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Navegando por Assunto "Hepatotoxicidade"

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    Alterações hepáticas por exposição a baixas doses de metilmercúrio em macacos prego, Cebus apella (Linnaeus 1758)
    (Universidade Federal do Pará, 2011-09-16) SILVA, Márcia Cristina Freitas da; SILVEIRA, Luiz Carlos de Lima; http://lattes.cnpq.br/9383834641490219
    Cebus apella were exposed to 1,5 ppm methylmercury (methylHg) in the diet for 120 days. Hepatotoxicity was investigated, concentrations of mercury in total blood were monitored each 30 days using atomic absorption spectrometry with cold vapor Hg201, aspartate transaminase (AST), alanine transaminase (ALT) and total bilirubin (BT) were determined. Liver was fixed by formaldehyde 10% and prepared by histopathology protocols. Significant difference was observed in groups exposed and control about total mercury (Hgtotal) in the periods of 60, 90 (P < 0,05) and 120 days (P < 0,01). The histopathology revealed moderate steatosis and hydropic degeneration, common in methylHg exposed in other species. No Significant difference between the levels of AST (p= 0.38), ALT (p= 0.83) and BT (p= 0.07) in groups exposed and control. The Pearson correlation with Hgtotal was negative (AST r= -0,7; ALT r=0,07; BT r= -0,3 e p > 0,05), suggests another studies to clarify the alert levels of mercury concentrations and liver dosages.
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    Estresse oxidativo na hepatotoxicidade aos medicamentos anti-tuberculose
    (Universidade Federal do Pará, 2016-06-30) COSTA, Maria Heliana Alencar da; MACCHI, Barbarella de Matos; http://lattes.cnpq.br/5330351659478942; NASCIMENTO, José Luiz Martins do; http://lattes.cnpq.br/7216249286784978
    Tuberculosis treatment involves a combination of drugs with possible interactions with each other and other drugs. The most common side effects are related to hepatotoxicity. The biotransformation of drugs may result in the formation of reactive metabolites that can produce cellular damage which has been considered as an important process in the pathogenesis of hepatotoxicity. Goals: Evaluate the role of oxidative stress in patients with hepatotoxicity that have used anti-TB drugs. Methodology: To reach the first goal a Review of hepatotoxicity as an adverse reaction to anti-TB drugs was performed. Such an review was done through a wide search in the Portal of the Virtual Library of Health that targeted Portuguese and English literature to find papers pub- lished until December 2014. On the other hand, a Case Control study was performed to reach the second goal. For the analysis of antioxidant enzymes, patients treated at HUJBB in Secondary Reference Clinic of Pulmonology Clinic and admitted in línica of Pulmonology, and the patients seen at the Basic Health Unit Guamá in Belém were included. Results: As for the literature review, it was found that hepatic impairment is among the highest incidence of adverse reactions associated with anti-tuberculosis drugs in the Brazilian scene and adverse reactions during treatment of tuberculosis are one of the main factors associated with therapy abandonment. Regarding the analysis of antioxidant enzymes, the analysis of glutathione in the control group with hepatotoxicity (PCH) and the group without hepatotoxicity with anti-TB drugs (PCT) achieved median glutathione levels of 221 nmol / ml, 227 nmol / ml, and 236 nmol / ml, respectively. The distribution of catalase in the control group with hepatotoxicity (PCH) and the group without hepatotoxicity with anti-TB drugs (PCT) showed medians of catalase activity with values of 213 nmol / ml, 319 nmol / ml and 2035 nmol / ml, respectively. The median levels of antioxidants glutathione to the PCT group was the largest. However, glutathione levels were not statistically significant when applying the ANOVA test. Distributions of catalase activity in the population of TB patients in the group who developed hepatotoxicity (PCH) and that evolved without hepatotoxicity (PCT) were larger when compared to healthy volunteers. In particular, there was a statistically significant difference in catalase activity in the group (PCT) compared to the remaining groups. Conclusion: The results suggest that hepatotoxicity is not only associated with antioxidants enzymes and further analysis with more explanatory variables should be made to better understand this phenomenon.
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    Investigação de polimorfismos no gene TNF em pacientes com hepatotoxicidade induzida por medicações antituberculosas no norte do Brasil
    (Universidade Federal do Pará, 2015-08-27) VALENTE, Sonia Lopes; SANTOS, Ney Pereira Carneiro dos; http://lattes.cnpq.br/1290427033107137; SORTICA, Vinicius de Albuquerque; http://lattes.cnpq.br/2046482071071824
    Tuberculosis still remains a serious public health problem worldwide. The hepatotoxicity induced by anti-tuberculosis drugs causes a large number of hospitalizations and may be fatal if treatment is not interrupted. The hepatitis induced by anti-tuberculosis drugs are not yet fully understood and clinical studies suggests that immunological mechanisms are involved in its pathogenesis. The cytokine TNF-α is a major mediator of inflammatory and immune changes in the levels of this cytokine may be related to pathogenesis of drug-induced hepatitis. These changes observed may be related to polymorphisms in the TNF gene. The knowledge of which polymorphisms in the TNF gene are involved in the risk of developing hepatotoxicity anti-tuberculosis drugs will permit the use of these molecular markers to improve the therapeutic management of these patients. This study investigated the influence of polymorphisms -308C>T (rs1800629), -1031C>T (rs1799964), -238A>G (rs361525) and -857C>T (rs1799724) in the TNF gene with drug-induced hepatotoxicity. The study included 68 patients with tuberculosis who had hepatotoxicity of the basic regimen consisting of rifampicin, isoniazid, pyrazinamide and ethambutol (2RHZE/4R) and 191 patients without adverse therapy effects. The polymorphisms were determined by real-time PCR with TaqMan probes. Comparing the frequency of genotypes between cases and controls, a significant difference in the distribution of genotypes of the SNP -1031C>T was identified (p = 0.003). The frequency of homozygous -1031CC was higher in the case group (8.8%) than in the control group (1.6%). The -1031CC homozygous patients had an increased risk for the development of hepatotoxicity when compared to homozygous -1031TT or the T allele carriers (OR = 8.632, p = 0.014, OR = 11.355, p = 0.004). We concluded that -1031C>T SNP was significantly associated with susceptibility to induced hepatitis anti-tuberculosis drugs in the north population of Brazil.
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