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Epstein-Barr virus (EBV) is a herpesvirus whose only reservoir host is the human. It is transmitted by oropharyngeal secretions. Primary EBV infection is usually asymptomatic, but sometimes it causes infectious mononucleosis with fever, lymphadenopathies, splenomegaly and pharyngitis. Acute infection is diagnosed by serology (heterophile or specific antibodies). Immunofluorescence and molecular biologic techniques may be used to demonstrate the presence of EBV in biopsy specimens. Mild and transient elevations of serum aminotransferases are common, thus liver biopsy is usually not necessary to confirm the diagnosis. Severe cholestasis is rare (5%). We describe a patient with cholestatic hepatitis and acute EBV infection with atypical lymphocytes and positive anti-VCA IgM. The patient had taken drugs (ibuprofen, paracetamol and valerian). The bad evolution of the patient, the history of exposure to drugs, and the few cases of cholestatic hepatitis due to EBV infection reported, led us to consider liver biopsy. Molecular biologic techniques confirmed the presence of EBV in liver tissue however histologic features did not exclude the toxic aetiology or the concomitant effect of drugs and EBV infection.

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Cyclosporine has recently been reported to produce in vitro suppression of hepatitis C virus replication driven by blockade of cyclophilins, an effect not shown for tacrolimus. However, the clinical consequence of this in vitro finding have not been well studied in vivo. We compared viral load and fibrosis in transplanted patients receiving monotherapy with tacrolimus or cyclosporine. Patients with recurrent hepatitis C after transplantation were selected from two tertiary centers with the following inclusion criteria: monotherapy with tacrolimus or cyclosporine for more than 12 months before viral load measurement, no antiviral treatment, corticosteroids stopped within 12 months after transplantation. HIV, hepatitis B, and active infection by cytomegalovirus were excluded. Patient characteristics, viral load, and fibrosis were compared by univariate analysis between the cyclosporine and tacrolimus groups. Significant variables, viral load, and fibrosis were included in a multivariate model. Sixty-six patients were included, 46 on tacrolimus and 20 on cyclosporine. Fifty-six were male, and the mean age was 55.3 +/- 10.1 years. Fibrosis (Ishak score) was 3.9 +/- 1.9 in the cyclosporine group and 2.7 +/- 1.9 in the tacrolimus group (P = .019). Viral load (log(10)IU/mL) was 5.8 +/- 0.5 and 5.9 +/- 0.5, respectively (P = .7) and time since liver transplantation was 95.3 +/- 47.7 and 41.1 +/- 16.8 months (P = .0001). In the multivariate model, viral load (P = .65) and fibrosis (P = .24) were not significantly different and only time since transplantation remained significant (P = .0001). In conclusion, viral load was not different in patients with tacrolimus as compared with cyclosporine, and the lower fibrosis observed in the cyclosporine group lacked significance when considered together with time since liver transplantation.

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Corticosteroid boluses, which are the treatment for acute rejection episodes, have been shown to produce transient increases in viremia. However, their effect on long-term viral load, histological activity index (HAI), and fibrosis has not been well established. The aim of our study was to compare late viral load, HAI, and fibrosis in patients with versus without steroid boluses in the immediate posttransplant period. We analyzed patients transplanted due to hepatitis C virus. Inclusion criteria were: no change in immunosuppression (cyclosporine or tacrolimus with/without mycophenolate); no steroids in the previous 4 months; no antiviral treatment; liver biopsy and viral load determination >12 months after transplantation. Exclusion criteria were HIV, hepatitis B, and active cytomegalovirus infection. Nonparametric tests were used to compare viral load, HAI, and fibrosis (Ishak-score) among patients who received steroid boluses for an acute rejection episode (group 1) versus those who did not (group 2). Among the 48 selected patients were 38 men with the overall mean age of the entire group of 55.6 +/- 10.9 years. The mean period from liver transplantation was 53.25 +/- 33.4 months. Thirty-four (70.1%) were treated with tacrolimus and the rest, cyclosporine. Eleven (22.9%) had and 37 (77.1%) had not received corticosteroid boluses. The viral load was similar in groups 1 and 2 (5.74 +/- 0.54 vs 5.98 +/- 0.53 Log(10) IU per mL, P = .32). Fibrosis was also similar (2.5 +/- 1.6 vs 2.2 +/- 1.7, P = .56). However, HAI was higher in group 1 (7.5 +/- 1.7 vs 6.0 +/- 1.7, P = .026). In conclusion, although long-term viral load was similar in patients who had versus had not received one cycle of steroid boluses, the HAI was significantly higher in the former cohort, but had not resulted in greater fibrosis during the study follow-up.

