In the present study, the levels of NT-proBNP, troponin T, and troponin I were measured in postmortem serum from femoral blood in a series of sepsis-related fatalities that had undergone forensic autopsies. We aimed to assess whether a possible increase in the concentrations of these biomarkers was correlated to macroscopic or microscopic observations that suggest myocardial damage or cardiac dysfunction. Two study groups were retrospectively formed, a sepsis-related fatalities group and a control group. Both groups consisted of 16 forensic autopsy cases. Unenhanced computed tomography scan, autopsy, histological, toxicological, microbiological, and biochemical analyses were performed for all cases in both groups. Levels of procalcitonin, C-reactive protein, NT-proBNP, troponin T, and troponin I were systematically measured in postmortem serum from femoral blood. The preliminary results suggest that the postmortem serum troponin I, troponin T, and NT-proBNP levels are increased in sepsis-related deaths in the absence of any relevant coronary artery disease, myocardial ischemia, or signs of heart failure. These findings corroborate clinical data from previous studies pertaining to the usefulness of troponins and natriuretic peptides as indicators of toxic and inflammatory damage to the heart in cases of severe sepsis and septic shock without concomitant underlying coronary syndromes.
Globally considered, our findings seem to suggest that, contrary to urine catecholamines and their O-methylated metabolites, vitreous levels of these compounds appear to be of limited value in characterizing human antemortem stress reactions due to cold exposure and can hardly be used in the forensic setting to support the diagnosis of hypothermia.
Endocan is a soluble molecule secreted from vascular endothelial cells of various organs. Its exact function in humans remains to be elucidated, though it has been postulated that increased tissue expression or serum levels of this molecule may be an indicator of endothelial activation and neovascularization. In the realm of forensic pathology, studies pertaining to endothelial activation following exposure to cold exclusively focused on thrombomodulin, a transmembrane protein specific to endothelial cells. In the study herein described, endocan concentrations were determined in postmortem serum, urine and vitreous humor samples collected during autopsy in a series of cases that underwent medicolegal investigations. A total of 76 autopsy cases were selected and three study groups (hypothermia group, sepsis group and non-hypothermia/non-sepsis group) prospectively formed during the study period. The obtained results seem to indicate that exposure to cold and subsequent death is not distinguished by significant endothelial dysfunction causing enhanced endocan secretion.
The aim of this study was to measure catecholamines and their O-methylated metabolites in urine and vitreous humor collected in cardiac deaths and noncardiac control cases that underwent medicolegal investigations. Our first goal was to assess whether cardiac events of different types are characterized by different catecholamine/metanephrine urine and/or vitreous profiles. Our second goal was to determine whether noncardiac causes of death with different survival intervals are characterized by different catecholamine/metanephrine urine and/or vitreous profiles. Two study groups were prospectively and retrospectively formed, a cardiac death group (including three subgroups, according to the cause of death) and a noncardiac death group (including two subgroups, according to the length of the agonal period). Postmortem angiography, autopsy, histology, toxicology, and biochemistry were performed in all cases. First results seem to indicate that absolute values measured in urine and vitreous for each of the analyzed markers display no significant differences relating to each of the tested cardiac death subgroups. In the control group, absolute concentrations measured in urine and vitreous for each of the analyzed parameters failed to show significant differences relating to the length of agonal period. Our preliminary findings do not seem to confirm the conclusions of former studies and fail to corroborate the usefulness of urine catecholamine and metanephrine analysis to characterize stress response intensity or length of the dying process in the postmortem setting.
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