Objective: To evaluate the utility of NT-proBNP in the emergency diagnosis and in-hospital monitoring of patients with acute dyspnoea and ventricular dysfunction. Background: Misdiagnosis of heart failure (HF) is common in the urgent care setting using clinical diagnostic tests. Reports show that BNP is useful to diagnose HF in patients with acute dyspnoea. Methods: Prospective study of 100 patients attending the Emergency Department (ED) for acute dyspnoea. Final diagnosis was determined on the basis of ED data sheets, echocardiography and pulmonary function tests. NT-proBNP levels were obtained on admission, at 24 h and at day 7. Results: Patients with ventricular dysfunction were sub-classified into decompensated HF and masked HF, defined as HF with concomitant signs of pulmonary disease. Decompensated and masked HF patients had significantly higher NT-proBNP values than patients with non-cardiac dyspnoea (normal ventricular function) (920"140 and 978"363 vs. 50"15 pmolyL; P-0.001 and P-0.01, respectively). The mean area under the ROC curve for NT-proBNP was 0.957 (95% CI, 0.918 to 0.996, P-0.001). In multiple logistic-regression analysis NT-proBNP)115 pmolyl was the strongest independent predictor of ventricular dysfunction (odds ratio 45.4; 95% CI: 4.5-452.3). At day 7, a significant and similar reduction in NT-proBNP was observed in the two groups of patients with ventricular dysfunction (P-0.001 vs. admission values), but complete clinical resolution was less frequent in masked HF patients (P-0.05 vs. decompensated HF). Conclusions: NT-proBNP is a new candidate marker for the detection and exclusion of ventricular dysfunction in patients attending the ED for acute dyspnoea. NT-proBNP may also serve to monitor outcome during hospitalization.

Ischemia-modified albumin (IMA) has been proposed as a biological marker of myocardial ischemia (1, 2 ). Exposure to ischemic myocardium modifies circulating albumin at its NH 2 terminus by different mechanisms, and this modification is the basis of IMA measurement by the albumin cobalt binding (ACB) test (3 ). The tissue-specific nature of the mechanism by which ischemia modifies albumin remains undetermined. Together with a nondiagnostic electrocardiogram and negative troponin values, IMA concentrations within the reference interval have high negative predictive value of myocardial ischemia in patients with suspected acute coronary syndromes (1, 2 ). However, IMA cardiospecificity has not been validated and needs an evidence base before routine clinical use. A recent report showed significant IMA increases 24 -48 h after a marathon race, with exercise-promoted gastrointestinal and/or delayed skeletal muscle ischemia being evoked as possible causes of such increases (4 ). However, because IMA has shown rapid kinetics of increase (in minutes) and return to baseline no longer than 12 h after angioplastic procedures (5 ), long-duration skeletal muscle ischemia (i.e., occurring during marathons) does not appear to be the most appropriate model to investigate the effect of such ischemia on IMA values or the kinetics of IMA occurring during acute coronary syndromes. The aim of this work was to analyze the possible contribution of skeletal muscle ischemia to IMA by investigating its short-term kinetics in an isolated skeletal-muscle ischemia model. Because lactate and ammonia concentrations increase sharply after a forearm ischemia test, their possible influence in the ACB assay was studied.Ten healthy volunteers (4 men and 6 women) from our laboratory staff (age range, 48 -61 years; median, 53 years) with no personal or family history of cardiovascular disease and no known cardiovascular risk factors after a medical examination underwent a forearm ischemia test (6 ). Briefly, after an overnight fast (10 -12 h) and 30 min of previous rest, a preexercise (0 min) blood sample was drawn, and blood systolic pressure was recorded twice within a 5-min interval. Thereafter, forearm ischemia was produced by inflating the blood pressure cuff up to 20 -30 mmHg higher than the maximum systolic pressure registered. Under these ischemic conditions, a hand-grip exercise at maximum possible strength was performed for 1 min. Thereafter, the cuff was removed, and serial blood samples were drawn at 1, 3, 5, 10, 15, and 30 min. Serum for IMA, creatine kinase, and potassium; EDTA plasma for ammonia; and fluoride plasma for lactate and glucose were collected at each time point into Vacutainer ® Tubes (Becton Dickinson). To establish reference values, IMA was tested in a group of 86 fasting (10 -12 h), ambulatory (median age, 57 years; 38 women) sedentary individuals who underwent blood sampling after health examinations or before minor surgical procedures. Individuals with cardiovascular risk factors or past or present signs or symptoms o...

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Asparaginase (ASP) is an essential component for the acute lymphoblastic leukemia (ALL) treatment, but toxicities, such as allergy, frequently limit its use. Although the potentially lower PEG-ASP formulation immunogenicity, few studies with conflicting results have compared the allergy incidence between Escherichia coli-ASP and PEG-ASP in the same protocol. We aimed at comparing the allergy incidence in children receiving native E. coli-ASP versus PEG-ASP within the same clinical protocol (Spanish Society of Pediatric Hematology and Oncology ALL-SEHOP-PETHEMA 2013). One hundred and twenty-six children (1-19 years) diagnosed with ALL from 2013 to 2020 were included. Patients in group 1 received a sequential scheme of native E. coli-ASP 10,000 IU/m 2 intramuscularly (IM) followed by PEG-ASP 1000 IU/m 2 IM. Patients in group 2 received PEG-ASP 1000 IU/m 2 IM upfront. Clinical allergy incidence was compared between both groups. Serum ASP activity (SAA) was measured in a subgroup of patients, and silent inactivation was recorded. The cumulative incidence of clinical allergy was significantly higher in group 1 (native followed by PEG-ASP) than in group 2 (PEG-ASP upfront), 24.7% versus 4.1% (p = 0.0085). Adequate ASP activity was achieved with PEG-ASP 1000 IU/m 2 dose in most patients (median SAA 412.5 and 453.0 IU/L at days 7 and 14).

Standardized serum peptidome profiling could be a useful tool to improve biochemical diagnosis of PC in combination with the classic tumor marker, CA 19-9.