Hepatitis E Diagnosis and Management After Liver, Kidney, or Heart Transplant: A Single-Center Experience.

BACKGROUND: Transplant-related hepatitis E virus (HEV) infection is a rarely recognized phenomenon with significant clinical importance given its potential to result in chronic hepatitis posttransplant. METHODS: We retrospectively evaluated HEV diagnosis and treatment after liver, kidney, and heart transplant in a single center. We identified patients diagnosed with HEV by serologic testing and evaluated their treatment regimens. RESULTS: Fifteen transplant recipients (12 liver, 2 kidney, and 1 heart) presented with elevated liver enzymes and were positive for HEV IgM antibody. Liver enzymes normalized in 4 patients after being treated with ribavirin. One of the 4 patients had 2 recurrences with positive HEV RNA results following ribavirin treatment but recovered after 12 months of ribavirin therapy. After treatment with reduction in immunosuppression without antiviral treatment, 6 of 8 patients' liver enzymes normalized. One of these patients died of acute pancreatitis 2 months after testing positive for HEV IgM antibody. CONCLUSIONS: The potential for complications related to active HEV infections in transplant recipients necessitates prompt diagnosis and treatment to prevent irreversible damage. Diagnosis with HEV reverse transcriptase-polymerase chain reaction should follow a positive HEV IgM antibody test. This manuscript provides evidence that ribavirin antiviral therapy and reducing immunosuppression are effective treatments for HEV infections in liver, kidney, and heart transplant recipients, which has not been sufficiently investigated in the population of the United States. Larger multicenter studies are needed to confirm the risks and benefits of using ribavirin antiviral therapy as first-line therapy of HEV posttransplant.

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Benign Recurrent Intrahepatic Cholestasis in Pregnancy: Fetal Death at 36 Weeks of Gestation.

INTRODUCTION: Benign recurrent intrahepatic cholestasis is a rare hepatologic disorder characterized by recurrent, self-limited episodes of severe pruritus, jaundice, and elevated bile acids. While there are guidelines for the management of intrahepatic cholestasis of pregnancy, the literature regarding benign recurrent intrahepatic cholestasis and pregnancy is limited. CASE: A 29-year-old G1P0 woman, with history of liver toxicity, had elevated total serum bile acid levels and liver enzymes documented at 8 weeks of gestation and throughout her pregnancy. She had a reactive nonstress test just 3 days prior to her induction. Fetal demise was noted when she presented at 36 weeks for her induction. CONCLUSION: We recommend that women with elevated total serum bile acid early in pregnancy due to a separate entity relative to intrahepatic cholestasis of pregnancy be managed in a more individualized approach.

Characterization of the RFX complex and the RFX5(L66A) mutant: implications for the regulation of MHC class II gene expression.

Major histocompatability complex class II (MHCII) molecules are an essential component of the mammalian adaptive immune response. The expression of MHCII genes is regulated by a cell-specific multiprotein complex, termed the MHCII enhanceosome. The heterotrimeric RFX complex is the key DNA-binding component of the MHCII enhanceosome. The RFX complex is comprised of three proteins, RFXB, RFXAP, and RFX5, all of which are required for DNA binding and activation of MHCII gene expression. Static light scattering and chemical cross-linking of the three RFX proteins show that RFXB and RFXAP are monomers and that RFX5 dimerizes through two separate domains. One of these domains, the oligomerization domain, promotes formation of a dimer of dimers of RFX5. In addition, we show that the RFX complex forms a 2:1:1 complex of RFX5.RFXAP.RFXB, which can associate with a further dimer of RFX5 to form a 4:1:1 complex through the oligomerization domain of RFX5. On the basis of these studies, we propose DNA-binding models for the interaction between the RFX complex and the MHCII promoter including a DNA looping model. We also provide direct evidence that the RFX5(L66A) point mutation prevents dimerization of the RFX complexes and propose a model for how this results in a loss of MHCII gene expression.