Postmortem Serum Research Articles

Postmortem Serum Amylase and Lipase Analysis in the Diagnosis of Acute Pancreatitis.

The diagnosis of acute pancreatitis, which can occur due to natural and nonnatural causes, is usually made at autopsy based on gross and microscopic examination. However, some pathologists choose to measure serum amylase and lipase levels in postmortem blood samples, which may provide corroborating evidence of acute pancreatitis when evaluated in the context of the autopsy findings. A small series of autopsy cases of deaths related to acute pancreatitis with corresponding postmortem serum amylase and lipase levels and a review of the literature are used to highlight the potential benefits and interpretation issues of postmortem serum amylase and lipase. In autopsies without decomposition, elevated postmortem serum amylase (greater than 1000 U/L) and lipase can provide supportive evidence of acute pancreatitis as a cause of death. However, relying on postmortem serum amylase and lipase alone to diagnose acute pancreatitis is insufficient and unreliable. Rather, one must have the gross and histologic evidence of acute pancreatitis. Acad Forensic Pathol. 2018 8(2): 311-323.

Diagnostic role of serum tryptase in anaphylactic deaths in forensic medicine: a systematic review and meta-analysis.

Postmortem diagnosis of sudden death due to anaphylaxis can be very difficult due to the non-specific pathological findings in forensic practice. Postmortem serum tryptase has been used as an indicator of possible ante-mortem anaphylaxis. Though many previous studies have been conducted to explore the diagnostic significance of serum tryptase for lethal anaphylaxis, inconsistent results were documented. In this study, we made a retrospective study and presented a systematic review and meta-analysis that aims to summarize the diagnostic significance of postmortem serum tryptase in the deceased with and without anaphylactic shock and to calculate a cutoff value for future reference in the identification of deaths due to anaphylactic shock. A complete literature search in the PubMed, Cochrane Library, CNKI and Embase databases (published prior to March 1st, 2017) was performed. The quality of the eligible literature was evaluated according to the Newcastle-Ottawa Quality Assessment Scale (NOS), and the relevant data was extracted. The procedure of meta-analysis was performed by RevMan 5.3 software. Subgroup analysis was performed according to different causes of death. A total of nine studies with 296 patients were identified. The NOS of each included study was equal to 7. The results indicated that high concentrations of tryptase were significantly associated with anaphylactic shock when compared to the other causes of death. The weighted mean difference (WMD) was 29.53 (95% CI = 7.58-51.47, p = 0.008). Similar results were detected in the subgroup analysis when compared to deaths due to cardiovascular disease (CVD). However, no obvious elevation of tryptase in decedents with CVD compared to the other cause of death was observed (WMD = 4.42, 95% CI = -0.94-9.79). We concluded that high serum tryptase is a promising diagnostic biomarker for deaths due to anaphylactic shock, especially when it is higher than 30.4μg/L.

Usefulness of liver function tests in postmortem samples

Liver function tests have been investigated in the forensic setting in several biological fluids collected at autopsy. Nevertheless, the results of these investigations have provided diverging information on postmortem stability of liver function markers and postmortem reliability of liver function assessment. The first aim of this study was to determine gamma-glutamyltransferase, alanine aminotransferase, aspartate aminotransferase, alkaline phosphatase, total bilirubin, total proteins, and albumin in antemortem and postmortem serum samples in a series of cases that underwent forensic investigations and had both samples available. The second aim was to measure total bilirubin and gamma-glutamyltransferase in cerebrospinal fluid. Preliminary results indicated that femoral (and cardiac) blood postmortem serum concentrations of bilirubin, total proteins, and albumin, as well as femoral blood postmortem serum concentrations of gamma-glutamyltransferase, can be considered to reliably reflect antemortem serum concentrations, thus suggesting that postmortem values could be used as surrogates for antemortem levels. Measurable bilirubin levels were demonstrable in cerebrospinal fluid samples in both preservative-free and sodium fluoride tubes, though with levels varying widely and unpredictably, irrespective of liver disease severity.

