Hepatotoxicidad por esteroides anabólicos androgénicos, reporte de 2 casos en Uruguay / Hepatotoxicity induced by anabolic-androgenic steroids, 2 cases report in Uruguay / Hepatotoxicidade por anabolizantes esteróides androgênicos, relato de 2 casos no Uruguai

El consumo ilícito de esteroides anabólicos androgénicos con fines estéticos ha aumentado en los últimos años y, aunque raro, es causa de hepatotoxicidad. Los casos con daño hepatocelular son más frecuentes, pero los colestásicos son más graves y pueden asociarse a falla renal. Salvo por la suspensión del fármaco, la hepatotoxicidad por anabólicos no tiene tratamiento específico. Se describe y discuten las historias clínicas de dos hombres jóvenes, deportistas aficionados que consultaron por ictericia y presentaron colestasis e insuficiencia renal. El reporte de casos, en patologías poco frecuentes, resulta fundamental para difundir y ampliar la información que ayude al clínico a considerar con firmeza este diagnóstico, incluso ante la falta de reconocimiento inicial del consumo por parte del paciente.

Illicit consumption of anabolic-androgenic steroids for aesthetic purposes has increased in recent years. Hepatocellular damage is more frequent, but cholestasis is more dangerous and may be associated with renal failure. The clinical records of two young men, amateur athletes who consulted for jaundice in the last year and denied its consumption at the beginning, are described. Except for the drug interruption, hepatotoxicity by anabolics has no specific treatment. Usually presented as cholestatic liver disease and renal failure, case reports are fundamental to characterize its clinical-evolutionary presentation. This may also allow clinicians to firmly consider diagnosis even when the patient denies consumption.

O uso ilícito de esteróides androgênicos anabólicos para fins estéticos tem aumentado nos últimos anos e, apesar de raro, é causa de hepatotoxicidade. Casos com dano hepatocelular são mais freqüentes, mas colestesia é mais grave e pode estar associada à insuficiência renal. Com exceção da suspensão do medicamento, a hepatotoxicidade anabólica não possui tratamento específico. As histórias clínicas de dois homens jovens, atletas amadores que consultaram para icterícia e apresentaram colestase e insuficiência renal, são descritos e discutidos. O relato de casos, em patologias pouco freqüentes, é fundamental para disseminar e ampliar as informações que auxiliam o clínico a considerar com firmeza esse diagnóstico antes mesmo do não reconhecimento inicial do consumo pelo paciente.

Amoxycillin Clavulanic Acid Induced Hepatotoxicity.

Drug-related hepatotoxicity is a serious health problem, with broad implications for patients, healthcare providers, the pharmaceutical industry and governmental regulatory agencies. Herein we report a rare case of amoxycillinclavulanic acid combination induced liver injury of cholestatic pattern in 40 years old, well educated male patient. Patient gave history that though other drugs were given to him by his physician for fever with chills & rigors, malaise, bodyache, except amoxycillin-clavulanic acid combination all other drugs were well tolerated previously by the patient, without appearance of jaundice. So jaundice in this patient was most probably due to amoxycillinclavulanic acid combination. Though severe liver injury is rare, proper history should be taken while prescribing amoxycillin-clavulanic acid combination. Attention must be paid to potential side-effects of the drugs and close follow-up with patients is a medical necessity to evaluate adverse reactions, especially in case of amoxycillinclavulanic acid combination.

Hepatic failure with flutamide.

A 41-year-old woman, who was on flutamide for hair loss for 3 months, presented with deep jaundice. She developed hepatic encephalopathy but gradually recovered after discontinuing flutamide. Flutamide can cause fatal toxic liver injury and hence should be used with close monitoring of liver profile.

Jaundice due to anti-tuberculous drugs--a dose related phenomenon.

Data of 429 cases proved to have tuberculosis and on anti-tuberculous short course chemotherapy was analysed to find the incidence of jaundice due to anti-tuberculous drugs. The group included 257 males and 172 females (M : F ratio of 3 : 2), aged 7 to 75 years. 336 patients received short course chemotherapy for a duration of 6 months, while 93 patients were cases of relapse and hence received treatment for 9 months duration. Of these, 7 patients developed drug induced jaundice; 2 each in the age group of 21 to 35 years, and 36 to 50 years while 3 patients were in the age group of 51-65 years. All of these patients developed jaundice within 2 months of treatment and 6 of these 7 patients were receiving drugs in doses which were not adjusted as per the weight of the patient. None of these 6 patients redeveloped jaundice when the drugs were started in doses adjusted accurately as per the weight of the patients, in accordance with IUAT recommendations. One patient (0.21%), who was staredon weight adjusted dosage of anti-TB drugs developed jaundice which was probably due to isoniazed hypersensitivity.

Study on hepatotoxicity and other side-effects of antituberculosis drugs.

