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Plasma transthyretin (TTR) is a plasma protein secreted by the liver that circulates bound to retinol-binding protein 4 (RBP4) and its retinol ligand. TTR is the sole plasma protein that reveals from birth to old age evolutionary patterns that are closely superimposable to those of lean body mass (LBM) and thus works as the best surrogate analyte of LBM. Any alteration in energy-to-protein balance impairs the accretion of LBM reserves and causes early depression of TTR production. In acute inflammatory states, cytokines induce urinary leakage of nitrogenous catabolites, deplete LBM stores, and cause an abrupt decrease in TTR and RBP4 concentrations. As a result, thyroxine and retinol ligands are released in free form, creating a second frontline that strengthens that primarily initiated by cytokines. Malnutrition and inflammation thus keep in check TTR and RBP4 secretion by using distinct and unrelated physiologic pathways, but they operate in concert to downregulate LBM stores. The biomarker complex integrates these opposite mechanisms at any time and thereby constitutes an ideally suited tool to determine residual LBM resources still available for metabolic responses, hence predicting outcomes of the most interwoven disease conditions., (© 2015 American Society for Nutrition.)

Background: A consensus document developed by a joint committee of the European Society of Cardiology and the American College of Cardiology redefines myocardial infarction (MI) using an increase of troponin I or T as compared to a reference control population (i.e., troponin T (TnT) of 0.01 microg/l). A clinical problem arises when an arbitrary cut-off point is selected for determination of MI (i.e., TnT> or =0.1 microg/l), as minor elevations of troponin are associated with increased cardiovascular risk in selected patients with acute coronary syndromes., Methods: We prospectively studied 420 unselected patients being evaluated for suspected myocardial ischemia in the emergency department (ED). We compared a 99th percentile MI cut-off limit for TnT, determined by constructing a standard receiver operator curve from our ED population in whom an acute coronary syndrome was excluded, to a standard MI cut-off limit of 0.1 microg/l in assessing cardiovascular risk. We also assessed the prognostic value of detectable TnT concentrations below this 99th percentile MI cut-off, but above the upper reference limit of healthy controls., Results: The diagnosis of acute coronary syndromes (ACS) was more frequent in groups with higher TnT concentrations: 16.8% with a normal TnT (<0.03 microg/l), 29.5% with detectable TnT below the 99th percentile MI limit (0.03-0.066 microg/l), 64.3% with detectable TnT between the 99th percentile and standard MI cut-offs (0.067-0.099 microg/l), and 85.4% with TnT> or =0.1 microg/l (p<0.001 for the trend). Thirty-day cardiovascular event rates increased for any detectable concentration of troponin: 1.3% with normal TnT, 4.8% with detectable TnT below the 99th percentile MI limit, 15.4% with TnT between the 99th percentile and standard MI cut-off limits, and 12.5% with TnT> or =0.1 microg/l (p<0.01 for the trend)., Conclusion: Using an MI cut-off concentration for TnT from a "non-ACS reference" improves risk stratification, but fails to detect a positive TnT in 11.7% of subjects with an acute coronary syndrome.

Background: Prior studies with cardiac markers have focused predominantly on subjects presenting to the emergency department with chest pain or unstable angina, and have relied on serial markers for the diagnosis of acute myocardial infarction. We evaluated the diagnostic utility of a single cardiac troponin T (cTnT) determination at the time of presentation as compared to serial creatine kinase (CK) MB determinations in a broad spectrum of patients with suspected myocardial ischemia., Methods: A total of 267 consecutive patients presenting to the emergency department with suspected myocardial ischemia had a single, blinded cTnT determination drawn at the time of presentation to the emergency department in addition to routine serial electrocardiographic and CK-MB determinations., Results: The specificity (93.7% vs. 87.1%; p<0.05) and positive predictive value (80.0% vs. 69.4%; p<0.05) of a single cTnT determination were superior to that of serial CK-MB determinations without compromising sensitivity. Forty-six percent of patients with confirmed myocardial infarction and an abnormal cTnT at presentation had a normal initial CK-MB determination. Conversely, 20% of patients without acute coronary syndromes had an abnormal CK-MB determination in the setting of a normal cTnT. The initial cTnT was abnormal in all patients with confirmed myocardial infarction and a symptom duration of at least 3.5 h., Conclusions: In a heterogeneous population of patients with suspected myocardial ischemia, the initial cTnT determination drawn at the time of presentation is a powerful diagnostic tool that, when used in context with symptom duration, allows for more rapid and accurate triage of patients than serial CK-MB determinations.

Background: Most laboratories using the Abbott FLM-II assay for assessing fetal lung maturity follow the manufacturer's recommendations for interpreting the surfactant to albumin ratio (S/A). Thus, values >55 mg/g are considered mature and values <40 mg/g, immature-leaving a wide range of indeterminate values. Little data is available to assist the clinician in interpreting values between 40 and 55 mg/g. The goal of this study was to determine decision levels that would more clearly identify risk for RDS based on S/A results., Methods: Respiratory distress syndrome was identified based on medical record review in 46 infants (born at six hospitals), who had S/A measurements on amniotic fluid within 72 h of delivery. An additional 257 women, who had had the S/A test requested but had non-RDS infants, were also identified for this study. The probability of RDS was calculated based on S/A values and on gestational age. Odds ratios were computed for different S/A ratios and different gestational ages., Results: Probability of RDS increased with decreasing S/A and decreasing gestational age. At gestational age >36 weeks, the probability of developing RDS ranged from 1% at S/A>44 mg/g to 39% at S/A44 mg/g to 92% at S/A