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El virus de Epstein-Barr (VEB) es un herpesvirus cuyo único huésped es el hombre, al que infecta por vía orofaríngea. La primoinfección generalmente es asintomática o cursa como una mononucleosis infecciosa que se caracteriza por fiebre, adenopatías, esplenomegalia y amigdalitis. El diagnóstico de la infección aguda suele ser serológico (anticuerpos heterófilos o específicos para el VEB), aunque el virus también puede detectarse en los tejidos mediante inmunohistoquímica o por técnicas de biología molecular. Habitualmente la infección por el VEB produce una alteración leve y autolimitada de las transaminasas (AST y ALT), por lo que no suele precisarse una biopsia hepática, y solo en el 5% causa una hepatitis aguda colestásica (HAC). Presentamos a un paciente con una HAC e infección aguda por el VEB, con linfocitos atípicos en sangre periférica y anticuerpos IgM contra la cápside VCA, que había tomado tóxicos (ibuprofeno, paracetamol y valeriana). La evolución tórpida del cuadro, la relación cronológica con la exposición a fármacos y los escasos casos publicados de HAC atribuidos al VEB, recomendaron realizar una biopsia hepática. Aunque el estudio de biología molecular en el tejido hepático resultó positivo para el VEB, los hallazgos morfológicos no permitieron excluir el origen tóxico ni la posible interacción entre fármacos y el propio virus en la etiología del cuadro

Epstein-Barr virus (EBV) is a herpesvirus whose only reservoir host is the human. It is transmitted by oropharyngeal secretions. Primary EBV infection is usually asymptomatic, but sometimes it causes infectious mononucleosis with fever, lymphadenopathies, splenomegaly and pharyngitis. Acute infection is diagnosed by serology (heterophile or specific antibodies). Immunofluorescence and molecular biologic techniques may be used to demonstrate the presence of EBV in biopsy specimens. Mild and transient elevations of serum aminotransferases are common, thus liver biopsy is usually not necessary to confirm the diagnosis. Severe cholestasis is rare (5%). We describe a patient with cholestatic hepatitis and acute EBV infection with atypical lymphocytes and positive anti-VCA IgM. The patient had taken drugs (ibuprofen, paracetamol and valerian). The bad evolution of the patient, the history of exposure to drugs, and the few cases of cholestatic hepatitis due to EBV infection reported, led us to consider liver biopsy. Molecular biologic techniques confirmed the presence of EBV in liver tissue however histologic features did not exclude the toxic aetiology or the concomitant effect of drugs and EBV infection

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Describimos el caso de una paciente que presentó un hidrotórax como primera manifestación de una cirrosis hepática. Ante la ausencia de respuesta al tratamiento diurético, a la realización de una pleurodesis y a la colocación de una derivación portosistémica percutánea intrahepática, se inició tratamiento con octreótido conlo que se obtuvo la resolución del mismo. Se trata del tercer caso publicado en la literatura de hidrotórax hepático refractario con respuesta completa y mantenida al tratamiento con octreótido

We report the case of a patient that developed hepatic hydrothorax as the first complication of liver cirrhosis. Due to the lack of response to diuretics, pleurodesis and TIPS, treatment with octreotide was started with resolution of hydrothorax. To the best of our knowledge, this is the third reported case of refractory hepatic ;;hydrothorax with complete and sustained response to octreotide

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We report the case of a patient that developed hepatic hydrothorax as the first complication of liver cirrhosis. Due to the lack of response to diuretics, pleurodesis and TIPS, treatment with octreotide was started with resolution of hydrothorax. To the best of our knowledge, this is the third reported case of refractory hepatic hydrothorax with complete and sustained response to octreotide.

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