Rifaximin in the prevention of alcoholic liver disease

Anti-fibrotic and molecular aspects of rifaximin in alcoholic liver disease: A randomized placebo controlled clinical trial

Status

Active, not recruiting

Phases

Phase 4

Study type

Interventional

Source

EU CTR

Registry ID

EUCTR2014-001856-51-DK

Enrollment

136

Registered

2014-06-10

Start date

2014-08-26

Completion date

Unknown

Last updated

2022-03-02

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

Conditions

Liver fibrosis MedDRA version: 20.0 Level: LLT Classification code 10016648 Term: Fibrosis liver System Organ Class: 100000004871

Interventions

Trade Name: Xifaxan Pharmaceutical Form: Tablet INN or Proposed INN: RIFAXIMIN CAS Number: 80621-81-4 Concentration unit: g gram(s) Concentration type: equal Concentration number: 550- Pharmaceutical

Eligibility

Sex/Gender

All

Inclusion criteria

Inclusion criteria: 1. Liver fibrosis estimated by an Ishak score from 1-4 2. Women of child-bearing potential should use safe anti-conception and provide a negative pregnancy test. Are the trial subjects under 18? no Number of subjects for this age range: F.1.2 Adults (18-64 years) yes F.1.2.1 Number of subjects for this age range 120 F.1.3 Elderly (>=65 years) yes F.1.3.1 Number of subjects for this age range 16

Exclusion criteria

Exclusion criteria: 1. Known allergy to rifaximin 2. The investigator judge that the patient would not be compliant with trial medicine 3. Antibiotic treatment the prior 4 weeks

Design outcomes

Primary

Measure	Time frame
Main Objective: We hypothesise that the gut microbiota is a major contributor to progression of fibrosis in alcoholic liver disease and that modulating gut flora by rifaximn halter disease progression. ;Secondary Objective: The effects of rifaximin on the gut microbiota, metabolomics and metatranscriptomic ;Primary end point(s): 1. Rifaximin increases the proportion of patients with an improvement in Ishak score of liver biopsies equal to or more than 1;Timepoint(s) of evaluation of this end point: 18 months	—

Measure

Time frame

Main Objective: We hypothesise that the gut microbiota is a major contributor to progression of fibrosis in alcoholic liver disease and that modulating gut flora by rifaximn halter disease progression. ;Secondary Objective: The effects of rifaximin on the gut microbiota, metabolomics and metatranscriptomic ;Primary end point(s): 1. Rifaximin increases the proportion of patients with an improvement in Ishak score of liver biopsies equal to or more than 1;Timepoint(s) of evaluation of this end point: 18 months

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Secondary

Measure	Time frame
Secondary end point(s): 1. Rifaximin reduces the surrogate markers of fibrosis: collagen proportionate area, hydroxylprolin level, TIMP-1, MMP2, key pro-fibrotic cytokines (TGF-ß1, PDGF-ß-R, CTGF) and key pro-inflammatory cytokines (TNF-a, MCP-1) and CD 163 2. Rifaximin inhibits activation of hepatic stellate cells estimated by a reduction in the area of a-smooth muscle actin positive cells 3. Rifaximin changes the composition of the microbiota estimated by 454 pyrusequencing technology of faecal samples 4. Rifaximin changes gene expression of the microbiota estimated by transscriptomic of faecal samples 5. Rifaximin reduces host pro-inflammatory gene expression in hepatic tissue estimated by transcriptomics and microRNA profiling 6. Rifaximin affects host metabolomics of blood and urine including micro-RNA profile ;Timepoint(s) of evaluation of this end point: 18 months	—

Measure

Time frame

Secondary end point(s): 1. Rifaximin reduces the surrogate markers of fibrosis: collagen proportionate area, hydroxylprolin level, TIMP-1, MMP2, key pro-fibrotic cytokines (TGF-ß1, PDGF-ß-R, CTGF) and key pro-inflammatory cytokines (TNF-a, MCP-1) and CD 163 2. Rifaximin inhibits activation of hepatic stellate cells estimated by a reduction in the area of a-smooth muscle actin positive cells 3. Rifaximin changes the composition of the microbiota estimated by 454 pyrusequencing technology of faecal samples 4. Rifaximin changes gene expression of the microbiota estimated by transscriptomic of faecal samples 5. Rifaximin reduces host pro-inflammatory gene expression in hepatic tissue estimated by transcriptomics and microRNA profiling 6. Rifaximin affects host metabolomics of blood and urine including micro-RNA profile ;Timepoint(s) of evaluation of this end point: 18 months

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Countries

Denmark

Contacts

Public ContactMads Israelsen

Dept of Gastroenterology Odense Universityhospital

mads.egerod.israelsen@rsyd.dk004520681060

Outcome results

None listed

Source: EU CTR (via WHO ICTRP) · Data processed: Feb 4, 2026