CirrhosisNCT07471542
Copper Supplementation in Cirrhosis
A study testing Copper Gluconate in people with Cirrhosis and Chronic Liver Disease, run by University of Washington at 1 site in United States.
Trial summary
End stage liver disease or cirrhosis is a major cause of mortality in the United States and the world. Other than targeting the underlying cause, such as alcohol cessation and antiviral therapy, very few medical treatments can change the natural history of cirrhosis. Read more about this study
- Who is it for?
- Ages 18 years and older
- Conditions the study is for
- Cirrhosis, Chronic Liver Disease, Fibrosis
- What is being tested?
- Copper Gluconate
- Type of treatment
- Pill or oral medicine
- Could I receive a placebo?
- No, everyone receives an active treatment
- How many people
- 30 participants
- Where
- 1 siteUnited States
- Study dates
- 15 Mar 2026to Dec 2028
- Phase
- Interventional
- Are there results?
- Not yet: the study is under way
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 years and older
- All sexes
- No healthy volunteers
- Adult, Older adult
Who may be able to join
- Adult patients age 18 or older with confirmed diagnosis of cirrhosis based on clinical history, exam, imaging, laboratory or histological criteria;
- Cirrhosis patients whose serum or plasma Cu are below the normal range (80-155 ug/dL for women and 70-140 ug/dL for men);
- Cirrhosis patients whose serum or plasma Cu are in the normal range but exhibit at least one clinical feature that has been associated with Cu deficiency. These include history of infections, unexplained anemia, severe leukopenia, iron overload, unexplained neurological symptoms such as ataxia or myelopathy, coagulopathy with spontaneous bleeding.
- Patients must meet inclusion criteria 1 AND 2, or 1 AND 3 in order to be considered for the trial
Who cannot join
- Patients with Wilson disease, cholestatic liver diseases including primary biliary cholangitis and primary sclerosing cholangitis, all of which are associated with Cu overload;
- Patients with fulminant hepatic failure;
- Renal failure with a creatinine clearance <25 ml/minute;
- Hepatic encephalopathy more than grade 2 (Hepatic Encephalopathy in Chronic Liver Disease, 2014);
- MELD score >25 to minimize subject dropout due to been too ill;
- Serious non-liver related medical illnesses such as cardiopulmonary and renal diseases and non-liver malignancies;
- Active alcohol use;
- Pregnancy
Trial locations and contacts
1 site in 1 country. Contact the study team or a site near you to ask about taking part.
United States1 site, 1 recruiting
- Recruiting
University of Washington Medical Center
Seattle, Washington, 98195
Shukriyah Samoun, BS, 2065433220, shukrs@uw.edu
Lei Yu, MD
About this study
Official title: A Pilot Randomized Controlled Trial to Determine the Biochemical Effect, Safety and Patient Reported Outcomes of Copper Supplementation in Patients With Cirrhosis
End stage liver disease or cirrhosis is a major cause of mortality in the United States and the world. Other than targeting the underlying cause, such as alcohol cessation and antiviral therapy, very few medical treatments can change the natural history of cirrhosis. Malnutrition is one of the few potentially modifiable factors that have been associated with cirrhosis severity and poor prognosis. The transition metal copper (Cu) is an essential trace metal that must be acquired from diet. Its metabolism is primarily regulated by the liver in its role as a master regulator of nutrients. In 2019, the investigators reported that Cu deficiency defined by below normal serum or liver concentrations occurred in a wide range of liver disorders and was associated with a severe disease phenotype. Improvement in liver function was observed in 2 of the 3 patients who received Cu supplementation. In 2023, the investigators conducted a longitudinal cohort study utilizing clinical, serum and liver explant tissue data from 183 cirrhosis patients. The investigators showed that Cu deficiency was associated with 2-fold higher infection rate and a more than 3-fold increase in the risk of death compared to patients with normal Cu status. These preliminary findings and the well-established importance of Cu in human health prompted the investigators to design the current pilot randomized, placebo-controlled, crossover trial to determine the effect of Cu supplementation on Cu dependent biochemical changes, patient safety and patient reported outcomes in cirrhosis.
