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Introduction: This study aimed to examine the recovery of spiked human cardiac troponin I (cTnI) results measured by four routine assays, and investigate possible interference from microclots. Materials and methods: 457 consecutive samples with cTnI concentration below limit of quantitation (12 ng/L), declared by the Vitros TnI ES assay (reference assay), were measured on Beckman Coulter Accu TnI+3, Siemens TnI-Ultra and Roche TnI STAT assays. These samples were enriched with native full-length cTnI to a concentration of 100 ng/L and retested. A post-spiking result that exceeded the critical difference at a predefined probability of 0.0005 of the target concentration (the median post-spiking result for each individual assay) was considered as outlier. To determine whether microclots were a significant cause of critically discrepant outlier results, a separate 50 samples were centrifuged twice between two postspiking measurements using the Vitros TnI ES assay. Results: The median recovery of the enriched cTnI was highest with the Roche assay (271 ng/L) and lowest with the Vitros assay (29 ng/L). The Vitros assay had the highest percentage of results that exceeded the critical difference (49%), followed by the Siemens (38%), Roche (18%) and Beckman Coulter (7%) assays. None of the 50 additional samples produced a critically lower cTnI result after re-centrifugation. Conclusions: Our findings underscored the variability of cTnI assays in measuring native cTnI. The lack of cTnI results that became significantly lower after re-centrifugation suggested that microclots are unlikely to be a major cause of the outlier results. [ABSTRACT FROM AUTHOR]

Primarily perceived as an anti-inflammatory and antimicrobial mediator in mucosa and skin, interleukin-22 (IL-22) has emerged as a pivotal metabolic regulator. Central to IL-22 signaling is its receptor, IL-22RA1. Through IL-22RA1, IL-22 orchestrates glucose homeostasis by modulating insulin secretion, reducing cellular stress in pancreatic islets, promoting beta-cell regeneration, and influencing hepatic glucose and lipid metabolism. These actions suggest its potential as a therapeutic for metabolic dysfunctions like diabetes, obesity, and steatohepatitis. However, clinical applications of IL-22 face challenges related to off-target effects and safety concerns. This review explores IL-22's physiological roles, regulatory mechanisms, and profound influence on metabolic tissues. It also underscores IL-22's dual role in metabolic health and disease, advocating further research to harness its therapeutic potential., Competing Interests: Declaration of interests S.Z.H, M.A.M., and J.B.P. are inventors on patents relating to IL-22 use in metabolic disease. Patents: (i) Modulation of cellular stress. AU2015268101B2. The University of Queensland. McGuckin, M.A., Prins, J., Hasnain, S.Z. Granted 2021. (ii) Modulation of cellular stress using a B-cell oxidative and/or endoplasmic reticulum stress inhibitor and a targeting agent. US10695406B2. The University of Queensland. McGuckin, M.A., Prins, J., Hasnain, S.Z. Granted 2020. (iii) Method of treating a metabolic disorder of the liver. US20200353048A1. The University of Queensland. McGuckin, M.A., Prins, J., Hasnain, S.Z. Filed/published 2020, pending decision. (iv) Method of treating fibrosis. US63/384149. Provisional patent, filed February 2023., (Copyright © 2024 The Author(s). Published by Elsevier Ltd.. All rights reserved.)