A Decline in 2 Consecutive Postmortem Serum Tryptase Levels in an Anaphylactic Death

Anne, S.; Tse, Rexson; Cala, Allan

doi:10.1097/paf.0000000000000185

Cited by 21 publications

(15 citation statements)

References 12 publications

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“…It must be pointed out that elevated levels of tryptase may be present in the circulation for several hours. Aortic postmortem tryptase measurements can be of value as soon as possible after death in cases where Kounis syndrome is suspected [101]. Histamine release from mast cells is rapid and short lived and circulates for only about 8 min after an allergic event, therefore blood samples should be collected immediate after the onset of chest pain and before any analgesic, especially morphine, administration [102].…”

Section: Diagnosismentioning

confidence: 99%

Kounis syndrome: an update on epidemiology, pathogenesis, diagnosis and therapeutic management

Kounis¹

2016

Clinical Chemistry and Laboratory Medicine (CCLM)

310

421

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Kounis syndrome has been established as a hypersensitivity coronary disorder induced by various conditions, drugs, environmental exposures, foods and coronary stents. Allergic, hypersensitivity, anaphylactic and anaphylactoid reactions are associated with this syndrome. Vasospastic allergic angina, allergic myocardial infarction and stent thrombosis with occluding thrombus infiltrated by eosinophils and/or mast cells constitute are the three reported, so far, variants of this syndrome. Apart from coronary arteries, it affects the cerebral and mesenteric arteries. Its manifestations are broadening and its etiology is continuously increasing. Kounis syndrome is a ubiquitous disease which represents a magnificent natural paradigm and nature's own experiment in a final trigger pathway implicated in cases of coronary artery spasm and plaque rupture. Kounis syndrome seems to be not a rare disease but an infrequently diagnosed clinical entity which has revealed that the same mediators released from the same inflammatory cells are also present and in acute coronary events of non allergic etiology. These cells are not only present in the culprit region before plaque erosion or rupture but they release their contents just before an actual coronary event. Therefore, awareness of etiology, epidemiology, pathogenesis and clinical manifestations seems to be important for its prognosis, diagnosis, treatment, prevention.

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Section: Diagnosismentioning

confidence: 99%

Kounis syndrome: an update on epidemiology, pathogenesis, diagnosis and therapeutic management

Kounis¹

2016

Clinical Chemistry and Laboratory Medicine (CCLM)

310

421

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“… 11 presented a case of an anaphylactic death with initially increased values which subsequently decreased; another similar case was reported by Sravan et al . 12 . This may have been due to a degradation of the released hormones 12 or just reflected the clinical development after anaphylaxis 38 .…”

Section: Discussionmentioning

confidence: 99%

“…However, there are, unrelated to the cause of death, hardly any published research attempts investigating the intra-individual stability of markers used in forensic medicine by serial peripheral venous blood measurements in the same body after the onset of death. Very few existing studies address the small number of biochemical markers of sepsis and anaphylaxis 8 – 12 , and myoglobin 13 in post-mortem serum; there remain many organ systems whose characteristic markers have not been evaluated considering intra-individual changes after death.…”

Section: Introductionmentioning

confidence: 99%

Intra-individual alterations of serum markers routinely used in forensic pathology depending on increasing post-mortem interval

Woydt

Bernhard

Kirsten³

et al. 2018

Sci Rep

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Post-mortem biochemistry of serum markers has been the subject of numerous studies, but in-situ marker stability after death has not been sufficiently evaluated yet. Such laboratory analyses are especially necessary in the cases of functional deaths without morphological evidence of the death causes and also in cardiac death cases with only very short survival times. The aim of the study was to determine the post-mortem stability of commonly-used serum markers at predefined time points. In 20 cases, peripheral venous samples were taken starting immediately after circulatory arrest and ending 48 hours after death. Serum creatinine, urea, 3-β-hydroxybutyrate, tryptase, myoglobin, troponin T, creatin kinase and creatin kinase-MB have been included. For all markers, we observed increasing marker levels for longer post-mortem intervals. Significant marker level changes began two hours after death. Excessive increases were observed for cardiac and muscle markers. Marker levels showed high intra-assay precision. Furthermore, the markers were robust enough to withstand freeze-thaw cycles. Potential contamination of arteriovenous blood did not influence the post-mortem marker levels. Post-mortem blood should be sampled as soon as possible, as increased post-mortem intervals may heavily change marker levels in-situ in individual cases, whereas the markers are mostly unaffected by laboratory conditions.

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“…Indeed, mast cell tryptase levels can be assessed in postmortem serum even days after death and significantly increased postmortem serum tryptase levels have been reported repeatedly in cases of fatal anaphylaxis (26,44-47,50,51). …”

Section: Discussionmentioning

confidence: 99%

“…Moreover, beyond cases of fatal anaphylaxis, increased levels of postmortem serum tryptase have been observed in subjects with causes of death unrelated to anaphylaxis. This leads to the conclusion that postmortem, straightforward diagnoses of anaphylaxis cannot be exclusively based on mast cell tryptase determination alone (26,44,45,51-58). …”

Section: Discussionmentioning

confidence: 99%

Vaccination and anaphylaxis: a forensic perspective

2017

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AimTo review the available literature pertaining to fatalities following vaccine administration and, in particular, cases of vaccine-related fatal anaphylaxis.MethodThe MEDLINE database was systematically searched up to March 2016 to identify all relevant articles pertaining to fatal cases of anaphylaxis following vaccine administration.ResultsSix papers pertaining to fatal anaphylaxis following vaccination were found relevant. Mast cell tryptase and total IgE concentration was assessed exclusively in one case. Laryngeal edema was not detected in any of these cases, whereas eosinophil or mast cell infiltration was observed in lymphoid organs. In one case, immunohistochemical investigations using anti-tryptase antibodies allowed pulmonary mast cells and degranulating mast cells with tryptase-positive material outside to be identified.ConclusionIn any suspected IgE-mediated fatal anaphylactic cases, biochemical investigations should be systematically performed for forensic purposes. Splenic tissue should be routinely sampled for immunohistochemical investigations in all suspected anaphylaxis-related deaths and mast cell/eosinophil infiltrations should be systematically sought out in the spleen, myocardium, and coronary artery wall. The hypothesis of fatal anaphylaxis following vaccination should be formulated exclusively when circumstantial data, available medical records, laboratory investigations, and autopsy or histology findings converge in a consistent pattern. The reasonable exclusion of alternative causes of death after all postmortem investigations is also imperative in order to establish or rule out a cause-and-effect relationship between vaccine administration and any presumptive temporarily-related death.

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A Decline in 2 Consecutive Postmortem Serum Tryptase Levels in an Anaphylactic Death

Cited by 21 publications

References 12 publications

Kounis syndrome: an update on epidemiology, pathogenesis, diagnosis and therapeutic management

Kounis syndrome: an update on epidemiology, pathogenesis, diagnosis and therapeutic management

Intra-individual alterations of serum markers routinely used in forensic pathology depending on increasing post-mortem interval

Vaccination and anaphylaxis: a forensic perspective

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