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Impact of Hemolysis on UCH-L1 Quantification in Serum and Plasma.
СтатьяНазвание и аннотация: Перевод в очереди
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Martín Paula García, Rodríguez Silvia Álvarez, Macarro Covadonga Solar, Obaya Rafael Venta, Martínez-Morillo Eduardo
Аннотация
INTRODUCTION: Ubiquitin carboxy-terminal hydrolase L1 (UCH-L1) is a neuron-enriched deubiquitinase widely used for the evaluation of mild traumatic brain injury (TBI). Although minimal hemolysis-related interference has been reported for the Abbott TBI assay, routine laboratory observations indicate that hemolysis may substantially influence UCH-L1 measurements. This study aimed to evaluate the effect of hemolysis on UCH-L1 concentrations in plasma and serum samples and its potential clinical implications.
METHODS: Hemolysis interference was evaluated in accordance with CLSI C56-A and EP07 guidelines using pooled plasma samples and paired individual patient samples. Controlled hemolysis was induced by adding graded amounts of erythrocyte hemolysate to non-hemolyzed samples. UCH-L1 concentrations were measured using the Abbott Alinity i system. In addition, a retrospective analysis of routine TBI biomarker requests was conducted to estimate the potential rate of hemolysis-induced false-positive results.
RESULTS: In pooled plasma, UCH-L1 increased linearly (R2 = 0.992) with the hemolysis index (HI), with a 10% analytical bias observed at HI values of 100 or lower. Erythrocyte-derived samples showed UCH-L1-related signals more than 20-fold higher than plasma. In individual patient samples, hemolysis induced a dose-dependent but highly variable positive bias. Retrospective analysis suggested that hemolysis could result in false-positive UCH-L1 results in up to 21.5% of TBI-negative patients with concentrations near the clinical cut-off.
CONCLUSIONS: Hemolysis induces a clinically relevant positive bias in UCH-L1 measurements, even at moderate HI levels. These findings underscore the importance of strict preanalytical control and cautious interpretation of UCH-L1 results obtained from hemolyzed samples.
METHODS: Hemolysis interference was evaluated in accordance with CLSI C56-A and EP07 guidelines using pooled plasma samples and paired individual patient samples. Controlled hemolysis was induced by adding graded amounts of erythrocyte hemolysate to non-hemolyzed samples. UCH-L1 concentrations were measured using the Abbott Alinity i system. In addition, a retrospective analysis of routine TBI biomarker requests was conducted to estimate the potential rate of hemolysis-induced false-positive results.
RESULTS: In pooled plasma, UCH-L1 increased linearly (R2 = 0.992) with the hemolysis index (HI), with a 10% analytical bias observed at HI values of 100 or lower. Erythrocyte-derived samples showed UCH-L1-related signals more than 20-fold higher than plasma. In individual patient samples, hemolysis induced a dose-dependent but highly variable positive bias. Retrospective analysis suggested that hemolysis could result in false-positive UCH-L1 results in up to 21.5% of TBI-negative patients with concentrations near the clinical cut-off.
CONCLUSIONS: Hemolysis induces a clinically relevant positive bias in UCH-L1 measurements, even at moderate HI levels. These findings underscore the importance of strict preanalytical control and cautious interpretation of UCH-L1 results obtained from hemolyzed samples.