Read the detailed description
Approximately 41,000 people die annually of chronic liver disease (CLD) including liver cancer in the United States. Compared to other chronic diseases, patients with CLD have high rates of healthcare utilization and death. The annual cost of care for patients with cirrhosis, the most advanced stage of liver disease, is approximately $21 billion. While liver transplantation is a curative, albeit costly, treatment, there are far fewer donors than patients in need of liver transplants. Other than targeting the causes of cirrhosis, such as alcohol cessation and antiviral therapy, very few medical treatments can change the natural history of cirrhosis. Malnutrition is one of the few potentially modifiable factors that have been associated with cirrhosis severity and poor prognosis. Current guidelines in nutrition management focus on protein and calorie intake, with little consideration for trace metals, which have wide ranging physiological effects.
The transition metal copper (Cu) is an essential trace metal that must be acquired from diet. Absorption, uptake, export and transport of Cu are tightly regulated because both too much and too little Cu can cause cell damage, compromised immune function and organ dysfunction. Systemic Cu metabolism is primarily regulated by the liver in its role as a master regulator of nutrients. Whole body Cu status is best estimated by its blood concentration. Depending on laboratory benchmarks and sex, the lower limit of normal serum Cu is between 70-80 g/dL where concentrations below this range likely reflect systemic Cu deficiency.
In 2019, the investigators began an effort to better understand the role of Cu in liver disease and reported a series of patients who presented with unexplained low blood Cu concentrations. In this detailed report, Cu deficiency defined by below normal serum or liver concentrations occurred in a wide range of liver disorders and was associated with a severe disease phenotype. Improvement in liver function was observed in 2 of the 3 patients who received Cu supplementation. To further these preliminary observation, in 2023, the investigators conducted a longitudinal cohort study utilizing clinical, serum and liver explant tissue data from 183 cirrhosis patients. The investigators showed that Cu deficiency was associated with significantly higher infections rates (42% vs. 20%, p=0.01) and a more than 3-fold increase in the risk of death compared to patients with normal Cu status. These results provide concrete evidence that a complex, and potentially causal relationship exist between Cu status, compromised immune and metabolic functions and worse clinical outcomes in cirrhosis patients.
These preliminary findings and the well-established importance of Cu in human health raise several important questions: Does reduced circulating Cu, the standard definition of Cu deficiency in the general population, similarly reflect a deficiency state in cirrhosis? Is the higher infection and mortality risk observed among patients with low serum Cu mediated by Cu dependent enzymes and immune cells? Is reduced circulating Cu a secondary response in cirrhosis, therefore should be "left alone," or should patients receive Cu supplementation in order to improve functional Cu store and its associated physiological functions? To answer these questions, the investigators designed a pilot randomized, placebo-controlled, crossover trial to determine the effect of Cu supplementation on Cu dependent biochemical changes, patient safety and patient reported outcomes.
- Conditions
- Cirrhosis, Chronic Liver Disease, Fibrosis, Infection
- Being tested
- Copper Gluconate
- Keywords
- copper, cirrhosis, malnutrition
- Medical subject headings
- Fibrosis, Infections, Malnutrition
What participants receive
What participants receive. In a randomised study each person is assigned to one group by chance.
Copper GluconateDietary supplement
Oral copper gluconate 4 mg daily
| Study group | Role | What they receive |
|---|---|---|
| Copper supplementation 1st arm | Experimental | copper supplementation first, washout, then placebo Receives: Dietary Supplement: Copper Gluconate |
| Placebo first arm | Experimental | Placebo first, washout, then copper supplementation Receives: Dietary Supplement: Copper Gluconate |
What is being measured
The primary outcome is the main question the study is designed to answer.
Plasma copper (Cu) concentration
The primary endpoint is the mean change in plasma Cu concentration between baseline and each intervention period
Measured: From randomization to 1. end 6-week; 2. end of 9-week; 3. end of 15 week. First 6 week is intervention period 1 (either copper or placebo); followed by a 3-week washout period; followed by another 6-week intervention period (either placebo or copper).
