Liver CirrhosisPhase 4NCT06630572
Rifaximin in Cirrhosis: Effects on Endotoxin and Haemostatic Indexes
A Phase 4 study testing Rifaximin in people with Liver Cirrhosis and Coagulation Disorder, run by University of Roma La Sapienza at 1 site in Italy.
Trial summary
Rifaximin is an antibiotic that acts locally in the gastrointestinal tract with a broad spectrum of antibacterial activity. The efficacy of rifaximin is well documented in the prevention of acute hepatic encephalopathy. There is no evidence on its benefit to modulate hypercoagulative state in cirrhotic patient. Read more about this study
- Who is it for?
- Ages 18 to 75 years
- Conditions the study is for
- Liver Cirrhosis, Coagulation Disorder, Platelet Disorder
- What is being tested?
- Rifaximin
- Could I receive a placebo?
- Yes, some participants may receive a placebo
- How many people
- 20 participants
- Where
- 1 siteItaly
- Study dates
- 3 Apr 2021to 1 Aug 2024
- Phase
- Phase 4
- Are there results?
- None posted in the registry
Key requirements
Who can take part, as listed by the sponsor. Only the study team can confirm whether you are eligible, so take this list to your doctor.
- Ages 18 to 75 years
- All sexes
- No healthy volunteers
- Adult, Older adult
Who may be able to join
- Patients aged 18-75 years
- Patients of Child-Pugh grade B or C (decompensated liver cirrhosis, as confirmed by clinical symptoms and signs, laboratory results, ultrasound and spiral computed tomography)
Who cannot join
- Presence of overt infection or sepsis
- Treatment with systemic or non-absorbable antibiotic, aspirin or other non-steroidal anti-inflammatory drugs, antidepressant drugs in the previous 30 days
- Recent need of transfusion of platelets or plasma
- Presence of extra-hepatic malignancy
- Active alcohol intake in the last 6 months
- Pregnancy or breast feeding
Show all 13Show fewer
- Presence of overt HE, GI haemorrhage, SBP or other concurrent infections during the previous one month
- Human immunodeficiency virus (HIV) infection
- Chronic renal and/or respiratory insufficiency
- Severe heart disease
- Allergy to rifaximin
- Active post-viral hepatitis requiring or on direct-acting antiviral (DAA) agents
- Previous or active intestinal obstruction.
Trial locations and contacts
1 site in 1 country.
Italy1 site
Sapienza University of Rome - Policlinico Umberto I Roma
Rome, 00161
About this study
Official title: Rifaximin Blunted Higher Levels of Endotoxin in Cirrhosis Patients: a Randomized, Double Blind, Short Term Interventional Trial
Rifaximin is an antibiotic that acts locally in the gastrointestinal tract with a broad spectrum of antibacterial activity. The efficacy of rifaximin is well documented in the prevention of acute hepatic encephalopathy. There is no evidence on its benefit to modulate hypercoagulative state in cirrhotic patient.
To assess the effect of a short-term treatment with rifaximin on systemic levels of intestinal endotoxin and on platelet and coagulation markers in patients with decompensated cirrhosis the study has been planned.
Read the detailed description
The term coagulopathy has been coined because of impaired clotting activation detected by laboratory tests in association with deterioration of liver function; the frequent coexistence of hyperfibrinolysis, low platelet count, and platelet dysfunction reinforced the concept that coagulopathy is associated with cirrhosis.
This concept has been recently challenged for several reasons. The prolongation of global tests of clotting activation does not actually reflect hemostatic changes in vivo and maybe a laboratory artefact. In addition, cirrhotic patients actually disclose a tendency to a hypercoagulation state, which seems to be related to endotoxemia and may be detected in both peripheral and portal circulation, and to an increased platelet activation.
Bacterial lipopolysaccharide (LPS, endotoxin) is elevated in cirrhosis, particularly in decompensated cirrhosis, with a mechanism related to an enhanced gut permeability and ensuing translocation of LPS in the peripheral circulation. Recent data demonstrated that cirrhosis is associated with a low-grade endotoxemia, which is more evident in Child-Pugh classes B and C. Of note, LPS significantly correlated with sCD40L and sPs, suggesting a role for LPS in eliciting platelet activation.
