scholarly journals Immune Thrombocytopenia Associated with Hepatitis B Virus and Autoimmune Hepatitis and Recovery of Platelet Count following Liver Transplantation

2021 ◽  
Vol 2021 ◽  
pp. 1-5
Author(s):  
Chloe Nobuhara ◽  
Diana M. Cardona ◽  
Murat O. Arcasoy ◽  
Carl L. Berg ◽  
Andrew S. Barbas
Keyword(s):  
Liver Transplantation ◽  
Hepatitis B Virus ◽  
Hepatitis B ◽  
Liver Failure ◽  
Acute Liver Failure ◽  
Autoimmune Hepatitis ◽  
Immune Thrombocytopenia ◽  
First Case ◽  
Thrombopoietin Receptor ◽  
B Virus

Immune thrombocytopenia is a consumptive coagulopathy that can be either idiopathic or associated with infectious or autoimmune etiologies. Here, we present a case of immune thrombocytopenia in the setting of acute liver failure due to coexisting diagnoses of hepatitis B virus and autoimmune hepatitis. Our patient underwent orthotopic liver transplantation and recovered hemostatic platelet counts after treatment with romiplostim, a thrombopoietin receptor agonist, 51 days after transplantation. To our knowledge, this is the first case report of immune thrombocytopenia secondary to both hepatitis B virus and autoimmune hepatitis in a patient with acute liver failure.

scholarly journals Human genomics of acute liver failure due to hepatitis B virus infection: an exome sequencing study in liver transplant recipients

2018 ◽  
Author(s):  
Samira Asgari ◽  
Nimisha Chaturvedi ◽  
Petar Scepanovic ◽  
Christian Hammer ◽  
Nasser Semmo ◽  
...  
Keyword(s):  
Liver Transplantation ◽  
Hepatitis B Virus ◽  
Mortality Rate ◽  
Hepatitis B ◽  
Liver Failure ◽  
Acute Liver Failure ◽  
Fulminant Hepatitis ◽  
Clinical Presentation ◽  
Hbv Infection ◽  
B Virus

AbstractAcute liver failure (ALF) or fulminant hepatitis is a rare, yet severe outcome of infection with hepatitis B virus (HBV) that carries a high mortality rate. The occurrence of a life-threatening condition upon infection with a prevalent virus in individuals without known risk factors is suggestive of pathogen-specific immune dysregulation. In the absence of established differences in HBV virulence, we hypothesized that ALF upon primary infection with HBV could be due to rare deleterious variants in the human genome. To search for such variants, we performed exome sequencing in 21 previously healthy adults who required liver transplantation upon fulminant HBV infection and 172 controls that were positive for anti-HBc and anti-HBs antibodies but had no clinical history of jaundice or liver disease. After a series of hypothesis-driven filtering steps, we searched for putatively pathogenic variants that were significantly associated with case-control status. We did not find any causal variant or gene, a result that does not support the hypothesis of a shared monogenic basis for human susceptibility to HBV-related ALF in adults. This study represents a first attempt at deciphering the human genetic contribution to the most severe clinical presentation of acute HBV infection in previously healthy individuals.Author SummaryInfection with hepatitis B virus (HBV) is very common and causes a variety of liver diseases including acute and chronic hepatitis, cirrhosis and liver carcinoma. Acute HBV infection is often asymptomatic, still about 1% of newly infected people develop a rapid and severe disease known as acute liver failure or fulminant hepatitis. Acute liver failure has a high mortality rate and is an indication for urgent liver transplantation. It is not clear why some people, who are otherwise healthy, develop such severe symptoms upon infection with a common pathogen. Here, we hypothesized that rare DNA variants in the human genome could contribute to this unusual susceptibility. We sequenced the exome (i.e. the regions of the genome that encode the proteins) of 21 previously healthy adults who required liver transplantation upon fulminant HBV infection and searched for rare genetic variants that could explain the clinical presentation. We did not identify any variant that could be convincingly linked to the extreme susceptibility to HBV observed in the study participants. This suggests that HBV-induced acute liver failure is more likely to result from the combined influence of multiple genetic and environmental factors.