Effect of perioperative lidocaine on metastasis after sevoflurane or ketamine-xylazine anaesthesia for breast tumour resection in a murine model

BackgroundBreast cancer accounts for 7% of female cancer deaths, usually attributable to metastasis. While surgery is a mainstay of treatment, perioperative interventions may influence risk of metastasis during breast tumour resection. Amide local anaesthetics influence cancer cell biology via numerous mechanisms in vitro, but in vivo data is lacking. We aimed to test the hypothesis that perioperative lidocaine reduces pulmonary metastasis after inhalation and i.v. anaesthesia in the 4T1 murine breast cancer model. Methods4T1 Cancer cells were injected into the mammary fat-pad of immunocompetent BALB/c female mice. After 7 days, the resultant tumour was excised under either sevoflurane or ketamine/xylazine anaesthesia with or without perioperative i.v. lidocaine (1.5 mg kg−1 bolus followed by 25 min infusion 2 mg kg−1 h−1). Fourteen days post-surgery, posthumous lung and liver specimens were examined for metastasis. Pro-inflammatory and pro-metastatic cytokines were profiled in post-mortem serum from a small number of the mice. ResultsPrimary tumour diameter was similar between groups. Lidocaine reduced lung metastatic colony count vs sevoflurane alone; median (inter-quartile range) 0 (0–2) compared with 22.5 (0–481), P=0.02 and reduced the proportion of animals with pulmonary metastasis (28.5% compared with 52.5%, P=0.04). In mice receiving ketamine-xylazine, lidocaine did not decrease the overall colony count: 60 (26–123) compared with 23.5 (0–225), P=0.43, but increased the proportion of animals with pulmonary metastasis (100% compared with 50%, P<0.01). Post-mortem serum analysis demonstrated reduced pro-inflammatory and angiogenic cytokine expression in animals without metastasis which received lidocaine with sevoflurane. ConclusionsIn this 4T1 murine model of breast cancer, lidocaine decreased pulmonary metastasis when combined with sevoflurane anaesthesia, perhaps via anti-inflammatory and anti-angiogenic effects. It had no such effect in mice given ketamine anaesthesia.

Cerebrospinal fluid Lyme multiplex assay results are not diagnostic in horses with neuroborreliosis.

BackgroundThe accuracy of the Lyme multiplex assay for the diagnosis of neuroborreliosis in horses is unknown.Hypothesis/ObjectivesTo describe Lyme multiplex results in horses with a postmortem diagnosis of neuroborreliosis. The hypothesis was that paired serum and cerebrospinal fluid (CSF) results and a CSF : serum ratio would allow differentiation of horses with neuroborreliosis from those with other neurologic diseases.AnimalsNinety horses that had neurologic examinations, serum and CSF Lyme multiplex analyses, and postmortem examination of the nervous system performed.MethodsRetrospective study. Data collected included signalment, ante‐ and postmortem diagnoses, and serum and CSF Lyme multiplex results. The CSF : serum ratio was calculated by dividing CSF median fluorescent intensity (MFI) by serum MFI for each result.ResultsTen horses had a final diagnosis of neuroborreliosis, 70 were diagnosed with other neurologic diseases, and 10 had no neurologic disease. Not all horses with neuroborreliosis had positive results: 4/10 had at least 1 positive serum result, 5/10 had at least 1 positive CSF result, and 3/10 had at least 1 CSF result 4‐fold higher than the corresponding serum result. Results were similar for the 70 horses with other neurologic diseases: 53% had at least 1 positive serum result, 50% had at least 1 positive CSF result, and 16% had at least 1 CSF result 4‐fold higher than the corresponding serum result.Conclusions and Clinical ImportancePositive Lyme multiplex results were common in horses with neurologic diseases and did not adequately differentiate horses with neuroborreliosis from horses with other disorders.

Post-mortem biochemistry of NSE and S100B: A supplemental tool for detecting a lethal traumatic brain injury?

PurposeTraumatic brain injury (TBI) is a very common entity that leads to numerous fatalities all over the world. Therefore, forensic pathologists are in desperate need of supplemental methodological tools for the diagnosis of TBI in everyday practice besides the standard autopsy. The present study determined post-mortem neuron specific enolase (NSE) and S100 calcium-binding protein B (S100B) levels as biological markers of an underlying TBI in autopsy cases. MethodsPaired serum and CSF samples of 92 fatalities were collected throughout routine autopsies. Afterwards, the marker levels were assessed using commercially available immunoassays (ECLIA, Roche Diagnostics). For statistical analysis, we compared the TBI cases to three control groups (sudden natural death by acute myocardial infarction, traumatic death without impact on the head, cerebral hypoxia). Moreover, the TBI cases were subdivided according to their survival time of the trauma. Brain specimens have been collected and stained immunohistochemically against the aforementioned proteins to illustrate their typical cellular staining patterns with an underlying TBI compared to non-TBI fatalities. Principal resultsCSF NSE and S100B levels were elevated after TBI compared to all control groups (p < 0.001). Although this finding can already be investigated among the TBI cases dying immediately subsequent to the trauma, the marker levels in CSF increase with longer survival times until a peak level within the first three days after trauma. There is a strong correlation between both marker levels in CSF (r = 0.67). The presence or absence of cerebral tissue contusion following the initial trauma does not seem to affect the CSF levels of both proteins (p > 0.05). Post-mortem serum levels of both proteins were not elevated in TBI cases compared to controls (p > 0.05). Former elaborated cut-off values in CSF were confirmed and were only exceeded when a TBI survival time of at least 30 min was reached. Major conclusionsThe present results report that post-mortem NSE and S100B CSF levels are significantly elevated subsequent to a fatal TBI.

