scholarly journals Early identification using the referral system prolonged the time to onset for hepatic encephalopathy after diagnosing severe acute liver injury

2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Keisuke Kakisaka ◽  
Yuji Suzuki ◽  
Hiroaki Abe ◽  
Takuya Watanabe ◽  
Kenji Yusa ◽  
...  
Keyword(s):  
Multivariate Analysis ◽  
Hepatic Encephalopathy ◽  
Liver Injury ◽  
Early Identification ◽  
Total Bilirubin ◽  
Acute Liver Injury ◽  
Referral System ◽  
Significant Difference ◽  
Risk Of Progression ◽  
Time To Onset

Abstract In 2004, we implemented a referral system for patients with acute liver injury (ALI) based on an established formula that estimates the risk of progression to acute live failure (ALF); however, the benefits of the system for patients with severe acute liver injury (SLI) remain unclear. We have evaluated the clinical significance of the referral system for SLI patients. Patients with ALI/SLI who were consecutively and prospectively listed on the system between 2004 and 2018 were analyzed. Of the 371 ALI/SLI/ALF patients on the system, 124 satisfied the criteria for SLI; 34 of these 124 progressed to SLI after registration. Multivariate analysis using age, sex, AST, ALT, creatinine, total bilirubin, prothrombin, presence of hepatic encephalopathy (HE), and SLI at registration revealed that HE was associated with high mortality. Among the 23 patients who developed HE, five who progressed to SLI after registration showed an increased time to HE development compared with patients who had SLI at the time of registration. However, there was no significant difference in survival time after HE development. We concluded that early identification of SLI patients using the referral system increased the time from SLI diagnosis to HE development.

Explore the mechanism of Swertia mussotii Franch. for hepatoprotective effects with iTRAQ-LC-MS/MS

2020 ◽  
Vol 23 ◽  
Author(s):  
Haixia Yun ◽  
Xinyu Wu ◽  
Yiwei Ding ◽  
Wendou Xiong ◽  
Xianglan Duan ◽  
...  
Keyword(s):  
Lipid Metabolism ◽  
Carbon Tetrachloride ◽  
Liver Injury ◽  
Aspartate Aminotransferase ◽  
Alanine Aminotransferase ◽  
Total Bilirubin ◽  
Acute Liver Injury ◽  
Proteome Analysis ◽  
Ppi Networks ◽  
Hepatoprotective Effects

Background and Objective : A Tibetan traditional herb named Swertia mussotii Franch., also called “Zangyinchen” by the local people of Qinghai-Tibet area, has been used to protect the liver from injury for many years. However, the curative effect and molecular mechanism of the herb have not been demonstrated clearly. Materials and Methods: In our study, serum alanine aminotransferase, aspartate aminotransferase, total bilirubin levels were examined after S. mussotii Franch. treatment in the acute liver injury of the carbon tetrachloride-induced rat model. Then, Proteome Analysis was applied to explore the potential mechanism of SMT for hepatoprotective effects after iTRAQLC-MS/MS analysis (isobaric tag for relative and absolute quantification-liquid chromatograph-mass spectrometer with tandem mass spectrometry). Results: Serum results showed, alanine aminotransferase, aspartate aminotransferase, total bilirubin levels of rats with acute liver injury were all improved with SMT treatment. Moreover, Proteome Analysis suggested that, with S. Mussotii Franch. treatment, the levels of lipid catabolic process and lipid homeostasis were all enhanced. And the results of protein-protein interaction (PPI) analysis illustrated that these proteins assembled in PPI networks were found almost significantly enriched in response to lipid, negative regulation of lipase activity, response to lipopolysaccharide etc. Furthermore, the downregulated MRP14 and MRP8 proteins were found involved in the lipid metabolism, which may indicate the mechanism of SMT protection liver from ALI induced by carbon tetrachloride. Conclusion: SMT herb could play a role in hepatoprotection and alleviate the effect of acute liver injury by impacting the lipid metabolism associated biological process.

scholarly journals CD36 deficiency ameliorates drug-induced acute liver injury in mice