It is difficult to believe that under these circumstances patients with cirrhosis are at high risk of bleeding; thus, apart from gastrointestinal tract bleeding, which is independent of changes of the clotting system, spontaneous bleeding in cirrhosis is rare. Conversely, in vivo data reporting the existence of platelet and clotting activation may explain the increased risk for thrombosis overall in portal circulation. This opens a new and interesting scenario as portal vein thrombosis, which may occur in approximately 20% of cirrhotic patients, should be treated with antithrombotic drugs (https://clinicaltrials.gov/ct2/show/NCT01470547). However, planning trials with anticoagulants in cirrhosis will be very difficult because the persistent concept of "coagulopathy in cirrhosis" is likely to be a barrier against the use of anticoagulants.
Interventional trials to modulate low-grade endotoxemia are warranted to assess if this therapeutic approach may reduce the risk of thrombosis in cirrhosis.
In a small cohort of cirrhotic, a previous study demonstrated that administration of non-absorbable antibiotic reduces thrombin generation coincidentally with serum LPS reduction suggesting a role for LPS as trigger of clotting activation. No data were provided, however, on the effect of this treatment on platelet activation or on the duration of clotting system inhibition.
Rifaximin is an antibiotic that acts locally in the gastrointestinal tract with a broad spectrum of antibacterial activity. The efficacy of rifaximin is well documented in the prevention of acute hepatic encephalopathy (HE). It is recommended as a first-line therapy for HE and was recently approved for the prevention of HE in high-risk populations. More recently, clinical trials have been performed to evaluate the effect of this drug on the prophylaxis of spontaneous bacterial peritonitis (SBP) and other cirrhosis-related complications. Although these studies demonstrated excellent prospects for the clinical application of rifaximin, there is no evidence on its benefit to modulate hypercoagulative state in the cirrhotic patient.
Study objective: to assess the effect of a short-term (14 days) treatment with rifaximin (1100 mg/die) on systemic levels of intestinal endotoxin and on platelet and coagulation markers in patients with decompensated cirrhosis.
- Conditions
- Liver Cirrhosis, Coagulation Disorder, Platelet Disorder, Endotoxemia
- Being tested
- Rifaximin, Placebo
- Keywords
- Rifaximin, Liver Cirrhosis, Endotoxin, Platelet function
- Medical subject headings
- Liver Cirrhosis, Hemostatic Disorders, Blood Platelet Disorders, Endotoxemia
What participants receive
What participants receive. In a randomised study each person is assigned to one group by chance.
RifaximinDrug
Patients randomized to receive Rifaximin for 14 days
PlaceboDrug
Patients randomized to receive Placebo for 14 days
| Study group | Role | What they receive |
|---|---|---|
| TREATMENT | Experimental | Rifaximin (1100 mg/die) - 550 b.i.d. Receives: Drug: Rifaximin |
| PLACEBO | Placebo comparator | Placebo - b.i.d. Receives: Drug: Placebo |
What is being measured
The primary outcome is the main question the study is designed to answer.
Decrease in serum endotoxemia after 14-day treatment with Rifaximin.
Significant decrease (-20%) in serum bacterial LPS (endotoxemia) after 14-day treatment with Rifaximin 550 mg b.i.d respect to the control group as well as after 30 and 60 days from the end of the treatment.
Measured: 14, 30, 60 Days
Secondary outcomes (3)
Impact of serum changes of LPS on coagulation and/or platelet indexes
Significant correlation between change in serum LPS and thrombin generation and/or platelet activation indexes in both groups to support the role of LPS as trigger of clotting activation and platelet activation.
Measured: 14, 30, 60 Days
Clinical Failure
Proportion of patients with clinical failure.
Measured: 14, 30, 60 Days
Safety and tolerability: Number of participants with adverse events as a measure of safety and tolerability
Number of participants with adverse events as a measure of safety and tolerability
Measured: 14, 30, 60 Days
Timeline
From the start of the study to its completion; the mark is today. Estimated dates are the sponsor’s plan.
- First posted8 Oct 2024
- Study start3 Apr 2021
- Primary completion3 Apr 2022
- Study completion1 Aug 2024
Why it stopped: Because drug is expired
Resources
- Official record on ClinicalTrials.govThe registry entry this page is built from, with its full change history.
- Publications (9)Papers the sponsor has linked to this study.
- Other trials for Liver CirrhosisStudies of the same condition, open and under way.
- More trials run by University of Roma La SapienzaThe sponsor's other registered studies.
- What the trial phases meanHow a treatment moves from first tests in people to approval.