Secondary outcomes (14)
Biomarkers of functional Copper (Cu) status
Plasma ceruloplasmin concentration and activity
Measured: From randomization to 1) end 6-week; 2) end of 9-week; 3) end of 15 week. First 6 week is intervention period 1 (either copper or placebo), followed by a 3-week washout period, followed by another 6-week intervention period (either placebo or copper)
Biomarkers of functional copper status
Plasma diamine oxidase concentration and activity
Measured: Time Frame: From randomization to 1) end 6-week; 2) end of 9-week; 3) end of 15 week. First 6 week is intervention period 1 (either copper or placebo), followed by a 3-week washout period, followed by another 6-week intervention period (either placebo or
Biomarker of functional copper status
Neutrophil and PBMC oxidative burst activity
Measured: Time Frame: From randomization to 1) end 6-week; 2) end of 9-week; 3) end of 15 week. First 6 week is intervention period 1 (either copper or placebo), followed by a 3-week washout period, followed by another 6-week intervention period (either placebo or
Biomarker of functional copper status
PBMC superoxide dismutase (CCS) mRNA expression
Measured: From randomization to 1. end 6-week; 2. end of 9-week; 3. end of 15 week. First 6 week is intervention period 1 (either copper or placebo); followed by a 3-week washout period; followed by another 6-week intervention period (either placebo or copper)
Biomarker of functional copper status
Platelet cytochrome-C oxidase (COX) activity
Measured: From randomization to 1) end 6-week; 2) end of 9-week; 3) end of 15 week. First 6 week is intervention period 1 (either copper or placebo), followed by a 3-week washout period, followed by another 6-week intervention period (either placebo or copper)
Safety measures
Patient death before liver transplantation
Measured: From randomization to 1) end 6-week; 2) end of 9-week; 3) end of 15 week. First 6 week is intervention period 1 (either copper or placebo), followed by a 3-week washout period, followed by another 6-week intervention period (either placebo or copper)
Safety measures
Change in liver function based on MELD (maximum 40, high school worse liver function) and CTP score (5 to 15, higher school worse liver function)
Measured: From randomization to 1) end 6-week; 2) end of 9-week; 3) end of 15 week. First 6 week is intervention period 1 (either copper or placebo), followed by a 3-week washout period, followed by another 6-week intervention period (either placebo or copper)
Safety measures
Incidence of hospital admission from infection or bleeding
Measured: From randomization to 1) end 6-week; 2) end of 9-week; 3) end of 15 week. First 6 week is intervention period 1 (either copper or placebo), followed by a 3-week washout period, followed by another 6-week intervention period (either placebo or copper)
Safety measure
Plasma ratio of reduced to oxidized glutathione (GSH/GSSG)
Measured: Time Frame: From randomization to 1) end 6-week; 2) end of 9-week; 3) end of 15 week. First 6 week is intervention period 1 (either copper or placebo), followed by a 3-week washout period, followed by another 6-week intervention period (either placebo or
Patient reported outcomes
Change in Chronic Liver Disease Questionnaire (CLDQ)
Measured: From randomization to 1) end 6-week; 2) end of 9-week; 3) end of 15 week. First 6 week is intervention period 1 (either copper or placebo), followed by a 3-week washout period, followed by another 6-week intervention period (either placebo or copper)
Patient reported outcomes
Short form health survey
Measured: From randomization to 1) end 6-week; 2) end of 9-week; 3) end of 15 week. First 6 week is intervention period 1 (either copper or placebo), followed by a 3-week washout period, followed by another 6-week intervention period (either placebo or copper).
Functional and nutritional status
Liver frailty index based on grip strength, chair stands and balance
Measured: From randomization to 1) end 6-week; 2) end of 9-week; 3) end of 15 week. First 6 week is intervention period 1 (either copper or placebo), followed by a 3-week washout period, followed by another 6-week intervention period (either placebo or copper).
Functional and nutritional status
triceps skin fold in centimeters
Measured: From randomization to 1) end 6-week; 2) end of 9-week; 3) end of 15 week. First 6 week is intervention period 1 (either copper or placebo), followed by a 3-week washout period, followed by another 6-week intervention period (either placebo or copper).
Functional and nutritional status
Mid-arm circumference in centimeter
Measured: From randomization to 1) end 6-week; 2) end of 9-week; 3) end of 15 week. First 6 week is intervention period 1 (either copper or placebo), followed by a 3-week washout period, followed by another 6-week intervention period (either placebo or copper).
Timeline
From the start of the study to its completion; the mark is today. Estimated dates are the sponsor’s plan.
- First posted13 Mar 2026
- Study start15 Mar 2026 (estimated)
- Primary completionDec 2028 (estimated)
- Study completionDec 2028 (estimated)
Resources
- Official record on ClinicalTrials.govThe registry entry this page is built from, with its full change history.
