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- Edston, Erik, 1948-, et al.
(author)
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Death in anaphylaxis in a man with house dust mite allergy
- 2003
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In: International journal of legal medicine. - : Springer Science and Business Media LLC. - 0937-9827 .- 1437-1596. ; 117:5, s. 299-301
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Journal article (peer-reviewed)abstract
- Up to recently the post-mortem diagnosis of anaphylaxis has been based solely on circumstantial evidence. With the development of assays for mast cell tryptase it is now possible to verify cases of suspected anaphylaxis. Here we present one such case, which initially appeared to be due to sudden death of unknown cause. A 47-year-old farmer was found dead in his bathroom around midnight. Hospital records revealed that he had previously been diagnosed with an allergy to house dust mites. He had also had infrequent episodes of airway symptoms, nausea, hypotension and diarrhoea usually after going to bed. The forensic autopsy did not give any clue to the cause of death. Serum tryptase in post-mortem blood was found to be substantially elevated in two samples (170 and >200 ╡g/L). Analysis of allergen-specific IgE showed high values for Dermatophagoides pteronyssinus and farinae. High mite allergen levels were found in dust obtained from the patient's mattress. The results of the immunological tests support the assumption that he died of anaphylactic shock. The circumstances and the patient's history of previous attacks after going to bed point to the fact that exposure to mite contaminated food and/or exposure to mite allergens in bed might have caused his death.
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| 3. |
- Edston, Erik, 1948-, et al.
(author)
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Mast cell tryptase and hemolysis after trauma
- 2003
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In: Forensic Science International. - 0379-0738 .- 1872-6283. ; 131:1
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Journal article (peer-reviewed)abstract
- Background: We have previously found increased mast cell tryptase in accidental deaths due to trauma, indicating that mast cell degranulation had occurred. The present study was designed to confirm the previous observation and to determine if tryptase release after trauma is acute or delayed. Furthermore, the importance of hemolysis and direct trauma to the mast cells was investigated. Materials and methods: Mast cell tryptase was measured in post-mortem blood from the femoral vein in 27 cases of death from trauma and in 27 control cases by means of a commercially available immunoassay. The trauma cases were further classified into groups with single versus multiple trauma, and groups with short survival time (i.e. death at the scene of the accident) versus longer survival time (death in hospital). In five multi-trauma deaths, blood was sampled locally from the sites of crush injury. Results: The mean value of tryptase in femoral vein blood was 35.6▒34.6╡g/l in the entire trauma group and 14.7▒6.5╡g/l in the controls (P<0.005). In bloody liquid sampled from crush injuries, tryptase was substantially elevated in all cases, with a mean of 227▒146╡g/l. In cases with short survival time, tryptase was significantly higher than in those who died after several hours or days in hospital (P<0.001). No statistically significant difference was seen between multi- and single-trauma cases. A correlation between hemolysis in the samples and elevated tryptase was found only in the trauma cases (P<0.05), but experimentally induced hemolysis in vitro was not found to influence the measurements. Conclusion: Mast cell tryptase becomes elevated in trauma deaths and this seems to be ascribable either to direct mechanical injury to tissue mast cells and/or to cell lysis. In patients initially surviving severe injuries, the effects of massive release of histamine and other mast cell mediators might be of importance for treatment strategies and prognosis.
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| 4. |
- Edston, Erik, 1948-, et al.