More details
For doctors and researchers: how the study is designed, who runs it, and its registry IDs.
Study design
- Study type
- Interventional
- Phase
- Phase 4
- Primary purpose
- Treatment
- Allocation
- Randomised
- Intervention model
- Parallel groups
- Model description
- Randomized, placebo control, double-blind trial.
- Masking
- Quadruple blind
- Who is masked
- Participant, Care provider, Investigator, Outcomes assessor
- Enrolment
- 20 participants (actual)
Sponsor and investigators
- Lead sponsor
- University of Roma La Sapienza
- Sponsor type
- University, hospital or other
- Collaborators
- Azienda Policlinico Umberto I
- Responsible party
- Principal investigator, Stefania Basili, University of Roma La Sapienza
- Investigators
- Stefania BASILI, Prof., Study chair, SAPIENZA UNIVERSITY- Department of Translational and Precision MedicineOliviero Riggio, Prof., Principal investigator, SAPIENZA UNIVERSITY- Department of Translational and Precision MedicineManuela Merli, Prof., Principal investigator, SAPIENZA UNIVERSITY- Department of Translational and Precision MedicineLucia Stefanini, Prof., Principal investigator, SAPIENZA UNIVERSITY- Department of Translational and Precision MedicineRoberto Carnevale, Prof., Principal investigator, SAPIENZA UNIVERSITY
IDs, dates and publications
- ClinicalTrials.gov ID
- NCT06630572
- Sponsor's protocol ID
- EudraCT 2017-000488-34
- Status last verified
- Aug 2024
- First submitted
- 18 Jan 2018
- Last updated
- 8 Oct 2024
- Results posted
- No
- Data monitoring committee
- Yes
- FDA-regulated drug
- No
- FDA-regulated device
- No
- Individual data sharing
- No
Publications
Violi F, Ferro D. Clotting activation and hyperfibrinolysis in cirrhosis: implication for bleeding and thrombosis. Semin Thromb Hemost. 2013 Jun;39(4):426-33. doi: 10.1055/s-0033-1334144. Epub 2013 Mar 13.
PubMed 23487343Violi F, Ferro D, Basili S, Lionetti R, Rossi E, Merli M, Riggio O, Bezzi M, Capocaccia L. Ongoing prothrombotic state in the portal circulation of cirrhotic patients. Thromb Haemost. 1997 Jan;77(1):44-7.
PubMed 9031447Nolan JP. The role of intestinal endotoxin in liver injury: a long and evolving history. Hepatology. 2010 Nov;52(5):1829-35. doi: 10.1002/hep.23917.
PubMed 20890945Raparelli V, Basili S, Carnevale R, Napoleone L, Del Ben M, Nocella C, Bartimoccia S, Lucidi C, Talerico G, Riggio O, Violi F. Low-grade endotoxemia and platelet activation in cirrhosis. Hepatology. 2017 Feb;65(2):571-581. doi: 10.1002/hep.28853. Epub 2016 Nov 5.
PubMed 27641757Violi F, Basili S, Raparelli V, Chowdary P, Gatt A, Burroughs AK. Patients with liver cirrhosis suffer from primary haemostatic defects? Fact or fiction? J Hepatol. 2011 Dec;55(6):1415-27. doi: 10.1016/j.jhep.2011.06.008. Epub 2011 Jun 28.
PubMed 21718668Ferro D, Angelico F, Caldwell SH, Violi F. Bleeding and thrombosis in cirrhotic patients: what really matters? Dig Liver Dis. 2012 Apr;44(4):275-9. doi: 10.1016/j.dld.2011.10.016. Epub 2011 Nov 25.
PubMed 22119620Bass NM, Mullen KD, Sanyal A, Poordad F, Neff G, Leevy CB, Sigal S, Sheikh MY, Beavers K, Frederick T, Teperman L, Hillebrand D, Huang S, Merchant K, Shaw A, Bortey E, Forbes WP. Rifaximin treatment in hepatic encephalopathy. N Engl J Med. 2010 Mar 25;362(12):1071-81. doi: 10.1056/NEJMoa0907893.
PubMed 20335583Rivkin A, Gim S. Rifaximin: new therapeutic indication and future directions. Clin Ther. 2011 Jul;33(7):812-27. doi: 10.1016/j.clinthera.2011.06.007. Epub 2011 Jul 7.
