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At least 145 records · Page 8Linked to original sources
PubMed2000

Toxicology and pathology of deaths related to methadone: retrospective review.

OBJECTIVES: To clarify the mechanisms and risk factors of methadone toxicity and to describe the findings of deaths related to methadone use Design Retrospective review of case notes in the records of the San Francisco Medical Examiner comparing the findings in cases where methadone was deemed the cause of death with findings in decedents where methadone was an incidental finding, and with 50 age-matched, disease and drug free, trauma victims. RESULTS: 38 cases out of the 3317 processed by our office during 1997-1998 were identified in which methadone had been detected. Cases were mostly male 28/38 (74%) and white, 28/38 (74%). In 17 of 38 cases death was deemed to have been caused by methadone toxicity. For the group the mean blood methadone concentration for all 38 patients, was 957 ng/ml SD = .681, SE = .14). The mean blood concentration of the main methadone metabolite (EDDP) was 253 ng/ml, SD = 529 ng/ml, SE = .089. The mean ratio of methadone in the blood to EDDP in the blood was 13.6:1 Values were not significantly different between cases in which methadone toxicity was the cause of death and in those in which it was an incidental finding. Cocaine, or the cocaine metabolite benzoylecgonine, was detected in the blood or urine of 16/38 cases (42%); morphine in one-third (13/38) and methamphetamine in only one. Pulmonary edema was evident in all cases, coronary artery disease in 9/38 (24%) and cirrhosis in 7/38 (18%) of the methadone users. Necrotizing fasciitis was the cause of death in 4 of the 38 methadone users (11%). Nationally, a sizeable percent of methadone deaths are from drugs diverted from treatment programs. CONCLUSIONS: The presence of methadone is often an incidental finding during postmortem examination which is unrelated to the cause of death. Postmortem measurements of methadone or its metabolite, or both, cannot be used in isolation to identify which deaths are associated with methadone toxicity.

Adult↗
PubMed1987

The role of conventional pathology and toxicology in evaluating the immunotoxic potential of xenobiotics.

Investigating the immunotoxic potential of candidate drugs as part of a preclinical safety evaluation poses several problems. These include the need for practical, validated tests, the difficulty in establishing the toxicologic significance of positive findings, and a poor understanding of the predictive value such findings hold for drug effects in man. A key component of this investigation is the toxicologic profile generated through preclinical toxicity and safety studies. As this "routine" assessment becomes increasingly comprehensive and sophisticated, most toxicologically significant drug-associated effects are revealed. Such findings may serve as "triggers" for investigating possible immune mechanisms. Decisions to test specifically for immunotoxicity may also be influenced by the molecular structure and pharmacologic profile of the compound, as well as the intended use of the drug. Examples of such indications and follow-up studies are discussed in this review. We are presently poorly equipped to effectively screen drugs indiscriminately for an immunotoxic potential. We are better prepared, however, to investigate whether a drug-associated change is due to an adverse effect on the immune system. This problem-oriented approach to immunotoxicology challenges us as diagnosticians and immunopathologists, and requires a close working relationship among the toxicologic pathologist, the basic immunologist, the immunopharmacologist, and the clinician.

Animals↗
PubMedDate not supplied

The pathologist and toxicologist in pharmaceutical product discovery.

Significant change is occurring in the drug discovery paradigm; many companies are utilizing dedicated groups from the toxicology/ pathology disciplines to support early stage activities. The goal is to improve the efficiency of the discovery process for selecting a successful clinical candidate. Toxicity can be predicted by leveraging molecular techniques via rapid high-throughput, low-resource in vitro and in vivo test systems. Several important activities help create a platform to support rapid development of a new molecular entity. The proceedings of this symposium provide excellent examples of these applied concepts in pharmaceutical research and development. Leading biopharmaceutical companies recognize that a competitive advantage can be maintained via rapid characterization of animal models, the cellular identification of therapeutic targets, and improved sensitivity of efficacy assessment. The participation of the molecular pathologist in this quest is evolving rapidly, as evidenced by the growing number of pathologists that interact with drug discovery organizations.

Animals↗
PubMed1988

A pathologic and toxicologic evaluation of veal calves fed large amounts of zinc.

Tissues were examined from 26 male Holstein veal calves given large amounts of dietary zinc. All calves had been fed 706 micrograms zinc/g of milk replacer for 28 days before the first death occurred. Calves died naturally (14, group A) or were euthanatized (12, group B) after 23 days of feeding a lower concentration of zinc (150 micrograms/g). Average amounts of zinc in liver (wet weight) were 345.72 micrograms/g (group A) and 344.84 micrograms/g (group B). Mean kidney zinc concentrations were 219.0 micrograms/g (group A) and 252.38 micrograms/g (group B). Tissue manganese, copper, and iron levels were normal. Changes at necropsy included pneumonia, fluid digesta, and petechiae and infarcts in liver, kidney, and heart (as a result of bacterial infections). Histological changes that were directly attributed to dietary zinc intake were: marked atrophy and necrosis of pancreatic acinar tissue (group A); multifocal fibrosis of pancreatic acini (group B); multifocal renal cortical fibrosis with necrosis in convoluted tubules and loops of Henle, and with intratubular mineralization (groups A and B). Hepatic midzonal mineralization and fibrosis of the adrenal zona glomerulosa were seen in group B calves.

Animal Feed↗
PubMed1992

[Acute lead poisoning in calves: clinical, pathological and toxicological findings].

We present a case of acute lead poisoning in 10 calves. All calves died with few or no clinical signs prior to death. The clinical signs included neurologic and gastrointestinal symptoms but were of an unspecific nature. Several painted iron girders, stored on a field close to the farm, were determined as the source of the poisoning. Postmortem findings were minimal. Some animals presented acid-fast, intranuclear inclusion bodies in the renal tubules. A chemical analysis of some frozen parts of the liver and kidney revealed levels of lead as high as 12 ppm in the liver and 63 ppm in the kidney on a wet-weight basis. This article discusses the etiology, clinical signs, postmortem findings and diagnosis of lead poisoning in calves with special emphasis on the chemical analysis.

Acute Disease↗