- Publications (4)Papers the sponsor has linked to this study.
- Other trials for CirrhosisStudies of the same condition, open and under way.
- More trials run by University of WashingtonThe 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 N/A
- Primary purpose
- Treatment
- Allocation
- Randomised
- Intervention model
- Crossover
- Model description
- Randomized double blinded crossover trial
- Masking
- Quadruple blind
- Who is masked
- Participant, Care provider, Investigator, Outcomes assessor
- Enrolment
- 30 participants (estimated)
Sponsor and investigators
- Lead sponsor
- University of Washington
- Sponsor type
- University, hospital or other
- Collaborators
- National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK), University of Alaska Fairbanks
- Responsible party
- Principal investigator, Lei Yu, University of Washington
- Investigators
- Lei Yu, MD, Principal investigator, University of Washington
IDs, dates and publications
- ClinicalTrials.gov ID
- NCT07471542
- Sponsor's protocol ID
- STUDY00023686
- Other IDs
- 1R01DK142802-01
- Status last verified
- Mar 2026
- First submitted
- 2 Mar 2026
- Last updated
- 13 Mar 2026
- Results posted
- No
- Data monitoring committee
- No
- FDA-regulated drug
- No
- FDA-regulated device
- No
- Individual data sharing
- Undecided: For patient confidentiality, we likely will not share individual data.
Publications
Uauy R, Olivares M, Gonzalez M. Essentiality of copper in humans. Am J Clin Nutr. 1998 May;67(5 Suppl):952S-959S. doi: 10.1093/ajcn/67.5.952S.
PubMed 9587135Dhanda A, Atkinson S, Vergis N, Enki D, Fisher A, Clough R, Cramp M, Thursz M. Trace element deficiency is highly prevalent and associated with infection and mortality in patients with alcoholic hepatitis. Aliment Pharmacol Ther. 2020 Aug;52(3):537-544. doi: 10.1111/apt.15880. Epub 2020 Jun 23.
PubMed 32573823Yu L, Liou IW, Biggins SW, Yeh M, Jalikis F, Chan LN, Burkhead J. Copper Deficiency in Liver Diseases: A Case Series and Pathophysiological Considerations. Hepatol Commun. 2019 Jun 26;3(8):1159-1165. doi: 10.1002/hep4.1393. eCollection 2019 Aug.
PubMed 31388635Yu L, Yousuf S, Yousuf S, Yeh J, Biggins SW, Morishima C, Shyu I, O'Shea-Stone G, Eilers B, Waldum A, Copie V, Burkhead J. Copper deficiency is an independent risk factor for mortality in patients with advanced liver disease. Hepatol Commun. 2023 Feb 20;7(3):e0076. doi: 10.1097/HC9.0000000000000076. eCollection 2023 Mar 1.
PubMed 36809345
Study at a glance
From the registry record, last updated by the sponsor on 13 Mar 2026. Recruitment status is as the sponsor reported it: confirm with the study team.
- Official title
- A Pilot Randomized Controlled Trial to Determine the Biochemical Effect, Safety and Patient Reported Outcomes of Copper Supplementation in Patients With Cirrhosis
- ClinicalTrials.gov ID
- NCT07471542
- Acronym / sponsor ID
- STUDY00023686
- Conditions
- Cirrhosis, Chronic Liver Disease, Fibrosis, Infection
- Keywords
- copper, cirrhosis, malnutrition
- Study type
- Interventional
- Recruitment status
- Recruiting
- Enrolment
- 30 participants (estimated)
- Lead sponsor
- University of WashingtonUniversity, hospital or other
- Collaborators
- National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK), University of Alaska Fairbanks
- Study start
- 15 Mar 2026 (estimated)
- Primary completion
- Dec 2028 (estimated)
- Study completion
- Dec 2028 (estimated)
- First posted
- 13 Mar 2026 (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.
