Pulmonary edema in fatal heroin overdose: immunohistological investigations with IgE, collagen IV and laminin - no increase of defects of alveolar-capillary membranes
R. Dettmeyer et al., Pulmonary edema in fatal heroin overdose: immunohistological investigations with IgE, collagen IV and laminin - no increase of defects of alveolar-capillary membranes, FOREN SCI I, 110(2), 2000, pp. 87-96
Pulmonary edema complicating heroin overdosage is a well recognized entity
and regarded as the major mechanism contributing to death in heroin addicts
. It's pathogenesis is unknown, several mechanisms are discussed: hypoxia-i
nduced increase of pulmonary capillary permeability, depressed myocardial c
ontractility, centrally induced respiratory depression, primary toxic effec
ts on the alveolar capillaries and acute anaphylactic shock. The present st
udy included opiate-related deaths (n = 23) and a control group of sudden c
ardiovascular deaths (n = 12) to verify the hypothesis, that defects of the
alveolar capillary membranes and/or an acute anaphylactic reaction leads t
o pulmonary congestion, edema and hemorrhages. Lung specimens were obtained
from these 35 autopsies of persons autopsied in the Institute of Forensic
Medicine, University of Bonn, in 1997 and 1998. All specimens were examined
with hematoxylin-eosin, prussian blue and investigated with immunohistolog
ical methods using primary antibodies against collagen IV, laminin and IgE.
Defects of the basal laminae of the alveoli were found, demonstrated by la
minin and collagen IV, and the number of IgE-positive cells was counted in
both groups. There was an increased but not significant number of IgE-posit
ive cells in the heroin-group and defects of the epithelial and endothelial
basal laminae were found in both groups without significant differences. (
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