Journal ArticleDOI
The Pathology of Acute Liver Failure.
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TLDR
The liver pathology in ALF is reviewed, including forms of zonal necrosis and their etiologies, including marked loss of hepatocytes, variable degrees of inflammation, and a stereotypic proliferation of bile ductular structures (neocholangioles) derived from activated periportal hepatic progenitor cells.Abstract:
Acute liver failure (ALF) is a rare and severe liver disease that usually develops in 8 weeks or less in individuals without preexisting liver disease. Its chief causes worldwide are hepatitis virus infections (hepatitis A, B, and E) and drug hepatotoxicity (particularly intentional or unintentional acetaminophen toxicity). Massive hepatic necrosis is often seen in liver specimens in ALF and features marked loss of hepatocytes, variable degrees of inflammation, and a stereotypic proliferation of bile ductular structures (neocholangioles) derived from activated periportal hepatic progenitor cells. This paper reviews the liver pathology in ALF, including forms of zonal necrosis and their etiologies.read more
Citations
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Journal ArticleDOI
Acute liver failure induced by idiosyncratic reaction to drugs: Challenges in diagnosis and therapy
Shannan R. Tujios,William M. Lee +1 more
TL;DR: DILI that reaches the threshold of ALF will more often than not require transplantation, since survival without transplant is around 25%.
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IL-17 and IL-17-producing cells and liver diseases, with focus on autoimmune liver diseases.
Audrey Beringer,Pierre Miossec +1 more
TL;DR: Some of these observed beneficial effects suggest that targeting the IL-17 axis could be a new therapeutic strategy to prevent chronicity and progression of various liver diseases.
Journal ArticleDOI
An update on the use of benzoate, phenylacetate and phenylbutyrate ammonia scavengers for interrogating and modifying liver nitrogen metabolism and its implications in urea cycle disorders and liver disease.
TL;DR: Overall, as ammonia-scavenging drugs are usually safe and well tolerated among cancer patients, further studies should be instigated to explore the role of these drugs in liver cancer, and it is proposed that ammonia- scaventing drugs might also be used to non-invasively probe liver glutamine metabolism in vivo.
Journal ArticleDOI
The hepatoprotective effect of myricetin against lipopolysaccharide and D-galactosamine-induced fulminant hepatitis.
TL;DR: Myr exhibits a protective role against LPS/D-GalN-induced FH by suppressing hepatic apoptosis, inflammation, and oxidative stress, likely involving in the regulation of apoptosis-related protein, TLR4-NF-κB/-MAPK and NLRP3 inflammasome, and AMPK-Nrf2/HO-1 signaling pathway.
Journal ArticleDOI
Human Liver Regeneration: An Etiology Dependent Process
TL;DR: This manuscript focuses on the etiology-specific damage that is observed in different human diseases and how the liver regulates the regenerative response in an acute and chronic setting and describes the importance of morphological keynotes in different etiologies.
References
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Journal ArticleDOI
Acute liver failure: redefining the syndromes
TL;DR: Hyperacute liver failure is the authors' suggested term for cases in which encephalopathy occurs within 7 days of the onset of jaundice; this group includes the sizeable cohort likely to survive with medical management despite the high incidence of cerebral oedema.
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Acute liver failure: Summary of a workshop.
TL;DR: The outcome of ALF varies by etiology, favorable prognoses being found with acetaminophen overdose, hepatitis A, and ischemia, and poor prognosed with drug‐induced ALF, hepatitis B, and indeterminate cases, and excellent intensive care is critical in management of patients with ALF.
Journal ArticleDOI
Macropinocytosis in phagocytes: regulation of MHC class-II-restricted antigen presentation in dendritic cells.
Zhenzhen Liu,Paul A. Roche +1 more
TL;DR: Macropinocytosis plays a key role in DC-mediated antigen presentation to T cells against pathogens and the efficiency of macropinocytes in antigen capture is regulated during the process of DC maturation.
Journal ArticleDOI
Acetaminophen hepatotoxicity and repair: the role of sterile inflammation and innate immunity
TL;DR: The preponderance of experimental evidence suggests that the extensive sterile inflammatory response during APAP hepatotoxicity is predominantly beneficial by limiting the formation and the impact of pro‐inflammatory mediators and by promoting tissue repair.
Journal ArticleDOI
Activation of autophagy protects against acetaminophen‐induced hepatotoxicity
TL;DR: It is found that APAP overdose induces autophagy, which attenuates APAP‐induced liver cell death by removing damaged mitochondria, which suggests APAP mitochondrial protein binding and the subsequent production of reactive oxygen species may play an important role in AP AP‐induced autophagic flux assays.