End stage liver disease or cirrhosis is a major cause of mortality in the United States and the world. Other than targeting the underlying cause, such as alcohol cessation and antiviral therapy, very few medical treatments can change the natural history of cirrhosis. Malnutrition is one of the few potentially modifiable factors that have been associated with cirrhosis severity and poor prognosis. The transition metal copper (Cu) is an essential trace metal that must be acquired from diet. Its metabolism is primarily regulated by the liver in its role as a master regulator of nutrients. In 2019, the investigators reported that Cu deficiency defined by below normal serum or liver concentrations occurred in a wide range of liver disorders and was associated with a severe disease phenotype. Improvement in liver function was observed in 2 of the 3 patients who received Cu supplementation. In 2023, the investigators conducted a longitudinal cohort study utilizing clinical, serum and liver explant tissue data from 183 cirrhosis patients. The investigators showed that Cu deficiency was associated with 2-fold higher infection rate and a more than 3-fold increase in the risk of death compared to patients with normal Cu status. These preliminary findings and the well-established importance of Cu in human health prompted the investigators to design the current pilot randomized, placebo-controlled, crossover trial to determine the effect of Cu supplementation on Cu dependent biochemical changes, patient safety and patient reported outcomes in cirrhosis.
Detailed description
Approximately 41,000 people die annually of chronic liver disease (CLD) including liver cancer in the United States. Compared to other chronic diseases, patients with CLD have high rates of healthcare utilization and death. The annual cost of care for patients with cirrhosis, the most advanced stage of liver disease, is approximately $21 billion. While liver transplantation is a curative, albeit costly, treatment, there are far fewer donors than patients in need of liver transplants. Other than targeting the causes of cirrhosis, such as alcohol cessation and antiviral therapy, very few medical treatments can change the natural history of cirrhosis. Malnutrition is one of the few potentially modifiable factors that have been associated with cirrhosis severity and poor prognosis. Current guidelines in nutrition management focus on protein and calorie intake, with little consideration for trace metals, which have wide ranging physiological effects.
The transition metal copper (Cu) is an essential trace metal that must be acquired from diet. Absorption, uptake, export and transport of Cu are tightly regulated because both too much and too little Cu can cause cell damage, compromised immune function and organ dysfunction. Systemic Cu metabolism is primarily regulated by the liver in its role as a master regulator of nutrients. Whole body Cu status is best estimated by its blood concentration. Depending on laboratory benchmarks and sex, the lower limit of normal serum Cu is between 70-80 g/dL where concentrations below this range likely reflect systemic Cu deficiency.
In 2019, the investigators began an effort to better understand the role of Cu in liver disease and reported a series of patients who presented with unexplained low blood Cu concentrations. In this detailed report, Cu deficiency defined by below normal serum or liver concentrations occurred in a wide range of liver disorders and was associated with a severe disease phenotype. Improvement in liver function was observed in 2 of the 3 patients who received Cu supplementation. To further these preliminary observation, in 2023, the investigators conducted a longitudinal cohort study utilizing clinical, serum and liver explant tissue data from 183 cirrhosis patients. The investigators showed that Cu deficiency was associated with significantly higher infections rates (42% vs. 20%, p=0.01) and a more than 3-fold increase in the risk of death compared to patients with normal Cu status. These results provide concrete evidence that a complex, and potentially causal relationship exist between Cu status, compromised immune and metabolic functions and worse clinical outcomes in cirrhosis patients.
These preliminary findings and the well-established importance of Cu in human health raise several important questions: Does reduced circulating Cu, the standard definition of Cu deficiency in the general population, similarly reflect a deficiency state in cirrhosis? Is the higher infection and mortality risk observed among patients with low serum Cu mediated by Cu dependent enzymes and immune cells? Is reduced circulating Cu a secondary response in cirrhosis, therefore should be "left alone," or should patients receive Cu supplementation in order to improve functional Cu store and its associated physiological functions? To answer these questions, the investigators designed a pilot randomized, placebo-controlled, crossover trial to determine the effect of Cu supplementation on Cu dependent biochemical changes, patient safety and patient reported outcomes.