PubMed 21741091Danulescu RM, Ciobica A, Stanciu C, Trifan A. The role of rifaximine in the prevention of the spontaneous bacterial peritonitis. Rev Med Chir Soc Med Nat Iasi. 2013 Apr-Jun;117(2):315-20.
PubMed 24340510
Study at a glance
From the registry record, last updated by the sponsor on 8 Oct 2024. Recruitment status is as the sponsor reported it: confirm with the study team.
- Official title
- Rifaximin Blunted Higher Levels of Endotoxin in Cirrhosis Patients: a Randomized, Double Blind, Short Term Interventional Trial
- ClinicalTrials.gov ID
- NCT06630572
- Acronym / sponsor ID
- EudraCT 2017-000488-34
- Conditions
- Liver Cirrhosis, Coagulation Disorder, Platelet Disorder, Endotoxemia
- Keywords
- Rifaximin, Liver Cirrhosis, Endotoxin, Platelet function
- Phase
- Phase 4
- Study type
- Interventional
- Recruitment status
- TerminatedReason stopped: Because drug is expired
- Enrolment
- 20 participants (actual)
- Lead sponsor
- University of Roma La SapienzaUniversity, hospital or other
- Collaborators
- Azienda Policlinico Umberto I
- Study start
- 3 Apr 2021 (actual)
- Primary completion
- 3 Apr 2022 (actual)
- Study completion
- 1 Aug 2024 (actual)
- First posted
- 8 Oct 2024 (actual)
- Results
- Not posted in the source record
Clinical summary
The research question as the sponsor registered it. This describes what the study plans to test, not what it found.
Rifaximin is an antibiotic that acts locally in the gastrointestinal tract with a broad spectrum of antibacterial activity. The efficacy of rifaximin is well documented in the prevention of acute hepatic encephalopathy. There is no evidence on its benefit to modulate hypercoagulative state in cirrhotic patient.
To assess the effect of a short-term treatment with rifaximin on systemic levels of intestinal endotoxin and on platelet and coagulation markers in patients with decompensated cirrhosis the study has been planned.
Detailed description
The term coagulopathy has been coined because of impaired clotting activation detected by laboratory tests in association with deterioration of liver function; the frequent coexistence of hyperfibrinolysis, low platelet count, and platelet dysfunction reinforced the concept that coagulopathy is associated with cirrhosis.
This concept has been recently challenged for several reasons. The prolongation of global tests of clotting activation does not actually reflect hemostatic changes in vivo and maybe a laboratory artefact. In addition, cirrhotic patients actually disclose a tendency to a hypercoagulation state, which seems to be related to endotoxemia and may be detected in both peripheral and portal circulation, and to an increased platelet activation.
Bacterial lipopolysaccharide (LPS, endotoxin) is elevated in cirrhosis, particularly in decompensated cirrhosis, with a mechanism related to an enhanced gut permeability and ensuing translocation of LPS in the peripheral circulation. Recent data demonstrated that cirrhosis is associated with a low-grade endotoxemia, which is more evident in Child-Pugh classes B and C. Of note, LPS significantly correlated with sCD40L and sPs, suggesting a role for LPS in eliciting platelet activation.
It is difficult to believe that under these circumstances patients with cirrhosis are at high risk of bleeding; thus, apart from gastrointestinal tract bleeding, which is independent of changes of the clotting system, spontaneous bleeding in cirrhosis is rare. Conversely, in vivo data reporting the existence of platelet and clotting activation may explain the increased risk for thrombosis overall in portal circulation. This opens a new and interesting scenario as portal vein thrombosis, which may occur in approximately 20% of cirrhotic patients, should be treated with antithrombotic drugs (https://clinicaltrials.gov/ct2/show/NCT01470547). However, planning trials with anticoagulants in cirrhosis will be very difficult because the persistent concept of "coagulopathy in cirrhosis" is likely to be a barrier against the use of anticoagulants.
Interventional trials to modulate low-grade endotoxemia are warranted to assess if this therapeutic approach may reduce the risk of thrombosis in cirrhosis.
In a small cohort of cirrhotic, a previous study demonstrated that administration of non-absorbable antibiotic reduces thrombin generation coincidentally with serum LPS reduction suggesting a role for LPS as trigger of clotting activation. No data were provided, however, on the effect of this treatment on platelet activation or on the duration of clotting system inhibition.
