Albumin Modifications as Early Biomarkers of Chronic Liver Diseases
ConditionChronic Liver Disease
Trial statusRecruiting
Trial phaseNot applicable
Trial typeInterventional
Biological sexAll
Age18+
SponsorUniversity Hospital, Limoges
About this trial
Chronic liver diseases, affecting over 800 million people worldwide, lead to approximately 2 million annual deaths. The need for early, sensitive diagnostic strategies to prevent disease progression and reduce mortality is still unmet. The traditional serum markers lack sensitivity and specificity, leading to the integration of these biomarkers into panel tests with algorithms or imaging measures. Despite their widespread use, these tests have limitations at an individual level, including an inability to predict disease progression or response to treatment. To address these shortcomings, our project proposes utilizing albumin post-translational modifications (PTM) as a predictive biomarker for liver disease progression. The hypothesis is that albumin modifications occur in the early stages of hepatocellular damage and are indicative of future liver diseases. These modifications can be detected through serum albumin isoform determination, albumin isoforms profiles or the albumin's ligand-binding capacities. Innovatively, the study will use the Serum Enhanced Binding (SEB) test, which identifies reduced ligand-binding capacities, and discusses a second patent for determining a typical isoform profile based on the hepatic injury type.
Our preliminary results from animal models and a proof-of-concept studies with patients support this hypotheses. Our previous studies demonstrated also significant differences in albumin isoform profiles in response to different types of hepatic injury and high sensitivity and specificity in the SEB test among cirrhotic patients.
The primary objective of the MALAHBAR project is to evaluate the capacity of albumin PTM to predict liver disease progression over three years in chronic liver disease patients. Secondary objectives include assessing the predictive ability of different albumin isoforms and the SEB test for liver disease progression, evaluating diagnostic performances and confirming characteristic albumin isoform profiles related to specific hepatic injuries. The study could represent a significant advancement in liver disease diagnostics and management, offering new insights into the role of albumin in liver pathology.
Eligibility criteria
This trial does not accept healthy volunteersQualifiers
At least 18 years old
With a compensated fibrosis defined by an hepatic elasticity ≥10 kPa measured by FibroScan®
Having had blood test at the hospital as part of a consultation or an hospitalisation at the inclusion including usual parameters for the liver disease follow-up
Affiliated with or beneficiaries of a social security system
Disqualifiers
Patients suffering from decompensated cirrhosis or with an history of decompensated cirrhosis
Patients who received an albumin infusion in the month before the inclusion visit
Patients suffering from stage 4 or 5 renal failure (GFR < 29 ml/min/1,73m²)
Patients suffering from cancer
Trial design
Design model
Single group
Treatments tested in this trial
blood sampling
Procedure/SurgeryIf the patient does not object to participating in the study, a blood sample is taken at each visit (an additional tube may be added to a routine blood sample taken for standard care), or a residual blood sample is reused after routine tests have been performed, and data is collected from the medical record.
Treatment groups
756 Participants
are divided into 1 treatment groupGroup A: experimental armExperimental treatment 1 intervention
Trial outcomes
Primary outcomes
1
Ability of HSA PTM to predict the evolution of liver damage at 3 year in patients with an advanced chronic liver disease (ACLD) as recently defined in the BAVENO VII recommendations based on FibroScan.
The primary outcome is the positive predictive value (VPP) of post-translational HSA modifications related to the worsening of the liver damage at 3 years . This will be determined by an augmentation of more than 20% as compared to the initial state, documented by FibroScan® or a liver related event as defined in BAVENO VII.
Time frame
Years 3Secondary outcomes
1
ability of post-translational HSA modifications to predict the evolution of liver damage at 3 years based on liver-related events or on the worsening of the disease stage evaluated by the de Child Pugh or MELD score.
Positive predictive value (VPP) of post-translational HSA modifications related to the worsening of the liver damage at 3 years. This will be determined by the occurrence of one or several events of the following: 1. Liver-related events 2. Worsening of the disease stage evaluated by the Child Pugh score or of 2 points of the MELD score in case of cirrhosis.
Time frame
Year 32
ability of the different isoforms of HSA to predict the evolution of liver damage at 1 and 2 years provided that data are available in the medical file.
Positive predictive value (VPP) of post-translational HSA modifications related to the worsening of the liver damage at 1 and 2 years. This will be determined by the occurrence of one or several events of the following
Time frame
year 23
ability of SEB test to predict the evolution of liver damage at 3 years (and at 1 and 2 years provided data are available in the medical file).
Positive predictive value of the SEB test related to the worsening of the liver damage at 3 years, and at 1 and 2 years provided data are available in medical files.
Time frame
Year 34
diagnostic performances of the SEB test and of the different isoforms of HSA at each stage of the liver disease.
Sensibility and specificity of the SEB test and of the different isoforms of HAS, at each stage of the . liver disease (Child Pugh A5, A6, B7, B8, B9, et \> C10).
Time frame
year 3Sponsors and contacts
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Source ClinicalTrials.gov