ABSTRACT
Los problemas sanitarios por el consumo crónico de sustancias de abuso, se han transformado en problemas médico-legales en los últimos 10 años. Entre estos se destaca el Delirium Agitado Fatal por Cocaína, cuadro idiosincrático que deviene luego de 1 a 2 horas de una ingesta habitual y que puede causar la muerte sin que se detecte sobredosis en la autopsia. Esta revisión tiene como objetivo estudiar los cambios moleculares que provoca el consumo crónico de cocaína vinculados con el Delirium Agitado Fatal por Cocaína. La correlación molecular-clínica permite vincular los fenómenos inducidos por el consumo abusivo que se expresan en los distintos niveles de complejidad, desde lo bioquímico a lo social. De esta forma se pretende inducir un mayor conocimiento de este cuadro a fin mejorar su prevención, su diagnóstico temprano y su abordaje terapéutico-legal. En suma, el Delirium Agitado Fatal por Cocaína debe ser considerado como la consecuencia de varias modificaciones inadvertidas que, alcanzado un umbral crítico desencadena el cuadro fatal. Esto hace al consumo abusivo de cocaína y a la predisposición individual los únicos responsables de su aparición.
In the past 10 years, chronic drug abuse health problems have become complex medical-legal problems. These include Cocaine-Induced Agitated Delirium, an idiosyncratic illness appears 1-2 hours after regular drug intake and can cause death without overdose is detected at autopsy. This review studies the molecular changes caused by cocaine abuse that derived into Cocaine-Induced Agitated Delirium. The molecular-clinical correlation links the phenomena induced by the abuse expressed at different levels of complexity, from the biochemical to the social. The purpose here is to induce a greater awareness of this illness to improve its prevention, to obtain its early diagnosis and to achieve its appropriate therapeutic-legal approach. Cocaine-Induced Agitated Delirium should be considered as the result of several unseen changes, that if they reach a critical threshold trigger the fatal outcome. This makes the abuse of cocaine and the individual predisposition solely responsible for its appearance.
Subject(s)
Humans , Delirium/history , Delirium/chemically induced , Cocaine-Related Disorders/complications , Delirium/diagnosis , Delirium/prevention & control , Delirium/therapy , Forensic ToxicologyABSTRACT
To evaluate the risk factors involved in antituberculosis treatment-induced hepatotoxicity. In a retrospective study we analyzed the rate of drug-induced hepatotoxicity in a sample of 456 patients. Patients received a combination of drugs including isoniazid, rifampin, pirazinamide and streptomycinor or ethambutol. The association among hepatotoxicity and several risk factors (age, sex, alcoholism and HIV infection) was studied by univariate methods, stratified analysis and the multiple logistic regression model. Signs of liver injury were found in 9.86 percent of the treated patients. In the logistic model, the adjusted odds ratios (OR) and significance were found as follows: a) for alcoholism, OR=17.31 (95 percent CI:6.35-47.16), p<0.001; b) for HIV infection, OR=3.23 (95 percent CI:1.47-7.11), p=0.003 and c) for female Sex, OR=2.44 (95 percent CI:1.22-4.86), p=0.011. Age was not significantly associated with hepatotoxicity. Alcoholism, HIV infection and female sex were associated with an increased risk of hepatotoxicity in this study.