Rifaximin is an antibiotic that acts locally in the gastrointestinal tract with a broad spectrum of antibacterial activity. The efficacy of rifaximin is well documented in the prevention of acute hepatic encephalopathy (HE). It is recommended as a first-line therapy for HE and was recently approved for the prevention of HE in high-risk populations. More recently, clinical trials have been performed to evaluate the effect of this drug on the prophylaxis of spontaneous bacterial peritonitis (SBP) and other cirrhosis-related complications. Although these studies demonstrated excellent prospects for the clinical application of rifaximin, there is no evidence on its benefit to modulate hypercoagulative state in the cirrhotic patient.
Study objective: to assess the effect of a short-term (14 days) treatment with rifaximin (1100 mg/die) on systemic levels of intestinal endotoxin and on platelet and coagulation markers in patients with decompensated cirrhosis.
Study design
- Primary purpose
- Treatment
- Allocation
- Randomised
- Intervention model
- Parallel groups
- Masking
- Quadruple blind (participant, care provider, investigator, outcomes assessor)
- Number of arms
- 2
- Model description
- Randomized, placebo control, double-blind trial.
| Arm | Type | Receives |
|---|---|---|
| TREATMENT | Experimental | Drug: RifaximinRifaximin (1100 mg/die) - 550 b.i.d. |
| PLACEBO | Placebo comparator | Drug: PlaceboPlacebo - b.i.d. |
Who may qualify
- Ages
- 18 to 75 years
- Sex
- All
- Healthy volunteers
- Not accepted
- Age groups
- Adult, Older adult
Key inclusion criteria (2 listed)
- Patients aged 18-75 years
- Patients of Child-Pugh grade B or C (decompensated liver cirrhosis, as confirmed by clinical symptoms and signs, laboratory results, ultrasound and spiral computed tomography)
Key exclusion criteria (13 listed)
- Presence of overt infection or sepsis
- Treatment with systemic or non-absorbable antibiotic, aspirin or other non-steroidal anti-inflammatory drugs, antidepressant drugs in the previous 30 days
- Recent need of transfusion of platelets or plasma
- Presence of extra-hepatic malignancy
- Active alcohol intake in the last 6 months
Eligibility is decided by the study team after screening; this overview does not establish that a patient qualifies. Full inclusion and exclusion criteria.
Interventions
| Intervention | Type | Arms |
|---|---|---|
| RifaximinPatients randomized to receive Rifaximin for 14 days | Drug | TREATMENT |
| PlaceboPatients randomized to receive Placebo for 14 days | Drug | PLACEBO |
Primary outcome
Decrease in serum endotoxemia after 14-day treatment with Rifaximin.
Time frame: 14, 30, 60 Days
Significant decrease (-20%) in serum bacterial LPS (endotoxemia) after 14-day treatment with Rifaximin 550 mg b.i.d respect to the control group as well as after 30 and 60 days from the end of the treatment.
3 secondary outcomes
Impact of serum changes of LPS on coagulation and/or platelet indexes
Time frame: 14, 30, 60 Days
Clinical Failure
Time frame: 14, 30, 60 Days
Safety and tolerability: Number of participants with adverse events as a measure of safety and tolerability
Time frame: 14, 30, 60 Days
Results and safety
The study was stopped early (reason given: Because drug is expired). Results are not available in the source record.
Research links
- Official record on ClinicalTrials.govLast updated by the sponsor 8 Oct 2024.
- Background: PubMed 23487343Violi F, Ferro D. Clotting activation and hyperfibrinolysis in cirrhosis: implication for bleeding and thrombosis. Semin Thromb Hemost. 2013 Jun;39(4):426-33. doi: 10.1055/s-0033-1334144. Epub 2013 Mar 13.
- Background: PubMed 9031447Violi F, Ferro D, Basili S, Lionetti R, Rossi E, Merli M, Riggio O, Bezzi M, Capocaccia L. Ongoing prothrombotic state in the portal circulation of cirrhotic patients. Thromb Haemost. 1997 Jan;77(1):44-7.
- Background: PubMed 20890945Nolan JP. The role of intestinal endotoxin in liver injury: a long and evolving history. Hepatology. 2010 Nov;52(5):1829-35. doi: 10.1002/hep.23917.
- Background: PubMed 27641757Raparelli V, Basili S, Carnevale R, Napoleone L, Del Ben M, Nocella C, Bartimoccia S, Lucidi C, Talerico G, Riggio O, Violi F. Low-grade endotoxemia and platelet activation in cirrhosis. Hepatology. 2017 Feb;65(2):571-581. doi: 10.1002/hep.28853. Epub 2016 Nov 5.