Cardiac troponins and NT-proBNP in the forensic setting: Overview of sampling site, postmortem interval, cardiopulmonary resuscitation, and review of the literature

The possible use of biochemical markers in the postmortem diagnosis of myocardial ischemia is well known in the forensic setting, though several issues have limited its widespread adoption. The study presented herein focuses of N-terminal pro-B-type natriuretic peptide, troponin T, and troponin I, and the possible influence due to sampling site chosen, postmortem interval elapsed, and cardiopulmonary resuscitation attempts. Comparisons were performed between antemortem serum levels of these markers and postmortem levels measured in pericardial fluid and postmortem serum samples obtained from different sampling sites (n=16). Levels of these markers were also compared in cases characterized by various postmortem intervals (n=48, consisting of 24 ischemic heart disease cases and 24 controls) as well as in cases with and without cardiopulmonary resuscitation (n=22, consisting of 14 cases of hanging and 8 cases of drug intoxication). Our results indicate that N-terminal pro-B-type natriuretic peptide, troponin T, and troponin I values determined in postmortem serum from femoral blood (collected up to 24h after death) do not differ significantly from those measured in venous blood antemortem serum samples (collected at the upper limbs). In addition, our results reveal that the time elapsed after death should always be taken into consideration when cardiac troponins are measured in postmortem samples. Lastly, our findings reveal the absence of statistically significant differences between levels of the tested biomarkers (in postmortem serum from femoral blood) in cases without cardiopulmonary resuscitation compared to cases with cardiopulmonary resuscitation (at least for postmortem intervals up to 24h).

Postmortem biochemical investigation results in situations of fatal mechanical compression of the neck region.

Biochemical investigations performed in cases of mechanical asphyxia have provided diverging information over time. The purpose of the study presented herein was threefold: to investigate the postmortem stability of a series of molecules (thyroglobulin, iodothyronines, calcitonin, and parathyroid hormone) in blood after death, to determine the same molecules in a series of cases of suicidal hangings for which antemortem serum samples were available, and to measure the same molecules in postmortem serum obtained from different sampling sites thereby evaluating the distribution of these molecules in the specific samples. Preliminary results indicated postmortem stability of thyroglobulin, calcitonin, and parathyroid hormone levels, decreasing total and free T4 levels, and increasing total and free T3 concentrations. Our findings also showed that antemortem mechanical force applied to the neck region (hanging cases) may be accompanied by increased thyroglobulin in peripheral (femoral) blood, though a certain number of cases with nonincreased thyroglobulin levels may be observed. Lastly, our results revealed that hanging, manual, and ligature strangulation cases may be accompanied by increased thyroglobulin, total T3, and free T3 values in postmortem serum specimens obtained from blood sampled at different sampling sites, even in the absence of microscopically identified thyroid gland tissue damage. Such increases are more constant and important in arterial and venous blood samples obtained from sampling sites located in close vicinity of the thyroid gland.

Postmortem evaluation of cholesterol, triglyceride, and apolipoprotein levels.