2021 ◽  
Vol 27 (1) ◽  
Author(s):  
Chen Zhang ◽  
Xiao Shi ◽  
Zhongping Su ◽  
Chao Hu ◽  
Xianmin Mu ◽  
...  
Keyword(s):  
Liver Injury ◽  
Western Blot ◽  
Kinase Inhibitor ◽  
Inflammatory Responses ◽  
Acute Liver Injury ◽  
Protein Adducts ◽  
Sterile Inflammation ◽  
Inflammatory Factor ◽  
Cd36 Deficiency ◽  
Significant Difference

Abstract Background Acetaminophen (APAP) overdose causes hepatotoxicity and even acute liver failure. Recent studies indicate that sterile inflammation and innate immune cells may play important roles in damage-induced hepatocytes regeneration and liver repair. The scavenger receptor CD36 has its crucial functions in sterile inflammation. However, the roles of CD36 in APAP induced acute liver injury remain unclear and warrant further investigation. Methods WT C57BL/6 J and CD36−/− mice were intraperitoneally injected with APAP (300 mg/kg) after fasting for 16 h. Liver injury was evaluated by serum alanine aminotransferase (ALT) level and liver tissue hematoxylin and eosin (H&E) staining. Liver inflammatory factor expression was determined by real-time polymerase chain reaction (PCR). The protein adducts forming from the metabolite of APAP and the metabolism enzyme cytochrome P450 2E1 (CYP2E1) levels were measured by Western blot. Liver infiltrating macrophages and neutrophils were characterized by flow cytometry. RNA sequencing and Western blot were used to evaluate the effect of damage-associated molecular patterns (DAMP) molecule high mobility group B1 (HMGB1) on WT and CD36−/− macrophages. Moreover, PP2, a Src kinase inhibitor, blocking CD36 signaling, was applied in APAP model. Results The expression of CD36 was increased in the liver of mice after APAP treatment. Compared with WT mice, APAP treated CD36−/− mice show less liver injury. There was no significant difference in APAP protein adducts and CYP2E1 expression between these two strains. However, reduced pro-inflammatory factor mRNA expression and serum IL-1β level were observed in APAP treated CD36−/− mice as well as infiltrating macrophages and neutrophils. Moreover, CD36 deficiency impaired the activation of c-Jun N-terminal kinase (JNK) caused by APAP. Interestingly, the lack of CD36 reduced the activation of extracellular regulated protein kinases (Erk) and v-akt murine thymoma viral oncogene homolog (Akt) induced by HMGB1. RNA transcription sequencing data indicated that HMGB1 has a different effect on WT and CD36−/− macrophages. Furthermore, treatment with PP2 attenuated APAP induced mouse liver injury. Conclusion Our data demonstrated that CD36 deficiency ameliorated APAP-induced acute liver injury and inflammatory responses by decreasing JNK activation. CD36 might serve as a new target to reduce acute liver injury.

scholarly journals Valproic acid induced acute liver injury resulting in hepatic encephalopathy- a case report and literature review

2018 ◽  
Vol 8 (5) ◽  
pp. 311-314 ◽  
Author(s):  
Vijay Gayam ◽  
Amrendra Kumar Mandal ◽  
Mazin Khalid ◽  
Binav Shrestha ◽  
Pavani Garlapati ◽  
...  
Keyword(s):  
Valproic Acid ◽  
Case Report ◽  
Hepatic Encephalopathy ◽  
Liver Injury ◽  
Literature Review ◽  
Acute Liver Injury

MicroRNA from a 12-h versus 20-h acetylcysteine infusion for paracetamol overdose

2019 ◽  
Vol 38 (6) ◽  
pp. 646-654 ◽  
Author(s):  
A Wong ◽  
C Nejad ◽  
M Gantier ◽  
KW Choy ◽  
James Doery ◽  
...  
Keyword(s):  
Liver Injury ◽  
Acute Liver Injury ◽  
Alanine Transaminase ◽  
Paracetamol Overdose ◽  
Paracetamol Poisoning ◽  
Control Groups ◽  
Treatment Groups ◽  
Significant Difference ◽  
Risk Patients ◽  
And Control

