Urine high-sensitive troponin I in children cannot offer an applicable alternative to serum.

Introduction: In children, congenital heart defects represent the primary cause of increased serum troponin I. The elimination process of cardiac troponin I from the bloodstream and the factors influencing this process remain unknown. The objective of this study was to explore the role of troponin I as an indicator of cardiac damage in children both in serum and urine, a concept previously investigated in adults. Methods: Our prospective study involved 70 children under 24 months of age. The first group underwent ventricular septal defect repair, while the second group involved children who had undergone partial cavopulmonary anastomosis. For these groups, urine and serum troponin I were assessed on four occasions. The third group, consisting of healthy children, underwent a single measurement of urine troponin I. Results: Serum troponin I values exhibited an expected elevation in the early postoperative period, followed by a return to lower levels. Significantly higher concentrations of serum troponin I were observed in the first group of children (p < 0.05). A positive correlation was found between troponin I in the first three measurements and cardiopulmonary bypass and aortic cross-clamping time. There was no discernible increase in urine troponin I directly related to myocardial damage; troponin I couldn't be detected in most urine samples. Discussion: The inability to detect troponin I in urine remains unexplained. Potential explanatory factors may include the isoelectric point of troponin I, elevated urinary concentrations of salts and urea, variations in urine acidity (different pH levels), and a relatively low protein concentration in urine.

Exploratory analysis of glial fibrillary acidic protein and ubiquitin C-terminal hydrolase L1 in management of patients with mild neurological symptoms undergoing head computed tomography scan at the emergency department: a pilot study from a Croatian tertiary hospital.

BACKGROUND: Diagnostic accuracy of glial fibrillary acidic protein (GFAP) and ubiquitin C-terminal hydrolase L1 (UCH-L1) in identification of intracranial abnormalities detected by computed tomography (CT) in mild traumatic brain injury (mTBI), and in patients with mild neurological symptoms not caused by head trauma but suspected with a neurological disorder, was examined. METHODS: GFAP and UCH-L1 were determined using the chemiluminescence immunoassays on the Alinity i analyzer (Abbott Laboratories). RESULTS: Significantly higher GFAP (median 53.8 vs 25.7 ng/L, P < .001) and UCH-L1 (median 350.9 vs 153.9 ng/L, P < .001) were found in mTBI compared to non-head trauma patients. In mTBI diagnostic sensitivity (Se) and specificity (Sp) for the combination of GFAP and UCH-L1 were 100% and 30.9%, respectively, with area under the curve (AUC) 0.655. GFAP alone yielded Se 85.7%, Sp 41.8%, and AUC 0.638, while UCH-L1 yielded Se 57.1%, Sp 56.4%, and AUC 0.568. In non-head trauma patients, the combination of GFAP and UCH-L1 showed Se 100%, Sp 87.9%, and AUC 0.939, while GFAP alone demonstrated Se 100%, Sp 90.9%, and AUC 0.955. CONCLUSIONS: If these results are reproduced on a larger sample, GFAP and UCH-L1 may reduce CT use in patients with mild neurological symptoms after systemic causes exclusion and neurologist's evaluation.

Analytical validation of 39 clinical chemistry tests and 17 immunoassays on the Alinity analytical system.

The aim of this study was to perform the analytical validation of Alinity c and i analyzers (Abbott Laboratories, Chicago, IL, USA) for 39 clinical chemistry tests and 17 immunoassays. Precision was evaluated at least at two concentration levels for 5 days in quintuplicate, following CLSI EP15-A3. Method comparison included parallel analysis of leftover routine samples on Alinity analyzers and the previously used Cobas c501 and e601 (Roche Diagnostics, Mannheim, Germany). Linearity was tested by preparing sequential sample dilutions with high analyte concentration, following the CLSI EP6 document. For clinical chemistry tests, within-run coefficients of variation (CV) were up to 6.0% (beta-2-microglobulin), while between-run CVs up to 5.4% (immunoglobulin M). Among immunoassays, the highest within-run CV was obtained for vitamin B12 (6.9%), while between-run for CA 19-9 (4.3%). Complete agreement with Roche analyzers was observed for 16 (41%) clinical chemistry assays and 6 (35%) immunoassays. Half of all evaluated assays did not meet the desirable biological variation criteria for bias, being especially exceeded for alpha1-antitrypsin, apolipoprotein A1, ceruloplasmin, complement C3 and C4, hemoglobin A1c, lipoprotein (a) and myoglobin, as well as some tumor markers (CA 125, CEA, fPSA, AFP, and ferritin), hormones (cortisol, DHEA-S, insulin) and vitamins (25-OHD). Linearity in the tested ranges was confirmed. Overall, this study revealed that precision criteria derived from manufacturer's claims were not satisfied for all assays while comparison study for some assays yielded differences that imply the need for additional assay evaluation prior to introduction into routine practice.

