Transcriptional analysis of mechanisms in liver failure and sepsis

  • Research type

    Research Study

  • Full title

    Transcriptional analysis of mechanisms and predictors in acute liver failure and sepsis

  • IRAS ID

    350924

  • Contact name

    Andrew Conway-Morris

  • Contact email

    ac926@cam.ac.uk

  • Sponsor organisation

    Cambridge University Hospitals NHS Foundation Trust and University of Cambridge

  • Duration of Study in the UK

    2 years, 0 months, 1 days

  • Research summary

    Acute liver failure (ALF) is a life-threatening condition that occurs on the background of a normal healthy liver. The most common cause of ALF in the UK is paracetamol overdose, although there are other causes including infection and autoimmune conditions. ALF is characterised by injury to the liver which results in activation of the immune system. However, the body’s immune system rapidly becomes overwhelmed resulting in damage to other organs such as the kidneys, brain, and heart which causes them to fail and requires the patient to be admitted to intensive care (ICU). Sepsis is often used as a paradigm to understand ALF as similar disturbances to the immune system are seen.
    The only effective rescue treatment available for ALF is liver transplant (LT). However, given the shortage of organs, lack of alternative therapies, and poor survival rates particularly for patients who do not receive a LT, there is an urgent need to better understand the mechanism of disease in ALF and establish other therapies. It is likely that a person’s genetics play a significant role in determining their initial immune response to ALF and that this influences how quickly and severely their organs begin to fail.

    This research aims to understand how our genes influence our body’s immune response to ALF, how similar or different this is to sepsis, and whether there are any gene pathways that we can target with medications to alter the course of a destructive immune response.

    In this project, we will use patient blood samples to look for genes which are abnormally over-active or under-active in patients who develop ALF and compare this to patients who develop sepsis because of severe chest infection (pneumonia). We will use this knowledge to propose potential treatments which can target affected gene pathways to change the course of disease.

  • REC name

    London - Bromley Research Ethics Committee

  • REC reference

    25/LO/0601

  • Date of REC Opinion

    3 Oct 2025

  • REC opinion

    Further Information Favourable Opinion