AER was correlated with HDL-cholesterol (r = 0.58, P less then 0.0001) and apoA1 levels (r = 0.56, P less then 0.0001). Kaplan-Meier survival plot showed subjects in the lowest quartile of AER experienced a significantly higher rate of incident major adverse cardiovascular events (MACE = myocardial infarction, stroke, or death) (P less then 0.0069 log rank). Moreover, compared to subjects in the lowest AER quartile, the remaining subjects showed significantly lower incident (3 year) risk for MACE, even after adjustment for traditional risk factors and apoA1 (HR 0.58; 95% CI 0.40-0.85; P = 0.005). Conclusions In a prospective cohort of stable subjects undergoing elective diagnostic cardiac evaluations, low AER was associated with increased incident risk of MACE.Background B-type natriuretic peptide (BNP) is a cardiac hormone released with an N-terminal fragment (NTproBNP) under conditions of ventricular pressure or volume overload. BNP has been proposed for use as a biomarker of cardiac dysfunction in premature infants in the setting of hemodynamically significant patent ductus arteriosus (HsPDA) and bronchopulmonary dysplasia (BPD). In adult settings the presence of proBNP and glycosylated isoforms may affect assay interpretation. However, there are limited data on how immature preterm physiology may affect BNP or NTproBNP levels and no published data on post-translational BNP processing in premature infants. Methods Pooled serial plasma samples from preterm infants born at less than 30 weeks gestation were analyzed for BNP congeners using Luminex® assay and high performance liquid chromatography. Samples were grouped according to clinical status Group 1, no HsPDA and no BPD, Group 2 HsPDA and no/mild BPD, Group 3 HsPDA and moderate/severe BPD. Results Plasma from 15 infants was analyzed, and across all three groups NTproBNP predominated with minimal amounts of other isoforms; no glycosylation was detected. Conclusions NTproBNP appears to be the predominant isoform across each of our clinical groups in our pooled sample analysis with no evidence of significant glycosylation. This suggests NTproBNP is likely to be a robust marker in this clinical setting.Background Laboratory tests that use streptavidin-biotin binding mechanisms have the potential to be affected by high circulating biotin concentrations, which would produce positive and negative interference in biotinylated competitive and noncompetitive (sandwich) immunoassays, respectively. Consumption of high-dose biotin supplements for cosmetic or health-related reasons has drawn attention to biotin interference in clinical laboratory tests. Case reports and in vivo studies show that ingestion of supplemental biotin can cause clinically significant errors in select biotinylated immunoassays. Content This AACC Academy document is intended to provide guidance to laboratorians and clinicians for preventing, identifying, and dealing with biotin interference. In vivo and in vitro spiking studies have demonstrated that biotin concentrations required to cause interference vary by test and by manufacturer. This document includes discussion of biotin's mechanisms for interference in immunoassays, pharmacokinetics, and results of in vitro and in vivo studies and cites examples of assays known to be affected by high biotin concentrations. This document also provides guidance recommendations intended to assist laboratories and clinicians in identifying and addressing biotin interference in laboratory testing. Summary The recent increase in the use of high-dose biotin supplements requires laboratorians and clinicians to be mindful of the potential for biotin interference in biotinylated immunoassay-based laboratory tests. Laboratories, clinicians, regulators, and patients should work together to ensure accurate laboratory results. Laboratories have several options for identifying suspected biotin interference in specimens. Alternatively, the relatively fast elimination of biotin allows the potential for rapid follow-up specimen analysis if necessary.Background Traumatic brain injury (TBI) is a significant cause of morbidity, mortality, and disability in the US, with >2.8 million patients presenting to the emergency department (ED) annually. However, the diagnosis of TBI is challenging and presents a number of difficulties, particularly at the mildest end of the spectrum concussion. A number of groups have researched biomarkers to aid in the evaluation of TBI, and most recently in 2018 the Food and Drug Administration approved a new blood-based immunoassay biomarker using ubiquitin carboxyl hydrolase L1 and glial fibrillary acidic protein to aid in head computed tomography (CT) triage. Content This review clarifies the practical challenges in assessing and implementing a new blood biomarker. It then examines the clinical context and need, as well as the evidence used to validate this new immunoassay. Summary Concussion is a multifaceted diagnosis with a need for biomarkers to assist in diagnostic and prognostic assessment. Recent articles in the lay press have revealed misunderstanding about the function of this new test, expressing hopes that this biomarker serves patients at the mildest end of the spectrum and is useful for athletes and children. None of these assumptions are correct, as this biomarker has been evaluated in patients only at the moderate end of the spectrum and has been validated only in adults presenting to the ED who have already been triaged to receive head CT, not in athletes or children. read more The next steps for this assay should consider clinical work flow and clarifying its intended use, including integration with existing triage methods, and validating the assay for a broader population.Background Serum glial fibrillary acidic protein (GFAP) and ubiquitin carboxyl-terminal esterase L1 (UCH-L1) have recently received US Food and Drug Administration approval for prediction of abnormal computed tomography (CT) in mild traumatic brain injury patients (mTBI). However, their performance in elderly patients has not been characterized. Methods We performed a posthoc analysis using the A Prospective Clinical Evaluation of Biomarkers of Traumatic Brain Injury (ALERT-TBI) study data. Previously recorded patient variables and serum values of GFAP and UCH-L1 from mTBI patients were partitioned at 65 years of age (herein referred to as ≥65, high-risk; 0.9999, respectively). Specificity was significantly lower in elderly patients (0.131 vs 0.442; P less then 0.0001) and decreased stepwise with older age. Compared to younger patients, elderly mTBI patients without abnormal (i.e., normal) CT findings also had a significantly higher GFAP (38.6 vs 16.2 pg/mL; P less then 0.0001) and UCH-L1 (347.4 vs 232.1 pg/mL; P less then 0.