Paracetamol overdose is common and microRNA (miR)-122 expression is increased with liver injury. We aimed to measure miR-122 in the setting of an abbreviated paracetamol overdose treatment regimen. We compared miRNA expression in patients treated for paracetamol poisoning with an abbreviated 12-h intravenous acetylcysteine regimen (200 mg/kg over 4 h, 50 mg/kg over 8 h) or a 20-h regimen (200 mg/kg over 4 h, 100 mg/kg over 16 h) (NACSTOP trial). miR-122 expression is increased (decreased cycle threshold (Ct) values) with paracetamol liver injury. We assessed miR-122 expression in patients receiving the two acetylcysteine regimens and in a separate group with acute liver injury (ALI). We examined 121 blood samples in 38 patients. After 20 h of acetylcysteine, median alanine transaminase (ALT) was 12 U/L (18, 14) versus 16 U/L (11, 21) ( p = 0.17) and median miR-122 Ct was 30.1 (interquartile range (IQR): 28.9, 33.3) versus 31.4 (28.9, 33.9) ( p = 0.7) in the NACSTOP abbreviated and control groups, respectively. Median normalized miR-122 Ct after 20 h of acetylcysteine was 2.2 (IQR 1.9, 6.4), 1.1 (0.7, 2.9), 63.9 (2.5, 168), 123.2 (40.9, 207.8) in the NACSTOP-abbreviated, NACSTOP-control, ALI and hepatotoxicity groups, respectively. There was no significant difference in ALT or miRNA between NACSTOP treatment groups and no signal of increased liver injury from an abbreviated 12-h acetylcysteine regimen. These findings suggest that an abbreviated acetylcysteine regimen in low-risk patients who have overdosed on paracetamol is safe. Further study is required to validate this finding utilizing miRNA as a comparative biomarker.

scholarly journals Dexmedetomidine attenuates lipopolysaccharide-induced acute liver injury in rats by inhibiting caveolin-1 downstream signaling pathway

2021 ◽  
Vol 41 (3) ◽  
Author(s):  
Fei Tong ◽  
Wenchao Shen ◽  
Pengtao Song ◽  
Jiafeng Song ◽  
Yonghe Hu ◽  
...  
Keyword(s):  
Lactic Acid ◽  
Liver Injury ◽  
Signaling Pathway ◽  
Liver Tissue ◽  
Acute Liver Injury ◽  
Male Rats ◽  
Tissue Homogenate ◽  
Caveolin 1 ◽  
Significant Difference ◽  
Group D

Abstract Objective: The aim of the present study is to investigate the anti-injury and anti-inflammatory effects of dexmedetomidine (Dex) in acute liver injury induced by lipopolysaccharide (LPS) in Sprague–Dawley rats and its possible mechanism. Methods: The acute liver injury model of male rats was established by injecting LPS into tail vein. The mean arterial pressure (MAP) of rats was recorded at 0–7 h, and lactic acid was detected at different time points. Wet/dry weight ratio (W/D) was calculated. Pathological changes of rat liver were observed by HE staining. ALT and AST levels in serum were detected. The activities of myeloperoxidase (MPO) and superoxide dismutase (SOD) in liver tissue homogenate and the levels of IL-1β and IL-18 in serum were detected by ELISA. Protein levels of Caveolin-1 (Cav-1), TLR-4 and NLRP3 in liver tissue were tested by immunohistochemistry method. The expression of Cav-1, TLR-4 and NLRP3 mRNA in liver tissue was detected by quantitative polymerase chain reaction (qPCR) to explore its related mechanism. Results: Compared with NS group, serum lactic acid, W/D of liver tissue, MPO, SOD, IL-1β and IL-18 were significantly increased and MAP decreased significantly in LPS group and D+L group. However, compared with NS group, D group showed no significant difference in various indicators. Compared with LPS group, MPO, SOD, IL-1β and IL-18 were significantly decreased and MAP was significantly increased in D+L group. D+L group could significantly increase the level of Cav-1 protein and decrease the level of TLR-4 and NLRP3 protein in liver tissue caused by sepsis. The expression of Cav-1 mRNA was significantly up-regulated and the expression of TLR-4 and NLRP3 mRNA was inhibited in D+L group. Conclusion: Dex pretreatment protects against LPS-induced actue liver injury via inhibiting the activation of the NLRP3 signaling pathway by up-regulating the expression of Cav-1 by sepsis.

scholarly journals Natural history and predictors of poor outcomes in acute liver injury patients in a setting without liver transplant facility

