Browsing by Author "Evert, Christine"

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    Calprotectin (S100A8/A9) as a marker of inflammation and treatment monitoring in cases of juvenile idiopathic arthritis in the Western Cape, South Africa
    (Stellenbosch : Stellenbosch University, 2023-03) Evert, Christine; Glashoff, Richard H. ; Abraham, Deepthi Raju; Stellenbosch University. Faculty of Science. Dept. of Microbiology.
    ENGLISH ABSTRACT: Background: Juvenile Idiopathic Arthritis (JIA) is a common rheumatic disease affecting children and is characterised by persistent inflammation of the joints. The socio-economic climate of South Africa can delay access to treatment to achieve remission. Joint inflammation is currently monitored through C-reactive protein (CRP) and erythrocyte sedimentation rate (ESR) measurements. Recent studies have shown that these markers may correlate less well with disease activity than calprotectin. Calprotectin is released by activated monocytes or macrophages at the site of joint damage and binds the TLR4 surface receptor. This protein has also been used to detect subclinical inflammation and may predict risk of relapse. This study aimed to compare standard markers of inflammation with calprotectin, and its relation to other inflammatory markers. Methodology: Blood samples were collected from 22 consented JIA participants. Clinical information and history for each participant was obtained from patient files at Tygerberg Hospital. Monocyte distribution and phenotypic marker expression was investigated using whole blood for surface marker flow cytometry. Plasma levels of calprotectin and JIA associated inflammatory markers (including CCL2, CCL11, CD163, CXCL9, CCL3, CCL22, CD25, CXCL10, IL-1β, MIF, IL12, TNF-α and IFN-γ) were assessed by means of ELISA and Luminex™ multiplex assays. Routine CRP and ESR results were collected from the NHLS TrakCare database. For longitudinal follow up, blood samples were collected from the same cohort 6 months later and assays were repeated. A study database was created with all participant results, at both visits, to investigate relationships between calprotectin and JIA disease activity, as well as the effect of treatment over time. Results: The majority (95%) of participants were already undergoing treatment. Calprotectin was within the normal range for children (127 – 1395 ng/mL) in 86% of baseline samples with a median of 628.6 ng/mL (IQR: 406.2 - 979.8). Only ESR changed significantly (p=0.0079) over time and showed the most evidence for changes in inflammation thereby inspiring analysis by stratification. To evaluate impact of disease phenotype (active vs. remission) and inflammatory state based on ESR expression (high vs. low ESR), participants were stratified into respective groups and compared. Expression of intermediate monocytes at baseline was higher than the expected range (2 - 10 %), with a median of 27 % (IQR: 9 - 43). This distribution is characteristic of inflammatory diseases. Calprotectin correlated significantly (p<0.05) with CRP and ESR at baseline in the returning, remission and high ESR analysis groups. Several notable cases displaying high calprotectin expression were linked to a relapse in disease. Conclusions: Despite limitations, this study confirmed the predictive value of calprotectin in risk of disease relapse and the need for such a marker in the clinical setting to allow for a more tailored approach to treatment. The relationship between intermediate monocyte expansion, calprotectin and disease phenotype also needs to be examined further. Future studies which include treatment naïve participants would be beneficial in assessing the usefulness of calprotectin in monitoring response to treatment.