Cholesterol and triglyceride levels have been analyzed in the forensic setting and their values correlated with atherosclerotic lesions found at autopsy and histology. Nevertheless, the results of these investigations have provided diverging information on postmortem molecule stability and postmortem measurement reliability. The aim of this study was to determine triglycerides, total cholesterol, low-density and high-density lipoprotein cholesterol, apolipoprotein B100, and apolipoprotein A-I in antemortem and postmortem serum samples in a series of cases (N=10, including cardiac and noncardiac deaths) that underwent forensic investigations and had both samples available, measure the same molecules in postmortem serum from femoral blood and pericardial and pleural fluids (N=39, including cardiac and noncardiac deaths), and evaluate whether different levels of these molecules could be observed in cases characterized by different degrees of coronary artery atherosclerosis (N=39, including cardiac and noncardiac deaths). Preliminary results indicated that total cholesterol and low-density and high-density lipoprotein cholesterol levels in postmortem serum samples tended to be lower than those in antemortem specimens, whereas triglyceride levels in postmortem serum samples tended to be higher than those in antemortem samples. No relationship could be found between postmortem serum and pericardial fluid levels or between postmortem serum and pleural fluid levels of all tested biomarkers. Lastly, cases characterized by severe coronary artery atherosclerosis revealed higher postmortem serum levels of total cholesterol and apolipoprotein B. Globally considered, these data confirm that femoral blood postmortem serum levels of cholesterol and apolipoproteins may be considered suitable to estimate their antemortem values in forensic cases characterized by coronary artery atherosclerosis.

Endocan concentrations in postmortem serum, vitreous humor and urine in victims of lethal 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.

Mediators of Inflammation in Asthma: A Forensic Perspective.

In the clinical setting, the role of systemic inflammation in patients with asthma has attracted increased attention, and some authors showed that increased IL-6 and high-sensitivity C-reactive protein characterized a group of asthmatic patients. In the realm of forensic pathology, a postmortem diagnosis of asthmatic death can be extremely challenging. The aim of this study was to determine the postmortem serum levels of C-reactive protein, IL-6, and tumor necrosis factor α in a series of severe acute bronchial asthma deaths that underwent medicolegal investigations. A total of 35 autopsy cases were retrospectively selected and included deaths in asthmatic subjects (related and unrelated to severe acute bronchial asthma, in situations characterized or not by systemic inflammation) as well as deaths in nonasthmatic individuals (in situations characterized or not by systemic inflammation). Our findings suggest that IL-6 is selectively increased in the systemic circulation of individuals with asthma, irrespective of whether the cause of death depends on a fatal asthma attack, compared with other biomarkers. Accordingly, postmortem serum IL-6 values in cases of death during severe acute bronchial asthma can be measured and considered of diagnostic relevance to estimate the magnitude of the systemic inflammation responses characterizing the disease.

Commentary: CSF and Plasma Testosterone in Attempted Suicide.

Commentary: CSF and Plasma Testosterone in Attempted Suicide.

Metabolic Characteristics of Lethal Bradycardia Induced by Myocardial Ischemia

To explore the metabolic characteristics of lethal bradycardia induced by myocardial ischemia in rat's serum. A rat myocardial ischemia-bradycardia-sudden cardiac death （MI-B-SCD） model was established, which was compared with the sham-operation group. The metabolic profile of postmortem serum was analyzed by gas chromatography-mass spectrometry （GC-MS）, coupled with the analysis of serum metabolic characteristics using metabolomics strategies. The serum metabolic profiles were significantly different between the MI-B-SCD rats and the control rats. Compared to the control rats, the MI-B-SCD rats had significantly higher levels of lysine, ornithine, purine, serine, alanine, urea and lactic acid; and significantly lower levels of succinate, hexadecanoic acid, 2-ketoadipic acid, glyceraldehyde, hexendioic acid and octanedioic acid in the serum. There were some correlations among different metabolites. There is obvious metabolic alterations in the serum of MI-B-SCD rat. Both lysine and purine have a high value in diagnosing MI-B-SCD. The results are expected to provide references for forensic and clinical applications of prevention and control of sudden cardiac death.

Postmortem Serum Tryptase Levels with Special Regard to Acute Cardiac Deaths.

An elevated serum tryptase concentration is considered a specific marker for systemic mast cell activation, a central feature of anaphylaxis. However, in some cases of acute cardiovascular death, high concentrations of serum tryptase are also observed. We compared the postmortem serum tryptase concentrations in 74 cases assigned to the following four groups: anaphylactic deaths (Group A, n = 20), acute cardiac deaths (Group ACD, n = 30), acute dissecting aneurysm ruptures (Group ADA, n = 10), and controls (Group C, n = 14). Additionally, the cutoff between Group A and the other groups was calculated using receiver-operating characteristic (ROC) curve analysis. Tryptase concentrations were markedly elevated in Group A (p < 0.001), Group ACD (p = 0.015), and Group ADA (p = 0.005). The optimal cutoff was 43 ng/mL, the sensitivity was 90%, and the specificity was 98%. While elevated concentrations of tryptase were noted in practical autopsy cases, due attention should be paid to the differential diagnosis between anaphylactic and acute cardiovascular deaths.

