This test may exhibit interference when sample is collected from a person who is consuming a supplement with a high dose of biotin (also termed as vitamin B7 or B8, vitamin H, or coenzyme R). It is recommended to ask all patients who may be indicated for this test about biotin supplementation. Patients should be cautioned to stop biotin consumption at least 72 hours prior to the collection of a sample.
1 - 3 days
Turnaround time is defined as the usual number of days from the date of pickup of a specimen for testing to when the result is released to the ordering provider. In some cases, additional time should be allowed for additional confirmatory or additional reflex tests. Testing schedules may vary.
For more information, please view the literature below.
Plasma (lithium-heparin), frozen
0.8 mL (Note: This volume does not allow for repeat testing.)
Green top (lithium-heparin) tube. Lithium heparin plasma tubes containing separating gel can be used.
Centrifuge and transfer separated heparin plasma to a plastic transport tube. To avoid delays in turnaround time when requesting multiple tests on frozen samples, please submit separate frozen specimens for each test requested.
24 hours (stability provided by manufacturer or literature reference)
12 months (stability provided by manufacturer or literature reference)
Stable x1 (stability provided by manufacturer or literature reference)
Sample other than lithium heparin plasma
Immunoassay for the in vitro quantitative determination of cardiac troponin T (cTnT) in lithium heparin plasma. The immunoassay is intended to aid in the diagnosis of myocardial infarction.
For diagnostic purposes, the results should always be assessed in conjunction with the patient’s medical history, clinical examination and other findings.
The Universal Definition of AMI takes into consideration the ESC/ACC/AHA/WHF definition recommending the detection of a rise and/or fall of cardiac troponin in the clinical setting with at least one value above the 99th percentile upper reference limit.1,2 Due to the release kinetics of cardiac troponin T, an initial test result may not be definitive in diagnosing MI. Serial cardiac troponin measurements are suggested.
Troponins are released during the process of myocyte necrosis. While they are cardiac-specific, they are not specific for MI, and detectable levels may be seen in other disease states that involve the heart muscle (e.g. arrhythmia, acute aortic syndrome, acute heart failure, hypertensive crisis, myocarditis, pericarditis, pulmonary embolism and Takotsubo cardiomyopathy), so that ACC/ESC/AHA guidelines and the Universal Definition of MI recommend serial sampling with a rise or fall in troponin to distinguish between acute and chronic cTn elevations.
A number of factors other than AMI are associated with elevated values.3-9 Published clinical studies have shown elevations of cardiac troponin T in patients with myocardial injury, as seen in stable or unstable angina, heart failure, myocarditis, pulmonary embolism, pericarditis, arrhythmias, cardiac contusions, and cardiac transplants. Elevations are also notable in patients with rhabdomyolysis and polymyositis.
Samples showing visible signs of hemolysis may cause interference. Falsely depressed results are obtained when using samples with hemoglobin concentrations > 0.1 g/dL.
For assays using antibodies, the possibility exists for interference by heterophileantibodies in the patient’s sample. Patients who have been regularly exposed to animals or have received immunotherapy or diagnostic procedures using immunoglobulin or immunoglobulin fragments may produce antibodies, e.g. HAMA, that interfere with immunoassays. Carefully evaluate the results of patients suspected ofhaving these antibodies.
In rare cases, interference due to extremely high titers of antibodies to analyte‐specificantibodies, streptavidin or ruthenium can occur. The reagent has been formulated to minimize this effect.
Samples should not be taken from patients receiving therapy with high biotin doses (i.e.> 5 mg/day) until at least 8 hours following the last biotin administration.
Electrochemiluminescence immunoassay (ECLIA)
Troponin T (TnT) is a component of the contractile apparatus of the striated musculature. Although the function of TnT is the same in all striated muscles, the cardiac isoform of TnT originating exclusively from the myocardium clearly differs from skeletal muscle TnT. As a result of its high tissue‐specificity, cardiac troponin T (cTnT) is a cardio‐specific, highly sensitive marker for myocardial damage. Cardiac troponin T increases rapidly10 after acute myocardial infarction (AMI) and may persist up to 2 weeks thereafter.11,12 In contrast to ST‐elevation myocardial infarction (STEMI), the diagnosis of non‐ST elevation myocardial infarction (NSTEMI) relies heavily upon elevated cardiac troponin (cTn) concentrations in the appropriate clinical context. The Third Universal Definition of Myocardial Infarction (MI) has confirmed cTn as the biomarker of choice.13 Diagnosis of MI is made with acute changes in cTn concentrations with at least one serial sample above the 99th percentile upper reference limit (URL), taken together with evidence of myocardial ischemia (symptoms, electrocardiogram (ECG) changes or imaging results). Various guidelines and publications recommend the optimal imprecision (coefficient of variation) of cTn assays at the 99th percentile upper reference limit be less than or equal to 10%.10,13-17
Several guidelines and research activities recognize that improved analytical sensitivity of cTn assays during the last several years has allowed for detection of other etiologies. Chronic cTn elevations can be detected in clinically stable patients such as patients with ischemic or non‐ischemic heart failure,18,19 patients with different forms of cardiomyopathy,20 renal failure,21-27 sepsis,28 and diabetes.29 Elevated concentrations of cTn can also occur in other clinical conditions such as myocarditis,30 heart contusion,31 pulmonary embolism,32 and drug‐induced cardiotoxicity.33
To distinguish between acute and chronic cTn elevations, the Universal Definition of MI stresses the need for serial sampling to observe a rise and/or fall of cTn above the 99th percentile upper reference limit consistent with the clinical assessment, including ischemic symptoms and electrocardiographic changes.13 Troponin elevations may persist for up to 14 days or occasionally longer.13 Other diagnostic tests such asNT‐proBNP and CRP can complement the diagnostic and prognostic information of cTnT in different indications.
By current universal definition of the disease (AMI), the 99th percentile URL should be used as a diagnostic cutoff of AMI,13 and is endorsed by major local guidelines.10,16,34 Higher cutoffs produce higher estimates of clinical specificity and positive predictive value (PPV), but tend to underestimate clinical sensitivity and negative predictive value (NPV).35 When switching to the Elecsys Troponin T Gen 5 STAT assay, users should be aware that the guideline compliant test using the 99th percentile URL as a diagnostic cutoff, can lead to a relative increase in the diagnosis of acute MIs compared to contemporary assays using other, often higher cutoffs.10,36-38
|Order Code||Order Code Name||Order Loinc||Result Code||Result Code Name||UofM||Result LOINC|
|140150||Troponin T||89576-3||140164||Troponin T(Highly Sensitive)||ng/L||67151-1|
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