Recurrent Fulminant Liver Failure Caused by Hepatitis B Virus After Liver Transplantation

1994 ◽  
Vol 19 (3) ◽  
pp. 238-241 ◽  
Author(s):  
Manuel de la Mata ◽  
Sebasti??n Rufi??n ◽  
Federico G??mez ◽  
Evaristo Varo ◽  
P L??pez-Cillero ◽  
...  
Keyword(s):  
Liver Transplantation ◽  
Hepatitis B Virus ◽  
Hepatitis B ◽  
Liver Failure ◽  
Fulminant Liver Failure ◽  
B Virus

scholarly journals Concomittant Liver Transplantation And  Low Anterior Resection in Patient with  Neuroendocrine Tumor and Chronic Hepatitis B Infection

2021 ◽  
Author(s):  
Adem Tuncer ◽  
Mehmet Zeki Öğüt ◽  
Sertac Usta ◽  
Sami Akbulut ◽  
Tevfik Tolga Sahin ◽  
...  
Keyword(s):  
Liver Transplantation ◽  
Liver Disease ◽  
Hepatitis B Virus ◽  
Hepatitis B ◽  
Liver Failure ◽  
Neuroendocrine Tumor ◽  
Anterior Resection ◽  
Low Anterior Resection ◽  
B Virus ◽  
End Stage

Abstract Aim: The treatment of end-stage liver disease is liver transplantation. There are studies regarding liver transplantation in patients with colorectal cancer and neuroendocrine tumor liver metastasis indicating comparable results with patients who were transplanted for hepatocellular carcinoma. The aim of the present study is to present a case of a patient with Hepatitis B virus related chronic liver disease and rectal neuroendocrine tumor who underwent concomitant living donor liver transplantation and low anterior resection. Case report: The patients was a 62 years old male patient with hepatitis B virus related end-stage liver failure and a rectal neuroendocrine tumor determined during colonoscopy surveillance. Model for end stage liver disease score was 21 and had two episodes of life-threatening variceal bleeding. We performed living donor liver transplantation and low anterior resection to the patient. Currently patient is doing well 2 years after the operation. Conclusion: Our case is the first in literature showing concomitant liver transplantation for hepatitis B virus related liver failure and rectal resection for neuroendocrine tumor. These procedures can be performed synchronously provided that the etiology of liver failure is unrelated to neuroendocrine tumor and the primary tumor has favorable tumor biologic characteristics. We reviewed the English literature, we did not find any case who underwent rectal NET surgery and HBV-related liver transplantation in the same operation. We wanted to present this first case in the literature.

scholarly journals Role of humoral immunity against hepatitis B virus core antigen in the pathogenesis of acute liver failure

2018 ◽  
Vol 115 (48) ◽  
pp. E11369-E11378 ◽  
Author(s):  
Zhaochun Chen ◽  
Giacomo Diaz ◽  
Teresa Pollicino ◽  
Huaying Zhao ◽  
Ronald E. Engle ◽  
...  
Keyword(s):  
Hepatitis B Virus ◽  
Hepatitis B ◽  
Liver Failure ◽  
Acute Liver Failure ◽  
Acute Hepatitis ◽  
B Cell ◽  
Core Antigen ◽  
Cell Disease ◽  
B Virus ◽  
Acute Hepatitis B

Hepatitis B virus (HBV)-associated acute liver failure (ALF) is a dramatic clinical syndrome leading to death or liver transplantation in 80% of cases. Due to the extremely rapid clinical course, the difficulties in obtaining liver specimens, and the lack of an animal model, the pathogenesis of ALF remains largely unknown. Here, we performed a comprehensive genetic and functional characterization of the virus and the host in liver tissue from HBV-associated ALF and compared the results with those of classic acute hepatitis B in chimpanzees. In contrast with acute hepatitis B, HBV strains detected in ALF livers displayed highly mutated HBV core antigen (HBcAg), associated with increased HBcAg expression ex vivo, which was independent of viral replication levels. Combined gene and miRNA expression profiling revealed a dominant B cell disease signature, with extensive intrahepatic production of IgM and IgG in germline configuration exclusively targeting HBcAg with subnanomolar affinities, and complement deposition. Thus, HBV ALF appears to be an anomalous T cell-independent, HBV core-driven B cell disease, which results from the rare and unfortunate encounter between a host with an unusual B cell response and an infecting virus with a highly mutated core antigen.

Sign in / Sign up

Export Citation Format

Share Document