Abstract 11581: False Positive Troponin Elevation Due to Heterophile Antibody

Abstract

Introduction: While highly specific, false positive Troponin I (TnI) can be caused by heterophile antibodies, autoimmune phenomena, and fibrin interference. The overreliance on TnI levels can lead to unnecessary patient work-up. Here we present a case of chronically elevated troponin over several hospitalizations most consistent with viral heterophile antibody cross reactivity. Case: A 71-year-old man with diabetes and polio-related paraplegia was admitted for pharyngitis. Initial TnI assay was significantly elevated at >90 (normal < 0.04 ng/mL) with a CK-MB of 21.7 (normal <20.0 U/L). ECG showed no evidence of ischemia (Figure 1). He had similar TnI elevation on two prior hospitalizations, with no significant coronary artery disease on angiography. Despite the absence of chest pain and normal ECG and TTE, myocardial perfusion stress test was performed due to the elevation in CK-MB, which was negative for ischemia (Figure 2). Troponin T, a sendout lab, was <12 ng/L. Patient was later confirmed to have positive CMV IgG and positive EBV viral capsid and nuclear antigen IgG, supporting the mechanism of heterophile antibody cross reactivity as the mechanism for false positive troponin. Discussion: Our case demonstrates a growing literature of patients presenting with chronically elevated TnI unrelated to myocyte damage. Focus of troponin levels without consideration of overall clinical picture and previous medical history can lead to unnecessarily invasive and expensive testing. For this patient, elevated troponin led to unnecessary testing and prolonged hospital admissions despite consistently negative cardiac workup. Heterophile cross reactivity can lead to false positive TnI in 1:2000 patients. If elevated troponin is concerning for a false positive, evaluation through other markers should be considered before undergoing more invasive procedures.