Background: PTLD is a clinical condition with high mortality. Monitoring EBV replication can be a useful tool to avoid the development of PTLD.
Materials and Methods:This was a retrospective analysis of 428 pediatric patients who underwent liver transplantation between 1989 and 2016. The patients were divided into 2 groups (transplanted before 2006, when PCR-EBV was not monitored, and after 2006, when PCR-EBV monitoring was started). Patients with continuous PCR measurements for EBV were evaluated for the impact of a reduction in immunosuppression or a change in immunosuppressants on the number of viral copies. A logistic regression model was applied to evaluate factors related to PTLD.
Results:The prevalence of PTLD was 4.2%. After monitoring patients with PCR for EBV levels, a predominance of the most severe, monomorphic form of lymphoproliferative disorder was observed (p = .009). The PTLD mortality was 5%. There was a change in the PCR level after tacrolimus reduction (p = .002) and after tacrolimus exchange for mTOR (p = .008). The number of EBV copies was significantly higher (p = .029) in patients who developed PTLD. In the multiple regression model, seropositivity for CMV was an independent protective factor for lymphoproliferative disorder (OR=0.09; 95% CI 0.02-0.42), reducing the chance of having PTLD adjusted by serology for EBV by 91%.
Conclusions:Monitoring the EBV viral load by PCR seems to prevent the emergence of milder forms of lymphoproliferative disorder. Pretransplant seropositivity for CMV is a protective factor for PTLD.
PURPOSE:To describe an animal model for acute liver failure by intraperitoneal d-galactosamine injections in rats and to define when is the best time to intervene through King's College and Clichy´s criteria evaluation.
METHODS:Sixty-one Wistar female rats were distributed into three groups: group 1 (11 rats received 1.4 g/kg of d-galactosamine intraperitoneally and were observed until they died); group 2 (44 rats received a dose of 1.4 g/kg of d-galactosamine and blood and histological samples were collected for analysis at 12 , 24, 48 , 72 and 120 hours after the injection); and the control group as well (6 rats).
RESULTS:Twelve hours after applying d-galactosamine, AST/ALT, bilirubin, factor V, PT and INR were already altered. The peak was reached at 48 hours. INR > 6.5 was found 12 hours after the injection and factor V < 30% after 24 hours. All the laboratory variables presented statistical differences, except urea (p = 0.758). There were statistical differences among all the histological variables analyzed.
CONCLUSION:King's College and Clichy´s criteria were fulfilled 12 hours after the d-galactosamine injection and this time may represent the best time to intervene in this acute liver failure animal model.
A disfunção precoce de enxerto hepático consiste em uma síndrome multifatorial caracterizada por alterações clínicas e laboratoriais associadas à alta morbidade nos primeiros dias pós-transplante. Relacionada à lesão de isquemia e reperfusão do fígado, pode levar em sua forma mais grave a alterações sistêmicas abruptas. Apesar de ser um quadro grave, as alterações podem ser transitórias, possibilitando recuperação do enxerto hepático. Sua ocorrência em população pediátrica é rara. A N-acetilcisteína, comumente utilizada no tratamento de hepatotoxicidade secundária à overdose por paracetamol, tem surgido como alternativa eficaz na melhora clínica de pacientes transplantados com má função de enxerto. Relatamos um caso de paciente do sexo masculino, dois anos, submetido a transplante de fígado por atresia de vias biliares, sem intercorrências intraoperatórias. Evoluiu com quadro de disfunção precoce grave de enxerto no segundo dia pós-operat óio, sem boa resposta às medidas de suporte, cogitando-se indicação de retransplante. Foi iniciada administração de n-acetilcisteína, dosagem de 100mg três vezes ao dia, progredindo com melhora clínica significativa, sobretudo da função hepática. O acompanhamento de dados clínicos e laboratoriais de pacientes no período pós-transplante é fundamental, tendo em vista riscos e graves repercussões da disfunção precoce do enxerto hepático. A N-acetilcisteína é uma droga que tem sido relatada atuando no aumento da oferta de oxigênio tecidual e na remodelação dos hepatócitos, a partir da recuperação dos níveis de glutationa. Os efeitos em pacientes com disfunções hepáticas pós -transplante têm sido promissores nos poucos relatos científicos de seu uso, como o caso em questão.
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