scholarly journals Parvovirus B19 in an Immunocompetent Adult Patient with Acute Liver Failure: An Underdiagnosed Cause of Acute Non-A-E Viral Hepatitis

2005 ◽  
Vol 19 (3) ◽  
pp. 161-162 ◽  
Author(s):  
J Kee Ho ◽  
Susan PL Tha ◽  
Robert Coupland ◽  
Bakul I Dalal ◽  
William R Bowie ◽  
...  
Keyword(s):  
Liver Failure ◽  
Acute Liver Failure ◽  
Acute Hepatitis ◽  
Viral Hepatitis ◽  
Adult Patient ◽  
Causative Agent ◽  
Hepatic Failure ◽  
Parvovirus B19 ◽  
Immunocompetent Adult ◽  
Parvovirus B19 Infection

There are occasional pediatric reports of parvovirus B19-associated transient acute hepatitis and hepatic failure. A case of a 34-year-old immunocompetent woman who developed severe and prolonged but self-limited acute hepatitis and myelosuppression following acute parvovirus B19 infection is reported. Parvovirus B19 may be the causative agent in some adult cases of acute non-A-E viral hepatitis and acute liver failure.

Parvovirus B19 Infection in a Fatal Case of Acute Liver Failure

2017 ◽  
Vol 36 (12) ◽  
pp. e355-e358 ◽  
Author(s):  
Luciane Almeida Amado Leon ◽  
Arthur Daniel Rocha Alves ◽  
Rita de Cássia Nasser Cubel Garcia ◽  
Juliana Gil Melgaço ◽  
Vanessa Salete de Paula ◽  
...  
Keyword(s):  
Liver Failure ◽  
Acute Liver Failure ◽  
Parvovirus B19 ◽  
Fatal Case ◽  
Parvovirus B19 Infection

Late Increase of Peripheral CD34+ Cells Number during Acute Liver Failure Recovery.

Blood ◽  
2005 ◽  
Vol 106 (11) ◽  
pp. 4223-4223
Author(s):  
Bernard Drénou ◽  
Anne Corlu ◽  
Yoann Desille ◽  
Christèle Sicot ◽  
Olivier Fardel ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Liver Function ◽  
Liver Failure ◽  
Acute Liver Failure ◽  
Acute Hepatitis ◽  
Hepatic Failure ◽  
Alcoholic Hepatitis ◽  
Factor V ◽  
Cd34 Cells ◽  
Over Time

Abstract Human Hematopoietic Stem Cells (HSC) of bone marrow origin are reported to transdifferentiate into various cell types, including cells of hepatic lineage, and to be involved in hepatic repopulation. As it has been previously reported in the course of myocardial infarction, we hypothesized that CD34+ cells would appear early in severe acute liver failure and could predict a favourable outcome. Methods: We quantified circulating CD34+ cells in peripheral blood of 146 patients without and with severe hepatic failure (HF) defined by factor V <50%: 20 acute hepatitis with HF, 26 acute alcoholic hepatitis with HF, 22 major right hepatectomy (6/23 developped HF) and 78 controls (31 healthy subjects, 23 cirrhosis, 24 cirrhosis with chronic HF). CD34+ cells were quantified by flow cytometry, according to ISHAGE guidelines in both one and dual platform approaches. Phenotypic and functional analyses were performed in selected cases. In case of acute HF, quantification was done every day until correction of liver function. One patient underwent liver transplantation. The number of circulating CD34+ cells was correlated with factor V level. Results were presented using median and range. Results : At inclusion, the numbers of CD34+ cells /mm3 were similar in different groups (healthy controls = 1.0 [0.1– 4.0]; cirrhosis = 0.9 [0.1–5.1]; cirrhosis with chronic HF = 1.0 [0.1–3.7]; alcoholic hepatitis with HF = 1.2 [0.1–6.0]; liver resection 24H after surgery = 0.8 [0.2–3.2]; acute hepatitis with HF = 0.7 [0.2–3.1]. For patients with acute hepatitis with HF, the number of CD34+ increased over time, from 0.7 [0.2–3.1] to 1.8 [0.5–9.6] at the 4th day after admission and was significantly (p <10–3) correlated with correction of factor V. There was no correlation between the number of CD34+ and the time between admission and onset of the disease. There was no significant increase over time in the hepatectomy group nor in the alcoholic hepatitis group. CD34+ cells detected during acute hepatitis regeneration presented an immature phenotype and coexpressed CD33, CD90, CD133, CD117, CD135 (FLT3-R), CD38, HLA-DR and not V-Cadherin. Clonogenic progenitor cell assays did not reveal specific features and correlation between number of CD34 and BFU-E colonies were in favour of their hematopoietic potentiality. Conclusion: By contrast with data reported in acute myocardial infarction in which early mobilisation of CD34+ cells was observed, we found that the increase of circulating CD34+ HSC is a late event occurring at the time of the recovery of liver function in acute severe hepatic failure. The hematopoietic potentiality of mobilized CD34+ cells suggests that they do not play a major role in liver repopulation in fulminant acute hepatitis.

Quantitative real-time PCR for differential diagnostics of parvovirus B19 infection in acute liver failure patients

2019 ◽  
Vol 19 (3) ◽  
pp. 259-266 ◽  
Author(s):  
Arthur Daniel Rocha Alves ◽  
Rita De Cassia Nasser Cubel Garcia ◽  
Oswaldo Gonçalves Cruz ◽  
Marcelo Alves Pinto ◽  
Luciane Almeida Amado Leon
Keyword(s):  
Liver Failure ◽  
Acute Liver Failure ◽  
Real Time ◽  
Real Time Pcr ◽  
Parvovirus B19 ◽  
Differential Diagnostics ◽  
Quantitative Real Time Pcr ◽  
Parvovirus B19 Infection

Acute Liver Failure as the Initial Manifestation of Wilson Disease Triggered by Human Parvovirus B19 Infection

2012 ◽  
Vol 31 (1) ◽  
pp. 103-104 ◽  
Author(s):  
Akira Shiraishi ◽  
Takayuki Hoshina ◽  
Kenji Ihara ◽  
Takehiko Doi ◽  
Shouichi Ohga ◽  
...  
Keyword(s):  
Liver Failure ◽  
Acute Liver Failure ◽  
Wilson Disease ◽  
Parvovirus B19 ◽  
Human Parvovirus B19 ◽  
Initial Manifestation ◽  
Parvovirus B19 Infection

scholarly journals Analysis of the safety of pretransplant corticosteroid therapy in patients with acute liver failure and late‐onset hepatic failure in Japan

JGH Open ◽  
2021 ◽  
Vol 5 (4) ◽  
pp. 428-433
Author(s):  
Takuro Hisanaga ◽  
Isao Hidaka ◽  
Isao Sakaida ◽  
Nobuaki Nakayama ◽  
Akio Ido ◽  
...  
Keyword(s):  
Liver Failure ◽  
Acute Liver Failure ◽  
Corticosteroid Therapy ◽  
Hepatic Failure ◽  
Late Onset ◽  
Late Onset Hepatic Failure
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