- Background: PubMed 21718668Violi F, Basili S, Raparelli V, Chowdary P, Gatt A, Burroughs AK. Patients with liver cirrhosis suffer from primary haemostatic defects? Fact or fiction? J Hepatol. 2011 Dec;55(6):1415-27. doi: 10.1016/j.jhep.2011.06.008. Epub 2011 Jun 28.
- Background: PubMed 22119620Ferro D, Angelico F, Caldwell SH, Violi F. Bleeding and thrombosis in cirrhotic patients: what really matters? Dig Liver Dis. 2012 Apr;44(4):275-9. doi: 10.1016/j.dld.2011.10.016. Epub 2011 Nov 25.
- Background: PubMed 20335583Bass NM, Mullen KD, Sanyal A, Poordad F, Neff G, Leevy CB, Sigal S, Sheikh MY, Beavers K, Frederick T, Teperman L, Hillebrand D, Huang S, Merchant K, Shaw A, Bortey E, Forbes WP. Rifaximin treatment in hepatic encephalopathy. N Engl J Med. 2010 Mar 25;362(12):1071-81. doi: 10.1056/NEJMoa0907893.
- Background: PubMed 21741091Rivkin A, Gim S. Rifaximin: new therapeutic indication and future directions. Clin Ther. 2011 Jul;33(7):812-27. doi: 10.1016/j.clinthera.2011.06.007. Epub 2011 Jul 7.
- Background: PubMed 24340510Danulescu RM, Ciobica A, Stanciu C, Trifan A. The role of rifaximine in the prevention of the spontaneous bacterial peritonitis. Rev Med Chir Soc Med Nat Iasi. 2013 Apr-Jun;117(2):315-20.
- Individual participant dataSharing planned: No
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Referral and contact
AzTrials does not enrol participants or take referrals. Contact the study team or a site listed below; they decide who can take part. This study is not recruiting at the moment.
Stefania BASILI, Prof. study chair
SAPIENZA UNIVERSITY- Department of Translational and Precision Medicine
Oliviero Riggio, Prof. principal investigator
SAPIENZA UNIVERSITY- Department of Translational and Precision Medicine
Manuela Merli, Prof. principal investigator
SAPIENZA UNIVERSITY- Department of Translational and Precision Medicine
1 site in 1 country: see every site and its status.
Questions about this trial
What is this clinical trial studying?
A Phase 4 study testing Rifaximin in people with Liver Cirrhosis and Coagulation Disorder, run by University of Roma La Sapienza at 1 site in Italy.
The full registered description is in the About this study section and the official record.
Who may be eligible to take part?
The sponsor lists 2 inclusion and 13 exclusion criteria. Eligibility is decided by the study team after screening, so read the full criteria and contact a listed site.
Is this clinical trial currently recruiting?
The record says: stopped early, as of the sponsor's last update on 8 Oct 2024. Status can change between updates, so confirm with the study contact before making plans.
Where is the study taking place?
The record lists 1 site in Italy. Whether a site is taking part right now should be confirmed with that site. See every site.
What are the possible benefits and risks?
They depend on the study and the treatment, and no study can promise a benefit. Some participants in this study may receive a placebo. The study team explains the known risks during informed consent, before anyone joins; the record itself does not list them.
What does this phase mean?
Phase 4 studies take place after a treatment is approved, to learn more about its long-term benefits and risks in everyday use.
Not every study follows the same path, and some studies (observational studies, device studies) have no phase.
Are results available for this study?
The study was stopped early (reason given: Because drug is expired). Results are not available in the source record.
How can a doctor refer a patient or contact the research team?
The record lists no contact. The official record names the sponsor, who can be asked directly. AzTrials does not enrol participants or take referrals.
What does the primary outcome measure?
Decrease in serum endotoxemia after 14-day treatment with Rifaximin. (time frame: 14, 30, 60 Days). It is what the study was designed to measure, not a finding.
Where can I read the original study information?
On the ClinicalTrials.gov record for NCT06630572, which also lists 9 linked publications.
Does a listing mean the treatment is approved or proven to work?
No. A listing means the study is registered. It does not show that the treatment is safe, works, or is approved by a regulator.
How often is this information updated?
AzTrials copies changed records from ClinicalTrials.gov every night and reloads the whole registry every week. The sponsor last updated this record on 8 Oct 2024.