2019 ◽  
Vol 2 (2) ◽  
pp. 6
Author(s):  
Alizeh Abbas
Keyword(s):  
Liver Injury ◽  
Natural History ◽  
Total Bilirubin ◽  
Acute Liver Injury ◽  
High Burden ◽  
Significant Burden ◽  
History Of ◽  
Causes Of Mortality ◽  
Poor Outcomes ◽  
Very High

Hepatitis is one of the leading causes of mortality globally and Pakistan, too, has a very high burden of liver disease and associated morbidity and mortality. Significant burden combined with lack of adequate transplant facilities make it crucial to understand predictors and natural history of more severe stages of liver damage or inflammation, such as acute liver injury, as is the aim of this study. Even though it is known that Acute Liver Injury (ALI) is defined as INR ≥ 2.0, ALT ≥ 10X ULN, and Total Bilirubin ≥ 3 mg/dl, there is a dearth of literature on factors and prognosis associated with ALI.

Exploration of the Hepatoprotective Effect and Mechanism of Swertia mussotii Franch in an Acute Liver Injury Rat Model

2020 ◽  
Vol 22 (9) ◽  
pp. 649-656
Author(s):  
Haixia Yun ◽  
Xianglan Duan ◽  
Wendou Xiong ◽  
Yiwei Ding ◽  
Xinyu Wu ◽  
...  
Keyword(s):  
Fatty Acid ◽  
Liver Injury ◽  
Rat Model ◽  
Aspartate Aminotransferase ◽  
Alanine Aminotransferase ◽  
Acid Metabolism ◽  
Total Bilirubin ◽  
Acute Liver Injury ◽  
Serum Alanine Aminotransferase ◽  
Metabolomics Analysis

Background and Objective: Swertia mussotii Franch, also known as “Zangyinchen”, is one of a Tibetan traditional herb used for treatment of liver diseases over thousands of years at Qinghai-Tibet Plateau, has been confirmed to be hepatoprotective. However, the underlying mechanism is largely unknown. Materials and Method: In this study, we evaluated the effect of S. mussotii treatment in a carbon tetrachloride-induced acute liver injury rat model by examining the serum alanine aminotransferase, aspartate aminotransferase, total bilirubin levels and performing histological observations of the liver tissues. Meanwhile, the metabolomics analysis was used to explore the molecular mechanism of S. mussotii treatment by high performance liquid chromatography tandem mass spectrometry. Results: The results showed that S. mussotii treatment could effectively improve the serum alanine aminotransferase, aspartate aminotransferase, total bilirubin in acute liver injury rat model. Histological observation showed that S. mussotii treatment could effectively alleviate liver injury. Moreover, the metabolomics analysis showed that S. mussotii treatment could normalize the levels of many fatty acid metabolism related metabolites. And the results of pathway analysis showed that these metabolites significantly enriched in fatty acid biosynthesis pathway (myristic acid, dodecanoic acid and capric acid) and linoleic acid metabolism pathway (13-OxoODE). Conclusion: The results indicated that S. mussotii treatment could significantly improve acute liver injury through affecting the pathways related to lipid metabolism.

scholarly journals Yellow fever in a traveller returning from Suriname to the Netherlands, March 2017

2017 ◽  
Vol 22 (11) ◽  
Author(s):  
Marjan Wouthuyzen-Bakker ◽  
Marjolein Knoester ◽  
Aad P van den Berg ◽  
Corine H GeurtsvanKessel ◽  
Marion PG Koopmans ◽  
...  
Keyword(s):  
Intensive Care ◽  
Hepatic Encephalopathy ◽  
Liver Injury ◽  
The Netherlands ◽  
Yellow Fever ◽  
Acute Liver Injury ◽  
World Health ◽  
Rt Pcr ◽  
The World ◽  
Health Organization

A Dutch traveller returning from Suriname in early March 2017, presented with fever and severe acute liver injury. Yellow fever was diagnosed by (q)RT-PCR and sequencing. During hospital stay, the patient’s condition deteriorated and she developed hepatic encephalopathy requiring transfer to the intensive care. Although yellow fever has not been reported in the last four decades in Suriname, vaccination is recommended by the World Health Organization for visitors to this country.

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