CONTEXT: Hepatotoxicity is a potential complication from the usage of various illicit drugs, possibly consequent to their liver metabolism, but information on this is scarce in the medical literature. OBJECTIVE:To study the occurrence of clinical and laboratory hepatic alterations in chronic marijuana users, from the use of marijuana on its own or in association with other legal or illicit drugs. TYPE OF STUDY: transversal studySETTING: Hospital Espírita de Marília, Marília, São Paulo, Brazil PARTICIPANTS:The study was made among 123 patients interned in the Hospital Espírita de Marília from October 1996 to December 1998, divided into 3 groups: 26 (21%) using only marijuana, 83 (67.5%) using marijuana and crack, and 14 (11.4%) consuming marijuana and alcohol. PROCEDURES AND MAIN MEASUREMENTS:Patients were examined clinically with special emphasis on types of drugs used, drug intake route, age when consumption began, length and pattern of usage, presence of tattooing, jaundice, hepatomegaly and splenomegaly. Serum determinations of total proteins, albumin, globulin, total and fractions of bilirubin, aspartate (AST) and alanine (ALT) aminotransferases, alkaline phosphatase (AP), gamma-glutamyltransferase and prothrombin activity were performed. RESULTS:Among users of only marijuana, hepatomegaly was observed in 57.7% and splenomegaly in 73.1%, and slightly elevated AST (42.3%), ALT (34.6%) and AP (53.8%). The three groups did not differ significantly in the prevalence of hepatomegaly, splenomegaly and hepatosplenomegaly. The group using both marijuana and alcohol showed the highest prevalence of alterations and highest levels of aminotransferases. Mean AP levels were above normal in all groups. CONCLUSIONS:Chronic marijuana usage, on its own or in association with other drugs, was associated with hepatic morphologic and enzymatic alterations. This indicates that cannabinoids are possible hepatotoxic substances.
In men and women, abusive ingestion of alcohol is associated with arterial hypertension [1][2][3] , cardiac arrhythmias 4 , and cardiac muscle impairment with several structural and functional abnormalities [5][6][7][8] . Myocardial lesions are expected to occur when the daily alcohol consumption is greater than 80g for an approximate period of 10 years 9 . However, lower daily doses (around 60g) for longer periods (approximately 25 years) may cause dilated cardiomyopathy, arrhythmias, and cardiac hypertensive disease 5,10 . A subgroup of chronic alcoholics with a greater sensitivity to development of hepatopathy, probably due to genetic reasons, exists. As such, vulnerability to cardiac changes may also depend on constitutional predisposition 11 . The following mechanisms have been cited as participating in the physiopathogeny of heart disease due to alcohol: direct action of alcohol or its metabolites on the cardiac muscle causing inflammation and fibrosis 12 , macro-and microangiopathic changes 13,14 , electrolytic changes, participation of metabolic and nutritional factors 15,16 , and the toxic effect of the additives present in alcoholic beverages 17 . Deficiency in thiamin itself does not seem to be the cause of alcoholic cardiomyopathy 18 , because it is associated with low cardiac output and systemic vasoconstriction, while, in the cardiomyopathy of beriberi, an elevated cardiac output occurs with reduced peripheral vascular resistance 4 . The increasing prevalence of female alcoholism among us 19,20 will certainly be a serious public health problem in the near future because of the increase in morbidity and mortality resulting from abusive alcohol consumption. If the cardiovascular problems of male alcoholism have not been sufficiently studied in Brazil, even less has been done in regard to female alcoholism. Women have been reported to be more susceptible than men are to diseases related to chronic alcoholism, even when ingesting a lower amount of alcohol. The difference in susceptibility between the sexes has been related to different proportions of body water and fat 21 and different rates of alcohol metabolism 22 . Therefore, women would be more susceptible than men in regard to Objective -To identify the electrocardiographic changes and their associations with metabolic and electrolytic changes in female alcoholics. Methods -
Prevalence of aspartate-aminotransferase alteration was consistently related to presence of histopathologic abnormalities; an enzyme level higher than 2N suggests the diagnosis of alcoholic hepatitis.
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