False-negative immunoassay results for cardiac troponin I probably due to circulating troponin I autoantibodies

Bohner, J; Pape, K W von; Hannes, Waltraud; Stegmann, T

doi:10.1093/clinchem/42.12.2046

Cited by 66 publications

(19 citation statements)

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“…In 1996, Bohner et al suspected the presence of such a complex in a patient after elective coronary artery bypass graft surgery. The patient had undetectable cTnI despite increased concentrations of creatine kinase isoenzyme MB (CK-MB) and cTnT (4 ). The authors added increasing amounts of cTnI to the sample, up to 38.5 g/L, and found that cTnI continued to be undetectable.…”

Section: And Clinical Findingsmentioning

confidence: 99%

Persistent Increase of Cardiac Troponin I in Plasma without Evidence of Cardiac Injury

Legendre-Bazydlo¹,

Haverstick²,

Kennedy

et al. 2010

Clinical Chemistry

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CASEA 69-year-old man with diabetes mellitus type II, hypertension, dyslipidemia, and prior ischemic strokes presented to the emergency department with complaints of balance difficulties and inability to stand unassisted of 2 weeks' duration. The patient's home medication regimen included atenolol, lisinopril, amlodipine, metformin, and glipizide. He is a retired chef and a former smoker (20 pack-years). He has 2 brothers, both of whom had myocardial infarctions in their 50s. The patient's physical examination was remarkable for frequent premature contractions, left lower extremity weakness, and impaired coordination. His electrocardiogram revealed sinus rhythm with frequent premature ventricular contractions and diffuse nonspecific T-wave abnormalities.Results of a comprehensive metabolic chemistry panel were within the reference intervals except for increases in glucose (158 mg/dL; reference interval, 74 -99 mg/dL) and creatinine (1.5 mg/dL; reference interval, 0.7-1.3 mg/dL). The hemoglobin A 1c value was 7.4% (reference interval, Ͻ6.0%). Cardiac troponin I (cTnI) 3 concentrations were increased at 0.27, 0.22, and 0.25 g/L (Abbott Architect assay; 99th percentile, Ͻ0.03 g/L) over a span of approximately 8 h. The patient was admitted to the cardiology service on the basis of these abnormal results.A transthoracic echocardiogram revealed a preserved left ventricular systolic function with evidence of impaired diastolic filling. A cardiac catheterization evaluation revealed an ulcerated plaque in the left anterior descending artery with Ͼ70% stenosis, which was treated with a bare-metal stent. The presenting symptom of balance difficulty failed to resolve after the coronary intervention, and the patient remained unable to stand unassisted. A neurologic evaluation included magnetic resonance imaging, which found no evidence of an acute stroke. He was discharged with a diagnosis of orthostatic hypotension.Three months later, the patient presented to the emergency department with several days of balance difficulty. The initial cTnI value was increased at 0.10 g/L, prompting admission to the cardiology service. Over the subsequent 12 h, cTnI values for 2 additional samples remained stable at 0.10 g/L. Other laboratory tests included a comprehensive metabolic panel and a complete blood count, with results within reference intervals except for a hemoglobin concentration of 12.5 g/dL (reference interval, 14.0 -18.0 g/dL) and a hematocrit of 35.5% (reference interval, 40.0%-52.0%). The patient's symptoms were not consistent with a cardiac etiology, and no further cardiac evaluation was pursued. A neurologic evaluation again found no evidence of acute stroke, and his symptoms were believed to reflect a combination of orthostatic hypotension, pontine gliosis, and cerebellar atrophy. The unexplained abnormal troponin results prompted the attending cardiologist to contact the director of clinical chemistry. DISCUSSIONCardiac troponins play a central role in diagnosis and risk stratification in acute coronary syndromes (1 ),...

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Section: And Clinical Findingsmentioning

confidence: 99%

Persistent Increase of Cardiac Troponin I in Plasma without Evidence of Cardiac Injury

Legendre-Bazydlo¹,

Haverstick²,

Kennedy

et al. 2010

Clinical Chemistry

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“…The immunogenic epitopes of cTnI have not been investigated in patients with MI. However, Bohner et al have proposed that ATIA interfere with some cTnI assays by reacting with midfragment epitopes (aa30-110) of cTnI [41]. This was supported by subsequent work, which found that cTnI recovery was unaffected by antibodies in assays utilizing the N-and C-terminal epitopes of cTnI [42,43].…”

Section: Anti-troponin Antibodiesmentioning

confidence: 99%

Anti-troponin antibodies following myocardial infarction

O’Donohoe

Ketheesan

Schrale

2017

Journal of Cardiology

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Recent improvements in medical and surgical coronary revascularization techniques have significantly improved outcomes for patients with acute myocardial infarction (MI). However, large infarctions are often followed by a poorly understood process of pathological ventricular remodelling, which fails to return the heart to its premorbid state. Although it remains incompletely understood, there is increasing interest in the role of the immune system in this process. One hypothesis is that released cardiac proteins become the focus of an immune response that results in the formation of functionally significant autoantibodies. This review summarizes the current literature, both human and animal, relating to the formation and clinical relevance of anti-troponin antibodies (ATAs) in patients with MI.

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“…IgG autoantibodies against cTnI have been known for many years. Interestingly one of the first reports was of a negative interference [28]. It appears that the autoantibodies are directed against cTnI but only when it is in the circulating cTnI-cTnC-cTnT (I-T-C) complex [29].…”

Section: Accepted Manuscriptmentioning

confidence: 99%

The investigation of interferences in immunoassay

Ward

Simpson

Boscato³

et al. 2017

Clinical Biochemistry

118

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Immunoassay procedures have a wide application in clinical medicine and as such are used throughout clinical biochemistry laboratories both for urgent and routine testing. Clinicians and laboratory personnel are often presented with immunoassay results which are inconsistent with clinical findings. Without a high index of suspicion interferences will often not be suspected. Artifactual results can be due to a range of interferences in immunoassays which can include cross reacting substances, heterophile antibodies, autoantibodies and the high dose hook effect. Further, pre-analytical aspects and certain disease states can influence the potential for interference in immunoassays. Practical solutions for investigation of artifactual results in the setting of the routine clinical laboratory are provided.

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False-negative immunoassay results for cardiac troponin I probably due to circulating troponin I autoantibodies

Cited by 66 publications

References 0 publications

Persistent Increase of Cardiac Troponin I in Plasma without Evidence of Cardiac Injury

Persistent Increase of Cardiac Troponin I in Plasma without Evidence of Cardiac Injury

Anti-troponin antibodies following myocardial infarction

The investigation of interferences in immunoassay

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