Commentary on the Paper of Thompson P. etal.: Phosphatidylethanol in Postmortem Brain and Serum Ethanol at Time of Death.

Alcohol: Clinical and Experimental ResearchVolume 41, Issue 3 p. 501-503 Commentary Commentary on the Paper of Thompson P. et al.: Phosphatidylethanol in Postmortem Brain and Serum Ethanol at Time of Death Wolfgang Weinmann, Wolfgang Weinmann Institute of Forensic Medicine , University of Bern, Bern, SwitzerlandSearch for more papers by this authorAlexandra Schröck, Alexandra Schröck Institute of Forensic Medicine , University of Bern, Bern, Switzerland Institute of Forensic Medicine , Kantonsspital Aarau, Aarau, SwitzerlandSearch for more papers by this authorFriedrich Martin Wurst, Corresponding Author Friedrich Martin Wurst [email protected] Paracelsus Medical University , Salzburg, Austria University of Basel, Basel, Switzerland Center for Interdisciplinary Addiction Research, University of Hamburg, Hamburg, GermanyReprint requests: Friedrich M. Wurst, Paracelsus Medical University, Strubergasse 21, 5020 Salzburg, Austria; E-mail: [email protected]Search for more papers by this author Wolfgang Weinmann, Wolfgang Weinmann Institute of Forensic Medicine , University of Bern, Bern, SwitzerlandSearch for more papers by this authorAlexandra Schröck, Alexandra Schröck Institute of Forensic Medicine , University of Bern, Bern, Switzerland Institute of Forensic Medicine , Kantonsspital Aarau, Aarau, SwitzerlandSearch for more papers by this authorFriedrich Martin Wurst, Corresponding Author Friedrich Martin Wurst [email protected] Paracelsus Medical University , Salzburg, Austria University of Basel, Basel, Switzerland Center for Interdisciplinary Addiction Research, University of Hamburg, Hamburg, GermanyReprint requests: Friedrich M. Wurst, Paracelsus Medical University, Strubergasse 21, 5020 Salzburg, Austria; E-mail: [email protected]Search for more papers by this author First published: 01 February 2017 https://doi.org/10.1111/acer.13319Citations: 2Read the full textAboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Citing Literature Volume41, Issue3March 2017Pages 501-503 RelatedInformation

Reliability of Post-mortem Biochemical Investigations after Fatal Traumatic Brain Injury

Objective: The aim was to test the reliability of former reported results of post-mortem laboratory investigations using cerebrospinal fluid (CSF) and serum levels of the biomarkers S100B and neuron specific enolase (NSE) to further evaluate the brain damage after fatal traumatic brain injuries. Methods: CSF and serum samples of 92 cases were collected during routine autopsies. The cases were divided into four groups regarding the causes of death in traumatic brain injury (TBI), isolated torso trauma, diffuse cerebral hypoxia and acute myocardial infarction. The samples were analysed using chemiluminescent immunoassays and the haemolytic index was quantified as internal control per sample (Roche Diagnostics). Results: There were significant differences in CSF values between TBI and all control cases (p<0.001), especially in comparison to fatal non-head injuries (p<0.05). Biochemical approaches in post-mortem serum are not suitable for both proteins. The marker levels increased with longer TBI survival time and peaked within the first three days after trauma. Former mentioned CSF cut-off values could be confirmed. Conclusion: Post-mortem investigations of CSF S100B and NSE can be declared a valuable tool in forensic practice since their levels indicate fatal TBI when empirically determined critical CSF values are reached.

Estimation of Postmortem Interval in Early Postmortem Period Using Serum Enzymes and its Correlation with Rigor Mortis and Postmortem Lividity

Determination of reasonably accurate time since death has a bearing on the issues of ‘alibi’ and ‘opportunity’. Post mortem interval is a critical step in most homicide or un-witnessed death investigations and remains one of the most challenging variables to establish. The present prospective study was designed to estimate time since death from postmortem serum enzyme levels and its correlation with rigor mortis and postmortem lividity. The sample group consisted of 127 cadavers from whom venous blood sample was collected at 6 hourly intervals and analyzed for SGOT, SGPT and Acid Phosphatase levels. The serum enzyme levels in individuals dying of different mechanisms were compared and a regression equation was derived to estimate time since death. From the equations derived, it was concluded that serum enzyme values can be a good indicator for determination of postmortem interval than that of routine parameters like rigor mortis and postmortem lividity.

