RESUMO
A 43 year old man with HIV and HCV infection and liver cirrhosis developed fatal lactic acidosis within five days from starting nifedipine for arterial hypertension. Multiple drug interactions, current and accumulated drug toxicities and the reduced liver function, might in combination have led to the acute lactic acidosis.
Assuntos
Acidose Láctica/induzido quimicamente , Dissuasores de Álcool/efeitos adversos , Antirretrovirais/efeitos adversos , Anti-Hipertensivos/efeitos adversos , Dissulfiram/efeitos adversos , Infecções por HIV/tratamento farmacológico , Hepatite C/complicações , Hipertensão/tratamento farmacológico , Nifedipino/efeitos adversos , Acidose Láctica/metabolismo , Adulto , Dissuasores de Álcool/farmacocinética , Alcoolismo/complicações , Alcoolismo/tratamento farmacológico , Antirretrovirais/farmacocinética , Anti-Hipertensivos/farmacocinética , Terapia Antirretroviral de Alta Atividade , Dissulfiram/farmacocinética , Interações Medicamentosas , Evolução Fatal , Infecções por HIV/complicações , Humanos , Hipertensão/induzido quimicamente , Fígado/efeitos dos fármacos , Fígado/enzimologia , Cirrose Hepática/etiologia , Masculino , Insuficiência de Múltiplos Órgãos/induzido quimicamente , Nifedipino/farmacocinéticaRESUMO
BACKGROUND: Acetaminophen overdose is a frequent cause of acute liver failure. Controversy exists over the rare association of severe hepatotoxicity or acute liver failure with therapeutic doses of acetaminophen. CASE SUMMARY: A 45-year-old white man weighing 85 kg with asymptomatic HIV, hepatitis B virus, and hepatitis C virus (HCV) infection presented with signs of severe hepatotoxicity: aspartate aminotransferase (AST), 8,581 IU/L; alanine aminotransferase (ALT), 5,433 IU/L; L-lactate dehydrogenase, 13,641 IU/L; and prothrombin international normalized ratio, 2.15. He reported taking acetaminophen 1,000 mg QID for the previous 4 days and 1,000 mg that morning because of a febrile illness. Immediate administration of continuous IV N-acetylcysteine 150 mg/kg for the first 90 minutes and then 50 mg/kg q4h for the next 3 days was followed by clinical improvement and a rapid decrease in AST and ALT. AST levels decreased from 8,581 to 42 IU/L within 11 days. Several potential risk factors for acetaminophen hepatotoxicity (ie, chronic alcohol, tobacco, and opiate consumption, malnutrition, illness-induced starvation, HIV infection, and HCV infection) were present in this patient. CONCLUSIONS: This patient with multiple risk factors and severe hepatotoxicity after therapeutic dosage of acetaminophen was successfully treated with N-acetylcysteine.
Assuntos
Acetaminofen/efeitos adversos , Acetilcisteína/uso terapêutico , Analgésicos não Narcóticos/efeitos adversos , Doença Hepática Induzida por Substâncias e Drogas/etiologia , Hepatite C/virologia , Acetaminofen/sangue , Acetaminofen/uso terapêutico , Consumo de Bebidas Alcoólicas , Analgésicos não Narcóticos/sangue , Analgésicos não Narcóticos/uso terapêutico , Soropositividade para HIV/virologia , Hepatite B/virologia , Humanos , Itália , Masculino , Pessoa de Meia-Idade , Fatores de Risco , Abuso de Substâncias por Via IntravenosaRESUMO
Shewanella putrefaciens is as yet rarely responsible for clinical syndromes in humans. However, a case involving multiple organs in an elderly male under treatment with appropriate steroids confirms that attention should be devoted to unusual pathogens.