Study design
- Primary purpose
- Treatment
- Allocation
- Randomised
- Intervention model
- Crossover
- Masking
- Quadruple blind (participant, care provider, investigator, outcomes assessor)
- Number of arms
- 2
- Model description
- Randomized double blinded crossover trial
| Arm | Type | Receives |
|---|---|---|
| Copper supplementation 1st arm | Experimental | Dietary Supplement: Copper Gluconatecopper supplementation first, washout, then placebo |
| Placebo first arm | Experimental | Dietary Supplement: Copper GluconatePlacebo first, washout, then copper supplementation |
Who may qualify
- Ages
- 18 years and older
- Sex
- All
- Healthy volunteers
- Not accepted
- Age groups
- Adult, Older adult
Key inclusion criteria (4 listed)
- Adult patients age 18 or older with confirmed diagnosis of cirrhosis based on clinical history, exam, imaging, laboratory or histological criteria;
- Cirrhosis patients whose serum or plasma Cu are below the normal range (80-155 ug/dL for women and 70-140 ug/dL for men);
- Cirrhosis patients whose serum or plasma Cu are in the normal range but exhibit at least one clinical feature that has been associated with Cu deficiency. These include history of infections, unexplained anemia, severe leukopenia, iron overload, unexplained neurological symptoms such as ataxia or myelopathy, coagulopathy with spontaneous bleeding.
- Patients must meet inclusion criteria 1 AND 2, or 1 AND 3 in order to be considered for the trial
Key exclusion criteria (8 listed)
- Patients with Wilson disease, cholestatic liver diseases including primary biliary cholangitis and primary sclerosing cholangitis, all of which are associated with Cu overload;
- Patients with fulminant hepatic failure;
- Renal failure with a creatinine clearance <25 ml/minute;
- Hepatic encephalopathy more than grade 2 (Hepatic Encephalopathy in Chronic Liver Disease, 2014);
- MELD score >25 to minimize subject dropout due to been too ill;
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 |
|---|---|---|
| Copper GluconateOral copper gluconate 4 mg daily | Dietary supplement | Copper supplementation 1st arm, Placebo first arm |
Primary outcome
Plasma copper (Cu) concentration
Time frame: From randomization to 1. end 6-week; 2. end of 9-week; 3. end of 15 week. First 6 week is intervention period 1 (either copper or placebo); followed by a 3-week washout period; followed by another 6-week intervention period (either placebo or copper).
The primary endpoint is the mean change in plasma Cu concentration between baseline and each intervention period
14 secondary outcomes
Biomarkers of functional Copper (Cu) status
Time frame: From randomization to 1) end 6-week; 2) end of 9-week; 3) end of 15 week. First 6 week is intervention period 1 (either copper or placebo), followed by a 3-week washout period, followed by another 6-week intervention period (either placebo or copper)
Biomarkers of functional copper status
Time frame: Time Frame: From randomization to 1) end 6-week; 2) end of 9-week; 3) end of 15 week. First 6 week is intervention period 1 (either copper or placebo), followed by a 3-week washout period, followed by another 6-week intervention period (either placebo or
Biomarker of functional copper status
Time frame: Time Frame: From randomization to 1) end 6-week; 2) end of 9-week; 3) end of 15 week. First 6 week is intervention period 1 (either copper or placebo), followed by a 3-week washout period, followed by another 6-week intervention period (either placebo or
Biomarker of functional copper status
Time frame: From randomization to 1. end 6-week; 2. end of 9-week; 3. end of 15 week. First 6 week is intervention period 1 (either copper or placebo); followed by a 3-week washout period; followed by another 6-week intervention period (either placebo or copper)
Biomarker of functional copper status
Time frame: From randomization to 1) end 6-week; 2) end of 9-week; 3) end of 15 week. First 6 week is intervention period 1 (either copper or placebo), followed by a 3-week washout period, followed by another 6-week intervention period (either placebo or copper)
Safety measures
Time frame: From randomization to 1) end 6-week; 2) end of 9-week; 3) end of 15 week. First 6 week is intervention period 1 (either copper or placebo), followed by a 3-week washout period, followed by another 6-week intervention period (either placebo or copper)
Safety measures
Time frame: From randomization to 1) end 6-week; 2) end of 9-week; 3) end of 15 week. First 6 week is intervention period 1 (either copper or placebo), followed by a 3-week washout period, followed by another 6-week intervention period (either placebo or copper)
Safety measures
Time frame: From randomization to 1) end 6-week; 2) end of 9-week; 3) end of 15 week. First 6 week is intervention period 1 (either copper or placebo), followed by a 3-week washout period, followed by another 6-week intervention period (either placebo or copper)
Safety measure
Time frame: Time Frame: From randomization to 1) end 6-week; 2) end of 9-week; 3) end of 15 week. First 6 week is intervention period 1 (either copper or placebo), followed by a 3-week washout period, followed by another 6-week intervention period (either placebo or
Patient reported outcomes
Time frame: From randomization to 1) end 6-week; 2) end of 9-week; 3) end of 15 week. First 6 week is intervention period 1 (either copper or placebo), followed by a 3-week washout period, followed by another 6-week intervention period (either placebo or copper)
Patient reported outcomes
Time frame: From randomization to 1) end 6-week; 2) end of 9-week; 3) end of 15 week. First 6 week is intervention period 1 (either copper or placebo), followed by a 3-week washout period, followed by another 6-week intervention period (either placebo or copper).
