Anti-animal antibodies (IgG, IgA, IgM, IgE class, anti-isotype, and anti-idiotype specificity) arise as a result of iatrogenic and noniatrogenic causes and include human anti-mouse, -rabbit, -goat, -sheep, -cow, -pig, -rat, and -horse antibodies and antibodies with mixed specificity

Anti-animal antibodies (IgG, IgA, IgM, IgE class, anti-isotype, and anti-idiotype specificity) arise as a result of iatrogenic and noniatrogenic causes and include human anti-mouse, -rabbit, -goat, -sheep, -cow, -pig, -rat, and -horse antibodies and antibodies with mixed specificity. detected by the monoclonal antibody-based assays currently in use [2]. This specificity for cardiac isoforms is the basis for the clinical utility of cTnT and cTnI assays. Relying on history, physical examination, and ECG abnormalities to diagnose acute myocardial infarction may often lead the clinician astray. Thus, the diagnosis of an acute myocardial infarction has become increasingly dependent upon the evaluation of cardiac enzymes, particularly cardiac troponins [2, 3]. In addition to acute myocardial infarction, elevated serum troponins can also be seen in a variety of other diseases including sepsis or critical illness, tachycardia, LVH, heart failure, pulmonary embolism, myocarditis, myocardial trauma, and renal failure [4, 5]. Although irreversible myocyte damage is the usual presumed mechanism responsible for troponin elevation, several additional mechanisms are believed to be responsible for elevated serum troponins in the aforementioned pathological states, including endothelial dysfunction, loss of membrane integrity with leakage of the free cytosolic troponin pool, stretch-mediated troponin release, and impaired renal excretion [6]. Falsely elevated troponin values caused by interference with current troponin assays have been reported. We report a unique case that demonstrates the fluctuation of falsely elevated troponin correlating with hemoglobin, serving as a marker of heterophile antibody levels EPZ-6438 (Tazemetostat) [7C17]. 2. Case Presentation A 74-year-old man, a retired railroad conductor, with a history of hypertension, hyperlipidemia, and noninsulin-dependent diabetes mellitus presented to our Emergency Department with a several-day history of increasing shortness Rabbit Polyclonal to GIT1 of breath associated with a new-onset chest pain. ECG performed in the Emergency Department showed a right bundle branch block, left ventricular hypertrophy, and left atrial enlargement. Troponin I was elevated at 77.28?ng/mL. (Beckman-Coulter’s Access AccuTnl Assay; reference range 0.00C0.04) The remainder of the cardiac enzymes were essentially normal: myoglobin (50?ng/mL), CK-MB (5.2?ng/mL), and creatine kinase (74?IU/L). D-Dimer was normal at 0.33?mcg/mL. BUN was 13?mg/dL and creatinine was normal at 0.65?mg/dL (reference range 0.64C1.27). Standard Acute Coronary Syndrome protocol was initiated, and the patient was admitted to the hospital. Transthoracic echocardiography showed left ventricular hypertrophy, mild EPZ-6438 (Tazemetostat) diastolic dysfunction, and a normal ejection fraction with no evidence of wall motion abnormality. Troponin levels remained elevated throughout the entire hospitalization, in continued disproportion to the other cardiac enzymes, (Myoglobin, CK-MB, and CK) which remained either normal or very mildly elevated throughout. His hospital course was complicated by bibasilar pneumonia and atelectasis requiring multiple bronchoscopies, intubation with ventilatory support, and ultimately a tracheostomy; bilateral lower extremity deep venous thromboses, EPZ-6438 (Tazemetostat) for which he underwent successful inferior vena cava filter placement; a progressive thrombocytopenia which proved to be Heparin-Induced Thrombocytopenia-antibody positive; and finally, a life-threatening bleeding duodenal ulcer. A complete blood count trend analysis revealed a significant two-week down-trending of the patient’s hemoglobin and hematocrit values; retrospectively a result of the slowly bleeding ulcer. Troponin levels was obtained serially throughout. Figure 1 is a graph showing all the patient’s troponin I levels recorded at our hospital, with a juxtaposed graphing of his hemoglobin levels. Open in a separate window Figure 1 As the duodenal ulcer proved to be incendiary, and refractory to temporizing measures, the patient ultimately developed hemorrhagic shock and was taken emergently to the operating room where he underwent EPZ-6438 (Tazemetostat) an exploratory laparotomy with pyloroplasty and successful suture ligation of the ulcer. In addition to extensive resuscitation with normal saline, the patient had required a total of 18 units of PRBC. 12 of these units were given within 24?hrs. Intraoperatively, the patient received 5 units of PRBC, 10 units of FFP, and 5 units of platelets. 3. Investigations A patient’s blood sample was sent out for a troponin I level on two EPZ-6438 (Tazemetostat) separate occasions to a near-by hospital laboratory that used the Siemens ADVIA Centaur Immunoassay as opposed to the Beckman-Coulter Access AccuTnl Assay used by our hospital. Both times the result returned at 0.01?ng/mL. Additionally, a random troponin T level measured by Associated Regional and University Pathologists Laboratories using the Electrochemiluminescent Immunoassay was only 0.13?ng/mL. A heterophile antibody by latex agglutination was also sent out to ARUP Laboratories and returned negative. However, since this screen only tests for.