Acute Liver Failure

Rajaram, Priyanka; Subramanian, Ram

doi:10.1055/s-0038-1673372

Cited by 33 publications

(30 citation statements)

References 105 publications

(199 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…In terms of etiology of ALF, acetaminophen (APAP) toxicity is the most prevalent cause in developed countries, whereas viral hepatitis accounts for the majority of ALF cases in developing countries . Other causes of ALF include non‐APAP drug‐induced liver injury (DILI), ischemic hepatitis, autoimmune hepatitis (AIH), fulminant Wilson disease (WD), pregnancy‐associated injury, and indeterminant etiology . Table summarizes the prevalence and evaluation of different etiologies of ALF.…”

Section: Epidemiology and Etiologymentioning

confidence: 99%

“…Hepatitis E virus (HEV) is endemic in parts of northern Africa and southern Asia and rarely seen in Western countries. It is transmitted enterically via contaminated water and food . Young adults and pregnant women (especially in the third trimester) are particularly vulnerable to HEV‐induced ALF .…”

Section: Epidemiology and Etiologymentioning

confidence: 99%

“…Patients can present with neurologic symptoms, chronic liver disease, or ALF . Fulminant WD represents about 3% of ALF cases and usually occurs in young female patients within the first 2 decades of life . In the setting of ALF, spontaneous recovery is rare, and LT is required for survival …”

Section: Epidemiology and Etiologymentioning

confidence: 99%

“…Pregnancy‐associated liver dysfunction that can progress to ALF includes acute fatty liver of pregnancy, preeclampsia, and HELLP (hemolysis, elevated liver enzymes, low platelets) syndrome . With any of these conditions, there is significant risk of placental abruption, disseminated intravascular coagulopathy, and death .…”

Section: Epidemiology and Etiologymentioning

confidence: 99%

See 3 more Smart Citations

Pathophysiology of Acute Liver Failure

2019

View full text Add to dashboard Cite

Acute liver failure (ALF) is a rare syndrome resulting from an acute insult to the liver in patients without known underlying chronic liver disease. It is characterized by loss of synthetic function in the form of jaundice and coagulopathy and development of hepatic encephalopathy. Multiorgan failure (MOF) eventually develops, leading to death. Many different etiologies have been identified, with acetaminophen (APAP) overdose and viral hepatitis being the most common causes worldwide. The pathophysiology of ALF can be divided into cause-specific liver injury pathophysiologies and pathophysiology related to occurrence of secondary MOF. In terms of liver injury pathophysiology, APAP toxicity is the most well known. Secondary MOF is often a result of the initial massive proinflammatory response generating a systemic inflammatory response syndrome followed by a compensatory anti-inflammatory response leading to immune cell dysfunction and sepsis. As the liver is a tremendously important metabolic organ involved in energy metabolism, protein synthesis, fat metabolism, and glycemic control, multiple aspects of nutrition also need to be considered as part of the overall pathophysiology of ALF. (Nutr Clin Pract. 2020;35:24-29)

show abstract

Section: Epidemiology and Etiologymentioning

confidence: 99%

Section: Epidemiology and Etiologymentioning

confidence: 99%

Section: Epidemiology and Etiologymentioning

confidence: 99%

Section: Epidemiology and Etiologymentioning

confidence: 99%

See 2 more Smart Citations

Pathophysiology of Acute Liver Failure

2019

View full text Add to dashboard Cite

show abstract

“…Acetaminophen is one of the most widely applied analgesic-antipyretic over-the-counter agents. It is relatively safe at therapeutic doses, but can cause liver injury, like acute centrilobular necrosis 23,24 even acute liver failure 25 at large dose or in certain risk groups. 26 The analysed result implied acetaminophen might cause toxicity even at a therapeutic dose when taken together with psoralen/isopsoralen.…”

Section: Prediction Of Diseases Related To Key Genes That Were Affementioning

confidence: 99%

The mechanism of Psoralen and Isopsoralen hepatotoxicity as revealed by hepatic gene expression profiling in SD rats

