ABSTRACT
Drug levels in decomposed individuals are difficult to interpret. Concentrations of 16 drugs were monitored in tissues (blood, brain, liver, kidney, muscle, and soil) from decomposing pigs for 1 week. Pigs were divided into groups (n = 5) with each group receiving four drugs. Drug cocktails were prepared from pharmaceutical formulations. Intracardiac pentobarbital sacrifice was 4 h after dosing, with tissue collection at 4, 24, 48, 96, and 168 h postdosing. Samples were frozen until assay. Detection and quantitation of drugs were through solid phase extraction followed by gas chromatograph/mass spectrometer analysis. Brain and kidneys were not available after 48 h; liver and muscle persisted for 1 week. Concentration of drugs increased during decomposition. During 1 week of decomposition, muscle showed average levels increasing but concentrations in liver were increased many fold, compared to muscle. Attempting to interpret drug levels in decomposed bodies may lead to incorrect conclusions about cause and manner of death.
Subject(s)
Pharmaceutical Preparations/analysis , Pharmacokinetics , Postmortem Changes , Animals , Brain Chemistry , Forensic Toxicology , Gas Chromatography-Mass Spectrometry , Kidney/chemistry , Liver/chemistry , Muscle, Skeletal/chemistry , Soil/chemistry , Swine , Time Factors , Tissue DistributionABSTRACT
Idiopathic hypereosinophilic syndrome is a rare systemic disease with an unexplained elevated eosinophil count. Loffler endomyocarditis is hypereosinophilic syndrome with endocardial fibrosis and restrictive cardiomyopathy. The atrioventricular valves are frequently involved, causing valvular regurgitation. Previously, there has been one case report of combined aortic and mitral valve involvement with Loffler endomyocarditis that was treated with bivalvular replacement. We describe a previously healthy 50-year-old man diagnosed with Loffler endomyocarditis complicated by peripheral thromboembolism and severe aortic regurgitation due to valve fibrosis and fibrotic vegetation on the aortic valve. He underwent embolectomy and aortic valve replacement in addition to treatment for his hypereosinophilia. He later presented with cardiomyopathy with severe aortic insufficiency due to the destruction of the aortic valve prosthesis by sterile fibrinous vegetation. To our knowledge, this is the second case in the literature in which Loffler endomyocarditis involves the aortic valve and the first patient in whom only the aortic valve is involved.