Fatal intravenous injection of potassium: Is postmortem biochemistry useful for the diagnosis?

Fatal cases of potassium overdoses have traditionally been considered indemonstrable due postmortem biochemical investigation limits (mainly potassium determination in postmortem serum and vitreous humor). Nevertheless, some authors have expressed a divergent opinion over the years based on the results of their own investigations. In this study, we investigated left vitreous, right vitreous, postmortem serum from peripheral blood, postmortem serum from cardiac blood, urine, pericardial and cerebrospinal fluid potassium concentrations in 21 forensic autopsy cases. One of these was a case of accidental, fatal intravenous potassium injection in a hospitalized patient. The other twenty cases were subjects with various causes of death unrelated to potassium administration and comparable postmortem intervals. Our aim was to assess whether postmortem biochemical investigations performed in several biological samples may be useful in diagnosing exogenous potassium administration. No statistically significant differences were observed between the measured concentrations in the fatal case of potassium intravenous administration and the control cases in any of the tested samples. Potassium concentrations in the investigated case of exogenous potassium injection were within the range of those measured in the control cases, irrespective of the tested biological sample. Our findings corroborate the conclusions of former authors who highlighted that circumstantial evidence provides the greatest diagnostic contribution in situations of suspected potassium poisoning. This is due to the objective limitations demonstrated by postmortem biochemical investigations in such cases, even when potassium measurements are carried out in several biological samples of satisfying quality and within a relatively short postmortem interval.

Postmortem serum levels of IgE and mast cell tryptase in fatal asthma

The aim of this study was to characterize the concentrations of total and specific IgE as well as mast cell-derived tryptase in postmortem serum from femoral blood and evaluate the usefulness of their determination for diagnostic purposes in cases of fatal asthma attacks. 36 autopsy cases were retrospectively selected including cases of witnessed death in asthmatic subjects, deaths in asthmatics and atopic subjects with causes of death unrelated to asthma or allergic anaphylaxis as well as deaths in non-atopic, non-allergic individuals with causes of death unrelated to asthma or allergic anaphylaxis. Initial results indicated increased postmortem serum total IgE in atopic and asthmatic individuals, irrespective of the cause of death. Conversely, increased mast cell tryptase levels were noted exclusively in fatal asthma attacks. This suggests that mast cell tryptase measurement in cases of death potentially caused by severe acute bronchial asthma may be useful for diagnostic purposes.

Phosphatidylethanol in Postmortem Brain and Serum Ethanol at Time of Death.

Phosphatidylethanol (PEth) is a metabolite of ethanol (EtOH), and its concentration in whole blood samples is a direct biomarker of alcohol consumption. Because PEth is also present in the brain and incorporated in lipid membranes, it can be used to classify deceased individuals on alcohol consumption status at the time of death. The purpose of this study was to detect PEth homologs in postmortem brains of individuals known to have had alcohol use disorder (AUD) and to determine the relationship between serum alcohol at the time of death and PEth in the cerebellum (CE) and orbital frontal cortex (OFC). Postmortem brain was collected and stored according to standard protocol. Psychiatric symptoms experienced prior to death were obtained by next of kin psychological autopsy to categorize subjects. Thirty male subjects were chosen for analyses: 10 with AUD with positive serum EtOH levels present at time of autopsy (AUD-W), 10 with AUD without positive serum EtOH levels (AUD-WO), and 10 controls. PEth 16:0/18:1 and 16:0/18:2 were quantified in 50mg of CE and OFC of human postmortem brain using HPLC and mass spectrometric detection (triple quadrupole). Results of this study were as follows: (i) PEth 16:0/18:1 and 16:0/18:2 were detected in the CE and OFC of all subjects diagnosed with AUD, (ii) PEth 16:0/18:1 levels were about 10-fold higher than PEth 16:0/18:2 in all subjects and both areas of brain, (iii) AUD-W subjects had higher PEth homolog levels in CE and OFC than controls and AUD-WO subjects, (iv) PEth 16:0/18:1, but not PEth 16:0/18:2, levels in CE and OFC of AUD-W subjects correlated significantly with serum EtOH levels at the time of death. Quantification of combined PEth homolog levels in postmortem human brain is a good candidate as a diagnostic factor to classify drinking status, especially for those with AUD at the time of death. For alcohol research studies with postmortem brain, verification of drinking status is essential.