Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020672 (hypothermia)
17,327 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In forensic pathology, previous studies have suggested the possible application of cardiac troponins in the diagnosis of myocardial infarction. However, there appears to be insufficient practical data on other causes of death. The present study was a comprehensive analysis of the cardiac, peripheral blood and pericardial levels of cardiac troponin T (cTnT) in serial medicolegal autopsy cases (n = 405) with a survival time <24 h and within 48 h postmortem to assess the validity of investigating myocardial damage with special regard to traumatic causes of death. These included blunt and sharp instrument injury (n = 122 and 21, respectively), asphyxiation (n = 35), drowning (n = 27), fire fatalities (n = 94), hyperthermia (n = 13), hypothermia (n = 6), fatal methamphetamine (MA) abuse (n = 12) and carbon monoxide (CO) poisoning (n = 5) in comparison with myocardial infarction (MI, n = 57) and cerebrovascular diseases (n = 13). Cases within 12h postmortem usually showed lower cardiac and pericardial cTnT levels than did those of longer postmortem time of 12-48 h. In the early postmortem period of <12 h, significantly elevated serum cTnT levels were observed for hyperthermia. Thereafter, fatal MA abuse, CO poisoning and MI cases also showed higher levels. However, cTnT remained at lower levels for hypothermia and drowning. The elevation of cTnT was associated with the pathology of advanced myocardial damage involving swelling and liquefactive necrosis. The above-mentioned differences were the smallest for peripheral blood. These findings suggest that elevations in postmortem serum and pericardial cTnT levels depend on the severity of myocardial damage at the time of death and are related to the pathological findings, although postmortem interference should be taken into consideration.
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PMID:Postmortem cardiac troponin T levels in the blood and pericardial fluid. Part 1. Analysis with special regard to traumatic causes of death. 1633 55

THIS CASE REPORT EXPOSES A PHENOMENON WHICH, ALTHOUGH PROPOSED, HAS NOT BEEN DESCRIBED IN CLINICAL LITERATURE: transient postictal hemiplegia (Todd's paralysis) with concomitant electrocardiographic J-point deflection (Osborn waves). Although typically associated with hypothermia, a prominent J-wave on the electrocardiogram (ECG) results from a transmyocardial voltage gradient during ventricular repolarization. Rarely, the Osborn wave may be observed in a non-hypothermic setting such as hypercalcemia or cerebral hemorrhage. Transient postictal hemiplegia has been attributed to localized cerebral hypoperfusion resulting from motor cortex exhaustion following an epileptic seizure. The same central nervous system autonomic dysfunction has been theorized to produce subendocardial hypoperfusion with electrocardiographic change and cardiac troponin T elevation. This is the first described ECG evidence of a dynamically displaced J-point in the setting of postictal hemiplegia.
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PMID:Dynamic J-Point Elevation Associated with Epileptic Hemiplegia: The Osborn Wave of Todd's Paralysis. 2346 97

The aim of the present study was to describe the findings of postmortem serum and pericardial fluid (PF) cardiac troponin T (cTnT) in various causes of death with regard to the postmortem interval (PMI) and comorbid cardiovascular disease, using 101 autopsy cases with PMI of 8-141 h divided into 9 groups: cardiovascular disease (CVD), other diseases (OD), poisoning (P), asphyxia (A), drowning (D), hypothermia (H), thoracic trauma (TT), other trauma (OT) and fire fatalities (F). The results suggest that cTnT levels may help to differentiate cardiovascular death from poisoning and non-thoracic trauma, as well as to differentiate cardiovascular and other diseases as cause of death from drowning and hypothermia. However, the effect of PMI, unlike comorbid cardiovascular disease, has to be taken into account.
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PMID:Cardiac troponin T in forensic autopsy cases. 2431 15

Previous studies suggested possible application of postmortem biochemistry of myocardial biomarkers to the investigation of sudden cardiac death; however, differences from clinical findings should be considered in autopsy materials. The present study involved a comprehensive investigation of cardiac troponin T and I (cTnT and cTnI), and creatine kinase MB (CK-MB) in cardiac and peripheral external iliac venous blood, pericardial fluid (PCF) and cerebrospinal fluid (CSF) for reassessment, with special regard to the estimated postmortem interval in relation to the cause of death, reviewing a large number of forensic autopsy cases (n=1923). These cardiac biomarkers showed cause-of-death- and postmortem-time-dependent differences: blood and PCF levels of each marker were higher in hyperthermia (heatstroke), bathwater drowning and chronic congestive heart disease in cases of postmortem interval (PMI) <12h. After 12h postmortem, these markers were also higher in fatal drug abuse, spontaneous cerebral/subarachnoid bleeding, electrocution and pulmonary embolism. In addition, most other causes of death, including ischemic heart disease, showed substantial elevations, while these markers remained low in acute hemorrhagic death from sharp instrument injury, hypothermia (cold exposure) and sea-/freshwater drowning during PMI of <48h. CSF cTnI and CK-MB showed similar findings. There was no difference between myocardial infarction and other causes of death to be discriminated, including asphyxiation, drowning and fire fatality. These findings are similar to clinical observations in critical ill patients, suggesting that elevated cardiac biomarkers cannot be a specific finding for death from acute ischemic heart disease, but indicate the severity of myocardial injury in postmortem investigation.
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PMID:Cardiac biomarkers in blood, and pericardial and cerebrospinal fluids of forensic autopsy cases: A reassessment with special regard to postmortem interval. 2605 7