(author)
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Postmortem measurements of thyroid hormones in blood and vitreous humor combined with histology
- 2001
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In: American Journal of Forensic Medicine and Pathology. - : Ovid Technologies (Wolters Kluwer Health). - 0195-7910 .- 1533-404X. ; 22:1, s. 78-83
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Journal article (peer-reviewed)abstract
- The aim of this study was to investigate whether clinical reference premortem values can be used to assess postmortem concentrations of thyroxine, triiodothyronine, and thyroid stimulating hormone (TSH), to compare the postmortem concentrations in blood and vitreous humor, and to study the possibility of diagnosing hyperthyroidism by comparing thyroid histologic appearance and postmortem hormone values. Biochemical analyses of free thyroxine (FT4), free triiodothyronine (FT3), and TSH in femoral blood and vitreous humor were made in 38 cases. In 40 cases, the hormones and thyroid histologic appearance were studied, 22 had no significant pathologic changes, and 18 showed focal hyperplasia of the follicular epithelium. A positive correlation was seen between the femoral blood and vitreous humor concentrations of FT4 (R = 0.66) but not between the corresponding concentrations of FT3 and TSH. A positive correlation was also seen between FT3 and FT4 in femoral blood (R = 0.74). In cases with normal thyroid histologic appearance, 58% were found to have FT4 values >24 pmol/L (clinical reference interval 9-24 pmol/L), mean value 27.5 ▒ 9.4 pmol/L), which did not differ from the FT4 values in the cases with hyperplasia, 31.6 ▒ 15 pmol/L. Only 5% of the T3 measurements in the group with normal histologic appearance were >9 pmol/L (clinical reference interval 3-9 pmol/L). The mean value of FT3 in cases with normal histologic appearance was 3.4 ▒ 1.3 pmol/L, and in the group with hyperplasia 8.6 ▒ 6.1 pmol/L. The difference was statistically significant P < .005). It is concluded that postmortem values of FT3 and FT4 in femoral blood are fairly comparable to premortem clinical reference values, but the upper normal limit, especially for T4. has to be adjusted upward. Analysis of vitreous humor cannot be used post mortem to assess thyroid function. Histologically, hyperplastic changes correlate well with elevated FT3 in femoral blood.
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| 6. |
- Wang, Jianpu, 1957-, et al.
(author)
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Effects of endothelin receptor antagonism on acute lung injury induced by chlorine gas
- 2006
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In: Critical Care Medicine. - 0090-3493 .- 1530-0293. ; 34:6, s. 1731-1737
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Journal article (peer-reviewed)abstract
- OBJECTIVE: To test the hypothesis that the endothelin system is involved in chlorine gas-induced lung injury.DESIGN: Experimental study.SETTING: Academic research laboratory.SUBJECTS: Twenty-four domestic juvenile pigs.INTERVENTIONS: Anesthetized, ventilated pigs were exposed to chlorine gas (400 parts per million in air) for 20 mins and then randomly allocated to four groups (n = 6 in each group). The tezosentan pretreatment group received the dual endothelin receptor antagonist tezosentan 20 mins before and hyperoxic gas (Fio2 0.6) after chlorine gas exposure. The tezosentan postinjury treatment group received hyperoxic gas after chlorine gas exposure and tezosentan 60 mins later. Animals in the oxygen group received hyperoxic gas after chlorine gas exposure. Pigs in the fourth group (air) were ventilated with room air (Fio2 0.21) throughout the experiment.MEASUREMENTS AND MAIN RESULTS: Hemodynamics, gas exchange, lung mechanics, and plasma endothelin-1 were evaluated for 6 hrs. Chlorine gas exposure induced an increase in circulating endothelin-1 by 90% (p < .05). The acute chlorine gas-induced rise in pulmonary vascular resistance was partly blocked by tezosentan pretreatment (p < .001). Tezosentan postinjury treatment also decreased pulmonary vascular resistance to levels significantly lower than in the air and oxygen groups (p < .001). Recovery of peak airway pressure was better in the tezosentan-treated groups than in the air group. There were significant linear relationships between circulating endothelin-1 and pulmonary vascular resistance (r = .47, p < .001) and endothelin-1 and peak airway pressure (r = .41, p < .001). These relationships were modified by tezosentan.CONCLUSIONS: Tezosentan modified chlorine gas-induced pulmonary dysfunction, indicating that the endothelin system is involved in this mode of acute lung injury.
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