Assessement of the Prevalence of Lysosomal Acid Lipase Deficiency in Liver Post-transplant Patients
NCT ID: NCT02851550
Last Updated: 2016-08-01
Study Results
The study team has not published outcome measurements, participant flow, or safety data for this trial yet. Check back later for updates.
Basic Information
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UNKNOWN
100 participants
OBSERVATIONAL
2015-12-31
2018-06-30
Brief Summary
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The accumulation of lipid is in hepatocytes, Kupffer cells and macrophages leading to a fatty liver, hepatic fibrosis that can evolve up to cirrhosis.
LAL deficiency is responsible for significant morbidity and early mortality in children, adolescents and adults in connection with a multi visceral disease reaching the liver, gastrointestinal tract and the vascular endothelium. The disease is caused by homozygous or heterozygous mutations in the gene (LIPA chromosome 10q23.2-23.3) which is responsible for the synthesis of the LAL.
The disease can be diagnosed by enzymatic analysis using few drops of blood absorbed onto blotting paper.
Patients with this deficiency LAL, have no or reduced activity of this enzyme. Because of its rarity, the deficit in LAL is under diagnosed or is diagnosed in patients with liver biological disturbances and / or lipid profile disturbances, steatohepatitis-hepatitis (NASH), the steatosis (NAFLD), the cryptogenic cirrhosis or Wilson disease.
Inclusion period of 12 to 18 months (100 patients).
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Detailed Description
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Conditions
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Study Design
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COHORT
PROSPECTIVE
Eligibility Criteria
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Inclusion Criteria
* patients with cryptogenic cirrhosis, NASH
Exclusion Criteria
18 Years
ALL
No
Sponsors
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Hospices Civils de Lyon
OTHER
Responsible Party
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Principal Investigators
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Sylvie Radenne, MD
Role: PRINCIPAL_INVESTIGATOR
Hospices Civils de Lyon
Locations
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Hépato-Gastro-Entérologie, Hôpital de la Croix Rousse, 103 gde rue de la Croix Rousse
Lyon, , France
Countries
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Central Contacts
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Facility Contacts
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Other Identifiers
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69HCL16_0485
Identifier Type: -
Identifier Source: org_study_id
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