A prospective study of different side-effects and toxicity of different antituberculosis drugs was made on 125 cases of pulmonary tuberculosis, divided into 3 groups according to the regime of treatment. Group A consisted of 50 patients, taking streptomycin, ethambutol and isoniazid. Group B of 50 patients received streptomycin plus ethambutol plus isoniazid and rifampicin and 25 patients comprising group C received streptomycin plus isoniazid plus ethambutol and pyrazinamide. The group B showed hepatotoxicity in 30% cases, out of which clinical jaundice with abnormal liver function tests being 26% and rest 4% cases were of anicteric hepatitis, while group A showed only 6% hepatotoxicity with 4% clinical jaundice and 2% anicteric hepatitis. In group A out of 50 cases only 2 patients complained of colour blindness, which reversed with the stoppage of drugs. In group C out of 25 cases 3 patients had gouty problems and responded with stoppage of drugs. Patients in group A developed jaundice in a mean of 50 days while those in group B developed jaundice in 17 days.

Tuberculosis e ictericia: estudio de 103 casos / Tuberculosis and jaundice: study of 103 cases

Entre enero de 1979 y diciembre de 1984 se estudiaron y trataron 103 enfermos con tuberculosis pulmonar e ictericia. En 59 enfermos, sin historia de enfermedad hepática y con los tests de función hepática normales al iniciar el tratamiento antituberculoso, la ictericia apareció durante el mismo; en el Grupo I y en la primera columna de Tabla I se indican sus características y el tratamiento que recibieron. Seis pacientes tuvieron hepatitis aguda viral confirmada por la positividad del HBsAg y la biopsia hepatica, la tuberculosis comprometía el hígado en otros 3 enfermos; en los restantes 50 la ictericia puede atribuirse a las drogas usadas en el tratamiento. En Tabla 2 se indica la histología hepática. El tratamiento fue suspendido al aparecer la ictericia y reinstituido cuando los tests de función eran normales y en sólo un caso, con enfermedad de Hodgkin, reapareció la ictericia. El tratamiento duró entre 6 y 8 meses; la evolución fue favorable - curaron la tuberculosis pulmonar - en 49 enfermos; 10 fallecieron, 2 debido a necrosis hepática mas va, 2 por cirrosis hepática y 6 por progresión de la tuberculosis pulmonar. El Grupo II está formado por 44 enfermos que ingresaron al hospital con ictericia, la tuberculosis pulmonar se diagnosticó después; sus características y el tratamiento que recibieron se indican en la segunda columna de Tabla 1. La mortalidad fue alta en este grupo y debida, en la mayoría, a la tuberculosis pulmonar; en Tabla 2 se indican las lesiones hepáticas; 20 enfermos tuvieron evolución favorable y en 18 los tests de función hepática se normalizaron entre los 20 y 30 días del tratamiento; en 2 pacientes con hepatitis alcohólica la bilirrubina total permaneció elevada los 6 meses de tratamiento. En base a estos hechos se considera que cuando aparece ictericia durante el tratamiento antituberculoso con estos esquemas terapéuticos se debe suspender el tratamiento...

Tuberculosis e ictericia: importancia de su asociación / Tuberculosis and jaundice: importance of its association

La Asociación de tuberculosis pulmonar (TP) e ictericia plantea una serie de situaciones en las que intervienen varios factores: 1) la tuberculosis puede ser la única enfermedad y, al localizarse en el higado, producir ictericia; 2) de las drogas antituberculosas más usadas, la isoniacida (INH), la rifampicina (RAMP) y la pirazinamida (PZ) son capaces de producir alteraciones hepáticas e ictericia; 3) un paciente con TP puede tener, durante el tratamiento, una hepatitis viral; 4) un paciente con una enfermedad hepática ictérica puede adquirir una tuberculosis. Estas situaciones diferentes obligan al médico a elegir, en cada una de ellas, cual es la conducta terapéutica adecuada. Hemos asistido a un grupo de pacientes que presentaron esta asociación y en ellos hemos estudiado los dos procesos, el pulmonar y el hepático, tratando de establecer las relaciones entre los mismos, así como de obtener conclusiones con respecto a la conducta terapéutica

Hepatitis and multi-drug therapy in leprosy with special reference to prothionamide.

Hepatotoxicity in two drug regimens was studied at Central Leprosy Teaching and Research Institute, Chengalpattu (Tamil Nadu) during 1983-84. In 'P' regimen-prothionamide 350 mg daily, dapsone 100 mg daily and rifampicin 600 mg at monthly intervals were given. In' C' regimen-dapsone 100 mg daily, rifampicin 600 mg once a month and clofazimine 300 mg once a month and 100 mg alternate day were given. Trial was started with fifty multibacillary adult leprosy patients in each group. Enzymatic hepatic dysfunction was noted in 52-58 per cent of the cases even before the therapy was started. In 'P' regimen, four cases of clinical jaundice and six cases of high bilirubinaemia was noticed during the trial as against two cases each of clinical jaundice and high bilirubinaemia in 'C regimen. Of the two cases of clinical jaundice in 'C' regimen, one turned out to be a case of HBV infection. The study which is in progress, indicated higher hepatotoxicity in 'P' regimen which is probably explained by the simultaneous use of two hepatotoxic drugs. Viral hepatitis is endemic in this area and might have aggravated the hepatotoxicity observed.