Allergic and pathologic findings in fifty insect-sting fatalities

Barnard, James H.

doi:10.1016/0021-8707(67)90104-9

Cited by 40 publications

(10 citation statements)

References 9 publications

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“…Allergy to bee venom is an extreme example of immediate-type hypersensitivity which may be fatal (Barnard, 1973), and interest in the antigenic properties of the high molecular weight protein constituents, phospholipase A 2 and hyaluronidase, dates back to 1956, when Habermann and El Karemi demonstrated the presence of antibodies that neutralised these two enzymes in rabbits immunised by bee venom. Allergy to bee venom is an extreme example of immediate-type hypersensitivity which may be fatal (Barnard, 1973), and interest in the antigenic properties of the high molecular weight protein constituents, phospholipase A 2 and hyaluronidase, dates back to 1956, when Habermann and El Karemi demonstrated the presence of antibodies that neutralised these two enzymes in rabbits immunised by bee venom.…”

Section: Immunologymentioning

confidence: 99%

Chemistry and Pharmacology of Honey-bee Venom

Banks

Shipolini

1986

Venoms of the Hymenoptera

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Section: Immunologymentioning

confidence: 99%

Chemistry and Pharmacology of Honey-bee Venom

Banks

Shipolini

1986

Venoms of the Hymenoptera

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“…Since these reactions are usually unexpected and occasionally fatal, opportunities to investigate systematically the detailed pathophysiology with controlled studies are exceedingly rare. Most of the available data concerning the pathophysiology and treatment ofhuman anaphylaxis are derived from anecodotal clinical case reports and postmortem studies (1)(2)(3)(4)(5).…”

mentioning

confidence: 99%

Physiologic manifestations of human anaphylaxis.

Smith¹,

Kagey‐Sobotka²,

Bleecker³

et al. 1980

J. Clin. Invest.

353

141

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A B S T R A C T In the course of a controlled study to evaluate different forms of immunotherapy for subjects with insect-sting hypersensitivity, we observed 11 subjects who had systemic cutaneous urticarial reactions and 3 subjects who experienced systemic anaphylaxis. With the exception of tachyeardia, there were no cardiopulmonary changes in the subjects with urticaria, whereas the major manifestation of anaphylactic shock in the other three subjects was severe hypotension that was probably secondary to peripheral vasodilation. Significant abnormalities in gas exchange developed in two subjects. In one, bronchospasm precipitated a respiratory arrest followed by endotracheal intubation with mechanical ventilation. Although plasma histamine levels were not related to the development of cutaneous reactions, the plasma histamine levels correlated with the severity and duration of the cardiopulmonary changes observed during anaphylactic shock. The two subjects with the most severe shock showed evidence of intravascular coagulation characterized by a diminution of Factor V, Factor VIII, fibrinogen, and high molecular weight kininogen, as well as changes in components of the complement system. Standard therapy with epinephrine and fluids, usually recommended for the treatment of systemic anaphylaxis, did not immediately reverse either the hemodynamic or the respiratory abnormalities in the two subjects with the most severe

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“…(Barnard, 1967;Da Broi & Moreschi, 2011;Delage & Irey, 1972;Di Maio & Di Maio, 2001;Edston & van Hage-Hamsten, 2005;James & Austen, 1964;Low & Stables, 2006;Lu et al, 2006;Menchel et al, 1987;Pumphrey & Roberts, 2000;Shen et al,2009;Yilmaz et al, 2009). You can find:  glottis edema and/or of the pharyngo-laryngeal districts;  congestion and/or pulmonary edema;  hyperinflation of the alveoli with acute emphysema;  endo-luminal bronchial secretions-this finding is more frequent if there's an asthmatic factor and it's usually related to a almost immediate death;  hemorrhagic petechiae: it's suggestive of an asphyxial component of the death and it's usually associated with an almost immediate death.…”

Section: Complete Necroscopic Exammentioning

confidence: 99%