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