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Hepatocellular Carcinoma in Patients With a Cirrhosis Due to an Alcoholic or a Non Alcoholic Fatty Liver Disease

Hepatocellular Carcinoma in Patients With a Cirrhosis Due to an Alcoholic or a Non Alcoholic Fatty Liver Disease

Status
Completed
Phases
Unknown
Study type
Observational
Source
ClinicalTrials.gov
Registry ID
NCT03307408
Acronym
CHALNA
Enrollment
180
Registered
2017-10-11
Start date
2017-02-28
Completion date
2022-09-01
Last updated
2026-06-16

For informational purposes only — not medical advice. Sourced from public registries and may not reflect the latest updates. Terms

Conditions

Hepatocellular Carcinoma

Brief summary

Global prevalence of Non Alcoholic Fatty Liver Diseases (NAFLD) ranges from 22% to 28%.The spectrum of these hepatic abnormalities extends from isolated steatosis to steatohepatitis (Non Alcoholic Steato-Hepatitis, NASH) and steatofibrosis leading to cirrhosis and hepatocellular carcinoma. NAFLD is one of the main causes of cirrhosis and increases the risk of liver-related death and hepatocellular carcinoma (developed in patients with or without cirrhosis). Despite this major public health concern, apart from lifestyle changes, treatment of NAFLD is still elusive as there is lack of efficacious pharmacological treatment. Alcoholic liver diseases are also frequent in Western countries. Alcoholic liver diseases and NAFLD share common pathological lesions and molecular pathways. This is illustrated by the emerging role of abnormalities of the microbiota (dysbiosis) in these 2 diseases leading to the concept of " liver-gut axis ". Whereas the molecular mechanisms responsible for the progression from a "safety" state to NASH or to a severe alcoholic steato-hepatitis are still unclear, hepatic inflammation is a key factor involved in the progression of NAFLD and alcoholic liver disease. The hypothesis is that cellular and molecular abnormalities and gut dysbiosis could be present in patients with simple steatosis or with steato-hepatitis and could be responsible for the occurrence of hepatocellular carcinoma particularly without cirrhosis. The main objective is to compare cellular and inflammatory pathways in liver with and without hepatocellular carcinoma in patients with alcoholic or non-alcoholic fatty liver diseases.

Interventions

OTHERblood collection

Standard routine practice clinico-biological data will be collected

Sponsors

Centre Hospitalier Universitaire de Nice
Lead SponsorOTHER

Study design

Observational model
COHORT
Time perspective
PROSPECTIVE

Eligibility

Sex/Gender
ALL
Age
18 Years to No maximum

Inclusion criteria

Group 1 Inclusion Criteria : * Available social insurance * Signed consent for the study enrollment * Age ≥ 18 years

Exclusion criteria

: * Patients in the group with metabolic fatty liver with hepatocellular carcinoma * Alcohol consumption ≤ 30 g/d (or 210 g/week) in men and ≤ 20 g/d (or 140 g/week) in women. * Decision (less than 3 months) to perform a liver biopsy of a tumor suspect of HCC and of adjacent liver in routine practice. * No systemic HCC treatment in the previous 6 months Group 2 Inclusion Criteria : * Available social insurance * Signed consent for the study enrollment * Age ≥ 18 years

Design outcomes

Primary

MeasureTime frameDescription
Dosage of immunity cells in liver8 weeksThe investigators determine the stage of liver by biochemical, genetic (and immunocytochemistry methods.
Dosage of the inflammatory cells in liver8 weeksThe investigators determine the stage of liver by biochemical, genetic and immunocytochemistry methods.

Secondary

MeasureTime frameDescription
Dosage of the glucose8 weeksThe investigators determine the genes implicated in oxidative stress, reticulum endoplasmic stress and autophagy .

Countries

France

Contacts

PRINCIPAL_INVESTIGATORRodolphe ANTY, MD

Centre Hospitalier Universitaire de Nice

Outcome results

None listed

Source: ClinicalTrials.gov · Data processed: Jun 17, 2026