Song

Yang

et al. 2019

Basic Clin Pharma Tox

View full text Add to dashboard Cite

Background The main bioactive components of Fructus psoraleae, such as psoralen and isopsoralen, are known to be hepatotoxic. However, its underlying mechanism is to be elucidated. Methods To address this, SD rats were randomly divided into control group, 60 mg/kg psoralen group and 60 mg/kg isopsoralen group. Blood was collected to detect serum biochemical indices. RNA was extracted from liver samples, and then, cDNA gene expression profiles were analysed. Results Psoralen administration significantly up‐regulated serum AST (aspartate aminotransferase) while addition of isopsoralen increased serum ALT (alanine aminotransferase), AST, TBA (total bile acid) and TG (total triglyceride) levels. A total of 172 differentially expressed genes (DEGs) were acquired between psoralen group and control group while 884 DEGs were screened between isopsoralen group and control group. Chemical Carcinogenesis and Metabolism of Xenobiotics by Cytochrome P450 were the two most significantly enriched pathways as revealed by DEGs. Liver was the most impacted organ, and endoplasmic reticulum was the most impacted organelle in subcellular level. Finally, some kinds of cancers and cytochrome p450 oxidoreductase deficiency were predicted. Taken together, psoralen and isopsoralen might cause hepatotoxicity mainly through cytochrome P450 metabolism of xenobiotics. Furthermore, Cyp1a1, Cyp1a2, Gstm1 and Akr7a3 worked as key genes in hepatotoxicity. Moreover, endoplasmic reticulum was the main target subcellular structure in hepatotoxicity induced by psoralen and isopsoralen.

show abstract

Upregulated microRNA‐450b‐5p represses the development of acute liver failure via modulation of liver function, inflammatory response, and hepatocyte apoptosis

Fang

Kuang

et al. 2023

Immunity Inflam & Disease

View full text Add to dashboard Cite

Objective: It has been evidenced that microRNAs (miRs) exert crucial effects on acute liver failure (ALF), while the detailed function of miR-450b-5p in ALF progression remained obscure. The purpose of this research was to unravel the regulatory mechanism of miR-450b-5p in ALF via modulating Mouse Double Minute 2 protein (MDM2).Methods: ALF was induced in mice by intraperitoneal injection of D-galactosamine (D-GalN) and lipopolysaccharide (LPS). Adenoviruses containing overexpressed miR-450b-5p, MDM2 shRNA, and overexpressed MDM2 sequences were utilized to manipulate miR-450b-5p and MDM2 expression in the liver before the mice were treated with D-GalN/LPS-induced ALF.Subsequently, miR-450b-5p and MDM2 expression levels in liver tissues of ALF mice were examined. Serum biochemical parameters of liver function were tested, serum inflammatory factors were assessed, and the histopathological changes and hepatocyte apoptosis in liver tissues were observed. The relation between miR-450b-5p and MDM2 was verified. Results: In ALF mice, miR-450b-5p was low-expressed while MDM2 was high-expressed. The upregulation of miR-450b-5p or downregulation of MDM2 could alleviate liver function, mitigate the serum inflammatory response and pathological changes in liver tissues, as well as inhibit the apoptosis of hepatocytes. MiR-450b-5p targeted MDM2. MDM2 overexpression reversed the repressive effects of elevated miR-450b-5p on ALF. Conclusion:The upregulated miR-450b-5p blocks the progression of ALF via targeting MDM2. This study contributes to affording novel therapeutic targets for ALF treatment.

show abstract

Acute Liver Failure

Cited by 33 publications

References 105 publications

Pathophysiology of Acute Liver Failure

Pathophysiology of Acute Liver Failure

The mechanism of Psoralen and Isopsoralen hepatotoxicity as revealed by hepatic gene expression profiling in SD rats

Upregulated microRNA‐450b‐5p represses the development of acute liver failure via modulation of liver function, inflammatory response, and hepatocyte apoptosis

Contact Info

Product

Resources

About