The missing slope: paradoxical shortening of activated partial thromboplastin time in a patient on unfractionated heparin therapy.

This case report describes false shortening of activated partial thromboplastin time (aPTT) due to erroneous optical reading of the clotting point in the presence of unfractionated heparin (UFH), and a biphasic waveform. Activated partial thromboplastin time performed on a coagulometer with photo-optical detection yielded an ambiguous clotting curve characterized by an early and steady decrease in light transmittance throughout the whole measuring range, with the clotting point read at 65 seconds. Further investigations included measurement of aPTT by means of a mechanical clot detection method as well as determination of another heparin-sensitive coagulation assay, that is thrombin time (TT), both being unmeasurably prolonged (> 150 seconds). Communication with clinicians revealed that the patient was on continuous UFH therapy and had an underlying sepsis, with highly elevated C-reactive protein (289 mg/L). The aPTT measurements requested at three timepoints later during the same day revealed gradual aPTT shortening and unveiled a peculiar biphasic waveform pattern. In this case, unmeasurably prolonged aPTT due to UFH therapy was masked by a biphasic aPTT curve pattern making only the first slope of the biphasic waveform visible within the measuring range. The early decrease in plasma light transmittance mimicked optical changes related to clot formation, thus causing erroneous optical reading and yielding a falsely shortened aPTT. This case emphasizes that such a pattern should be carefully inspected, especially when a combination of a critically ill condition and UFH therapy is present, in order to prevent erroneous reporting of aPTT and potential adverse effects on patient care.

Utility of procalcitonin in a medical intensive care unit in Croatia.

AIMS: To investigate the clinical benefit of routine procalcitonin (PCT) measurement in the medical intensive care unit (ICU) of a tertiary referral hospital. METHODS: Adult patients with suspected infections were included. White blood cells, C­reactive protein (CRP), and PCT were measured. RESULTS: In this study 129 patients of median age 64 years (interquartile range 39-89 years) were prospectively included. The Acute Physiology And Chronic Health Evaluation II (APACHE II) and Sequential Organ Failure Assessment (SOFA) scores were 21 ± 14 and 7 ± 6, respectively. Intensive care unit (ICU) mortality was 22.5%. Immunocompromised patients constituted 39.5%. A significant correlation was observed between PCT and APACHE II (Spearman's rho 0.461, p < 0.01), PCT and SOFA (Spearman's rho 0.494, p < 0.01) and PCT and CRP (Spearman's rho 0.403, p < 0.01). Most patients (n = 83, 64.3%) received antibiotics before admission. No difference in PCT (1.56 ± 8 µg/L vs. 1.44 ± 13 µg/L, p = 0.6) was observed with respect to previous antibiotic therapy. Levels of PCT and CRP were significantly increased in patients with positive blood cultures, the infection caused by Gram-negative microorganism regardless of disease severity and pneumonia with complications. PCT did not differ among patients with positive vs negative urine culture (4.6 ± 16 µg/L vs. 1.76 ± 11.9 µg/L) or positive vs. negative endotracheal aspirate (1.93 ± 11.4 µg/L vs. 1.76 ± 1.11 µg/L). PCT-guided stewardship was applied in 36 patients (28%). CONCLUSION: Increased initial PCT levels might point to the development of more severe disease caused by Gram-negative bacteria, regardless of previous antibiotic treatment. The results pertain to immunocompetent and immunocompromised patients. Implementation of PCT-guided stewardship in those patients is possible and relies on experience as well as knowledge of reference change value for a marker within the specific setting.