Functional and nutritional status
Time frame: From randomization to 1) end 6-week; 2) end of 9-week; 3) end of 15 week. First 6 week is intervention period 1 (either copper or placebo), followed by a 3-week washout period, followed by another 6-week intervention period (either placebo or copper).
Functional and nutritional status
Time frame: From randomization to 1) end 6-week; 2) end of 9-week; 3) end of 15 week. First 6 week is intervention period 1 (either copper or placebo), followed by a 3-week washout period, followed by another 6-week intervention period (either placebo or copper).
Functional and nutritional status
Time frame: From randomization to 1) end 6-week; 2) end of 9-week; 3) end of 15 week. First 6 week is intervention period 1 (either copper or placebo), followed by a 3-week washout period, followed by another 6-week intervention period (either placebo or copper).
Results and safety
This study is still under way. Results are not available in the source record yet.
Research links
- Official record on ClinicalTrials.govLast updated by the sponsor 13 Mar 2026.
- Background: PubMed 9587135Uauy R, Olivares M, Gonzalez M. Essentiality of copper in humans. Am J Clin Nutr. 1998 May;67(5 Suppl):952S-959S. doi: 10.1093/ajcn/67.5.952S.
- Background: PubMed 32573823Dhanda A, Atkinson S, Vergis N, Enki D, Fisher A, Clough R, Cramp M, Thursz M. Trace element deficiency is highly prevalent and associated with infection and mortality in patients with alcoholic hepatitis. Aliment Pharmacol Ther. 2020 Aug;52(3):537-544. doi: 10.1111/apt.15880. Epub 2020 Jun 23.
- Background: PubMed 31388635Yu L, Liou IW, Biggins SW, Yeh M, Jalikis F, Chan LN, Burkhead J. Copper Deficiency in Liver Diseases: A Case Series and Pathophysiological Considerations. Hepatol Commun. 2019 Jun 26;3(8):1159-1165. doi: 10.1002/hep4.1393. eCollection 2019 Aug.
- Background: PubMed 36809345Yu L, Yousuf S, Yousuf S, Yeh J, Biggins SW, Morishima C, Shyu I, O'Shea-Stone G, Eilers B, Waldum A, Copie V, Burkhead J. Copper deficiency is an independent risk factor for mortality in patients with advanced liver disease. Hepatol Commun. 2023 Feb 20;7(3):e0076. doi: 10.1097/HC9.0000000000000076. eCollection 2023 Mar 1.
- Individual participant dataSharing planned: Undecided. For patient confidentiality, we likely will not share individual data.
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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.
Lei Yu, MD principal investigator
University of Washington
1 site in 1 country: see every site and its status.
Questions about this trial
What is this clinical trial studying?
A study testing Copper Gluconate in people with Cirrhosis and Chronic Liver Disease, run by University of Washington at 1 site in United States.
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 4 inclusion and 8 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: looking for participants now, as of the sponsor's last update on 13 Mar 2026. 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 United States. 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. The study team explains the known risks during informed consent, before anyone joins; the record itself does not list them.
Are results available for this study?
This study is still under way. Results are not available in the source record yet.
How can a doctor refer a patient or contact the research team?
Contact Laura Sissons-Ross (206-616-0397, lsissons@uw.edu), or a site near the patient. AzTrials does not enrol participants or take referrals.
What does the primary outcome measure?
Plasma copper (Cu) concentration (time frame: From randomization to 1. end 6-week; 2. end of 9-week; 3. end of 15 week. First 6 week is intervention period 1 (either copper or placebo); followed by a 3-week washout period; followed by another 6-week intervention period (either placebo or copper).). 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 NCT07471542, which also lists 4 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 13 Mar 2026.