ABSTRACT
Introduction: There are many reports about hepatotoxicity associated with acute overdose or long-term use of acetaminophen, but few reports of that associated with therapeutic doses. We present a case of acute liver failure with hepatic coma caused by therapeutic doses of intravenous acetaminophen for cancer pain relief in palliative care setting. Case: The patient was a 56-year-old woman with stage IV lung cancer and normal liver function. She was admitted to the hospital because of anorexia and cancer pain. She received 1g intravenous acetaminophen every six hours for analgesia of pleural and rib metastasis. The patient’s AST/ALT levels were elevated at 3104/1212 IU/L, while she was receiving 11 doses of intravenous acetaminophen. She was treated with oral N-acetylcysteine, hemadsorption and plasma exchange therapy. Liver function returned to normal soon. Discussion: Therapeutic doses of intravenous acetaminophen is generally used in palliative care setting, and hepatic failure may occur due to glutathione depletion in patients with cancer anorexia. The potential hazard of rare but serious complications should always be kept in mind even with therapeutic doses.
ABSTRACT
JUSTIFICATIVA E OBJETIVOS: Mecanismos patogênicos desencadeados pelo Plasmodium berghei sugerem que suplementação prévia com antioxidantes possa exercer papel preventivo ao estabelecimento da malária. O objetivo deste estudo foi estudar os efeitos de suplementos antioxidantes sobre o estresse oxidativo cerebral e pulmonar e sobre a sobrevida de camundongos infectados. MÉTODOS: Estudo experimental que utilizou camundongos divididos em 3 grupos de 10 animais cada. O grupo I correspondeu ao grupo controle positivo, o grupo II foi formado por animais tratados com N-acetilcisteína e o grupo III com Agaricus sylvaticus.Observou-se a sobrevida e coletaram-se amostras de tecido pulmonar e cerebral no dia de óbito de cada animal. Avaliou-se a parasitemia,os níveis de malondialdeído e a capacidade antioxidante equivalente ao trolox. RESULTADOS: Não se encontrou relação significativa entre a administração prévia de Agaricus sylvaticus e N-acetilcisteína e o tempo de sobrevida ou sobre a parasitemia dos animais infectados. Entretanto, níveis de malondialdeído no cérebro dos animais do grupo controle foram significantemente maiores (p<0,0001) que do N-acetilcisteína e Agaricus sylvaticus, sendo os valores do N-acetilcisteína menores que do Agaricus sylvaticus.Para capacidade antioxidante equivalente ao trolox cerebral, o grupo N-acetilcisteína apresentou valores significantemente maiores (p<0,05) que o Agaricus sylvaticus. Encontrou-se moderada correlação negativa (r=-0,73; p=0,02) entre malondialdeído cerebral e sobrevida. CONCLUSÃO: Estes dados sugerem que, apesar do nível de estresse oxidativo apresentar correlação negativa com a sobrevida dos animais, o uso de suplementos antioxidantes não promoveu aumento na expectativa de vida dos animais suplementados. Isto pode ter decorrido das doses utilizadas de antioxidantes ou das substâncias empregadas.
BACKGROUND AND OBJECTIVES: Pathogenic mechanisms triggered by Plasmodium berghei suggest that prior supplementation with antioxidants may have a preventive role in the onset of malaria. The objective of this study was to study the effects of antioxidant supplements on brain and pulmonary oxidative stress and on the survival of infected mice. METHODS: An experimental study using mice, which were divided into 3 groups of 10 animals each. Group I corresponded to the positive control group, group II was formed by animals treated with N-acetylcysteine and group III with Agaricus sylvaticus. Survival was observed and samples of lung and brain tissues were collected on the day of death of each animal. Parasitemia, the levels of malondialdehyde, and antioxidant capacity equivalent to trolox were evaluated. RESULTS: There was no significant relationship between prior administration of Agaricus sylvaticus or N-acetylcysteine and the survival or parasitemia of infected animals. However, levels of malondialdehyde in the brain of animals from control group were significantly higher (p <0.0001) than those of N-acetylcysteine and Agaricus sylvaticus, and values from of N-acetylcysteine were lower than of Agaricus sylvaticus. For brain antioxidant capacity equivalent to trolox, N-acetylcysteine group showed significantly higher values (p < 0.05) than Agaricus sylvaticus. A mild negative correlation (p = 0.02 and R = -0.73) between brain malondialdehyde and survival was found. CONCLUSION: These data suggest that, although the levels of oxidative stress presented negative correlation with animals survival, the use of antioxidant supplements did not provide an increase in life expectancy of supplemented animals. This may have occurred due to the doses of antioxidants or of substances used.
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Animals , Adult , Mice , Antioxidants , Malaria , Oxidative Stress , Plasmodium bergheiABSTRACT
Objective To investigate the changes of peripheral insulin resistance after lipid infusion and the effect of N-acetylcystein(NAC) intervention.Methods Thirty-seven normal male SD rats,eight weeks old,were randomly divided into three groups,FFA group,NS group and NAC group(using into NAC 300 mg/(kg?d) two weeks before infusion).Catheters were implanted into right atrium via the jugular vein and left carotid artery.A technique for a 48-h infusion in unrestrained rats was used for triglyceride and heparin or saline infusion.The infusion period started on day 2 after surgery.48-h after infusion,we determined free fat acid(FFA),nitrotyrosine,malonaldehyde(MDA),reduced glutathione hormone(GSH) level in plasma.The glucose infusion rat(GIR) was measured by hyperinsulinemia euglycemic clamp to evaluated the perpherial insulin resistance.The expressions of IRS-1,IRS-2 gene in muscle were detected by real time PCR.Results(1)The FFA,nitrotyrosine and MDA con-centrations in FFA group were higher than that in NS group,but GSH level in plasma was lower.NAC intervention could reverse these effects.(2)GIR was decreased significantly in FFA group as compared with NS group[(8.34?1.8)mg/(min?kg)] vs[(13.56?1.7)mg/(min?kg)],(P