PTH-106 Plasma S100A8/A9: a novel mechanistic biomarker in innate immune activation in acute-on-chronic liver failure

Singanayagam, Arjuna; Nathwani, Rooshi; Triantafyllou, Evangelos; Patel, Vishal C.; Dhar, Anjan; McPhail, Mark; Bernsmeier, Christine; Wendon, Julia; Antoniades, C.G.

doi:10.1136/gutjnl-2018-bsgabstracts.262

Cited by 2 publications

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“…THBS1 was certified in regulating immune activation, enhancing inflammatory response, and accelerating fibrosis ( Lopez-Dee et al, 2011 ). S100A8 strongly correlated with activation of proinflammatory mediators and indices of ACLF disease severity, extrahepatic organ failure, and outcome ( Singanayagam et al, 2018 ). WNT5A overexpression has been positively correlated with ACLF prognosis ( Ji et al, 2015 ).…”

Section: Discussionmentioning

confidence: 99%

Transcriptomics reveals immune-metabolism disorder in acute-on-chronic liver failure in rats

et al. 2021

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Acute-on-chronic liver failure (ACLF) is clinical syndrome with high mortality rate. This study aimed to perform detailed transcriptomic analysis in liver cirrhosis–based ACLF rats to elucidate ACLF pathogenesis. ACLF was induced by combined porcine serum with D-galactosamine and lipopolysaccharide. Gene expression profile of liver tissues from ACLF rats was generated by transcriptome sequencing to reveal the molecular mechanism. ACLF rats successfully developed with typical characteristics. Total of 2,354/3,576 differentially expressed genes were identified when ACLF was compared to liver cirrhosis and normal control, separately. The functional synergy analysis revealed prominent immune dysregulation at ACLF stage, whereas metabolic disruption was significantly down-regulated. Relative proportions of innate immune–related cells showed significant elevation of monocytes and macrophages, whereas adaptive immune–related cells were reduced. The seven differentially expressed genes underlying the ACLF molecular mechanisms were externally validated, among them THBS1, IL-10, and NR4A3 expressions were confirmed in rats, patient transcriptomics, and liver biopsies, verifying their potential value in the ACLF pathogenesis. This study indicates immune-metabolism disorder in ACLF rats, which may provide clinicians new targets for improving intervention strategies.

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Section: Discussionmentioning

confidence: 99%

Transcriptomics reveals immune-metabolism disorder in acute-on-chronic liver failure in rats

et al. 2021

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“…Hyponatremia has appeared to have an independent prescient impact on 90 days survival [48] and copeptin concentrations in blood plasma showing changes in vasopressin level have appeared to ameliorate the ability of the CLIF-C ACLF score [49]. Additionally, urinary neutrophil gelatinase-associated lipocalin (N-GAL), plasma S100A8/A9 and soluble CD163 have also been shown to be increased in ACLF and correspond with the prognosis [50][51][52]. Apart from the above prediction models, the liver biopsy has also been found to be helpful in predicting the outcome and poor prognosis of ACLF, and further need for an early LT in these patients [53].…”

Section: Grades Of Acute-on-chronic Liver Failure (Aclf) Based On The...mentioning

confidence: 99%

Acute Decompensated Liver: When to Transplant?

Yadav¹,

Yadav²,

Liang³

2023

Controversies in Liver Transplantation - Recent Challenges and Future Perspectives

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Currently, liver transplant (LT) is only the effective treatment for an acute decompensated liver. Yet, a result of LT in the background of acute decompensated liver largely depends upon the cause of decompensation. Acute-on-chronic liver failure (ACLF) should not be confused with acute liver failure (ALF), where a patient with ACLF presents with a distinct clinical feature than ALF and often requires LT as the only definitive treatment option. However, ACLF patients are generally not listed for the emergency LT due to advanced age, ongoing sepsis, multiple organ failures and active alcoholism. Then again, about 40% of the patients with ALF recover spontaneously with medical care and hence do not need LT. In between these all perplexities and contentions, it’s critical to comprehend the clinical course of liver failure. In addition, physicians should also understand when it is necessary to enlist a patient for LT and which patient are likely to get benefit from LT. Thus, utilizing a “golden window” time for LT before the development of multi-organ failure. In this chapter, we focus on the current situation of LT for ALF and ACLF and further discuss the current decision making strategies used to indicate LT in this difficult clinical scenario.

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PTH-106 Plasma S100A8/A9: a novel mechanistic biomarker in innate immune activation in acute-on-chronic liver failure

Cited by 2 publications

References 0 publications

Transcriptomics reveals immune-metabolism disorder in acute-on-chronic liver failure in rats

Transcriptomics reveals immune-metabolism disorder in acute-on-chronic liver failure in rats

Acute Decompensated Liver: When to Transplant?

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