N-acetylcysteine interference of Trinder-based assays
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Updated: Mar 31, 2026

Preparation and In Vivo Use of an Activity-based Probe for N-acylethanolamine Acid Amidase
Published on: November 23, 2016
Jonathan R Genzen1, Joshua J Hunsaker2, Louis S Nelson3
1ARUP Institute for Clinical and Experimental Pathology, Salt Lake City, UT, 500 Chipeta Way, Salt Lake City, UT 84108, USA; Department of Pathology, University of Utah, Salt lake City, UT, 500 Chipeta Way, Salt Lake City, UT 84108, USA.
Objectives:
The primary objective of this study was to evaluate potential interference of Trinder-based chemistry assays by N-acetylcysteine (NAC). A secondary objective was to look for evidence of interference in patients treated with NAC for acetaminophen (APAP) overdose.
Design And Methods:
Dilutions of NAC in plasma were tested for interference using the following Roche Diagnostics Trinder-based assays on a cobas 8000 system: enzymatic creatinine (Cr), cholesterol (CHOL), high-density lipoprotein cholesterol (HDL-C), triglycerides (TRIG), and uric acid (UA). Two non-Trinder Roche assays - urea nitrogen (BUN) and glucose (GLUC) - were tested as controls. Sekisui N-geneous® low-density lipoprotein cholesterol (LDL-C) reagent was also evaluated. Retrospective chart review of APAP overdose cases over 49months was conducted to look for differences in plasma Cr before and after intravenous (IV) NAC administration.
Results:
NAC concentrations (shown in parentheses) that caused ≥10% inhibition for individual assays were (in order of sensitivity to interference): TRIG (570mg/L)>CHOL (740mg/L)≈Cr (790mg/L)>UA (1100mg/L)>HDL-C (1760mg/L)>LDL-C (2900mg/L). Neither BUN nor GLUC achieved significant inhibition up to 10,000mg/L NAC. Evidence for relatively minor inhibition of Cr was observed in patients after NAC administration.
Conclusions:
NAC inhibition of the assays investigated typically occurs at concentrations higher than expected during IV and oral NAC therapy.
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