Non-Alcoholic Fatty Liver DiseaseEMoHyNAFLDNCT05325398
Effect of Molecular Hydrogen in Patients With NAFLD
A study testing HRW drink, HRW Natural Health Products Inc., Made in Vancouver, Canada in people with Non-Alcoholic Fatty Liver Disease, run by Comenius University at 1 site in Slovakia.
Trial summary
Molecular hydrogen H2 acts as antioxidant which selectively reduces cytotoxic harmful reactive oxygen species ROS and concomitantly acts as biological messenger, which mediates several signaling pathways that play cytoprotective role in many human diseases. Read more about this study
- Who is it for?
- Ages 33 to 69 yearsHealthy volunteers can take part
- Conditions the study is for
- Non-Alcoholic Fatty Liver Disease
- What is being tested?
- HRW drink, HRW Natural Health Products Inc., Made in Vancouver, Canada
- Type of treatment
- Pill or oral medicine
- Could I receive a placebo?
- Yes, some participants may receive a placebo
- How many people
- 30 participants
- Where
- 1 siteSlovakia
- Study dates
- 1 May 2020to 18 Dec 2020
- Phase
- Interventional
- 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 33 to 69 years
- All sexes
- Healthy volunteers accepted
- Adult, Older adult
Who may be able to join
- People with age 33-69 years
- BMI ≥ 25
- Confirmation of fatty liver by ultrasonographic examination
- Signed informed consent
- Alcohol intake according to the AUDIT questionnaire 5 or less points for men or 4 or less points for women
Who cannot join
- Unsigned informed consent
- BMI < 25
- Presence of severe inflammatory disease with activity (Crohn's disease, ulcerative colitis, active tuberculosis, rheumatoid arthritis, etc.)
- Presence of acute infectious disease (acute hepatitis, peritonitis, cholecystitis, pancreatitis, etc.)
- Presence of active neoplastic disease
- Alcohol intake according to the AUDIT questionnaire more as 5 points for men or more as 4 points for women
Trial locations and contacts
1 site in 1 country.
Slovakia1 site
3rd Department of Internal Medicine Faculty of Medicine Comenius University in Bratislava
Bratislava, 83101
About this study
Official title: Effect of Molecular Hydrogen in Patients With Non Alcoholic Faty Liver Disease
Molecular hydrogen H2 acts as antioxidant which selectively reduces cytotoxic harmful reactive oxygen species ROS and concomitantly acts as biological messenger, which mediates several signaling pathways that play cytoprotective role in many human diseases. Due to their small size and high permeability, H2 is easily transportable into subcellular structures as mitochondria.
Read the detailed description
Non-alcoholic fatty liver disease, NAFLD, is the most common cause of liver disease. According to the forecasts, the non-alcoholic steatohepatitis will be the most common cause of liver transplantation and hepatic mortality in 2030. NAFLD is also a significant risk factor for the development of hepatocellular carcinoma, even in the non-cirrhotic stage of liver disease. The prevention of the progression of NAFLD to NASH (nonalcoholic steatohepatitis) is therefore a key factor in preventing this unfavorable prognosis.
Obesity and its associated comorbidities are among the most widespread and challenging conditions in the confrontation of the medical profession in the 21st century. The main metabolic consequence of obesity is insulin resistance, which is strongly associated with the storage of triacylglycerols in the liver. Hepatic steatosis may be associated with steatohepatitis, a condition that can lead to liver cirrhosis and, in the final stage, liver transplantation.
According to various sources, the incidence of NAFLD in the population is 20-30%, in obese up to 60%, which makes it the most common liver disease. In the USA, it is even 3 times more common than type 2 diabetes mellitus and 5-10 times more common than chronic hepatitis C. The incidence of non-alcoholic steatohepatitis NASH is 2-3% and is now thought to be the cause of up to 80% cryptogenic liver cirrhosis. The risk of developing cirrhosis in patients with simple hepatic steatosis is 1-2% over 8 years.
Insulin resistance, which is defined as an elevated HOMA (homeostasis model assessment) index above 1,4, is found in 70% of patients with NAFLD and plays a major role in the accumulation of triacylglycerols TAG (triacylglyceride) in the liver. Through the rise of hormone-sensitive lipase, hyperinsulinemia leads to the hydrolysis of free fatty acids FFA from visceral adipocytes to the portal vein, through which they enter directly into the liver, where they are esterified to TAG. Reducing the production of apolipoprotein B-100, which is an important part of their secretion from the liver into the circulation in the form of VLDL-lipoproteins, is also a potentiating factor in TAG deposition in the liver. Free oxygen radicals ROS (reactive oxygen species), which are formed due to the oxidative stress, are formed directly in the hepatocyte. However, their formation in visceral adipocytes has also been shown to be involved in liver damage. The main site of ROS are mitochondria. In NAFLD, known mitochondrial dysfunction leads to pathological oxidation of FFA (free fatty acid) in peroxisomes and microsomes, making them another source of ROS. ROS, through damage of the mitochondrial membrane by lipoperoxidation and induction of Fas-ligand expression on the hepatocyte, leads to cell apoptosis.
By activating stellate cells, a larger amount of extracellular matrix is formed - Mallory's hyaline, which is associated with the formation of balloon degeneration of hepatocytes, that is a typical histological feature of NASH.
From the cytokines, TNF-alpha is mainly used. It is formed by hepatocytes due to the increased supply of FFA. The diagnostic process is often random. One of the options for non-invasive measurement of liver fibrosis is transient elastography FibroScan, which is used for direct measurement of liver elasticity or use of noninvasive fibrosis indexes (NFS, Fib-4, APRI etc) as nondirect tools. Initial studies have confirmed that H2 penetrates cell membranes and protects mitochondria and cell nuclei from acute oxidative stress. Several studies have reported the effect of H2 on mitochondrial function. With H2, the investigators protect the potential of the mitochondrial membrane, increase ATP production and reduce organelle swelling. There are at least four possible mechanisms for H2 through which gene expression can be altered through mitochondrial bioenergetics, of which ghrelin is probably the most important. Ghrelin is the hormone responsible for appetite.
It reaches its maximum level during hunger. Obestatin has the opposite effect, which in turn suppresses the feeling of hunger. The role of ghrelin as an energy modulator in H2 intervention may be promoted by interaction with expressed glucose transporters, which increase glucose consumption and modulate oxidative phosphorylation in mitochondria. Exercise led to a significant change in ghrelin levels but had no effect on plasma levels of obestatin.
Molecular hydrogen has been shown to relieve oxidative stress, have an anti-inflammatory effect and improve lipid, glucose and energy production in patients as well as in animal models of hepatic steatosis and atherosclerosis. The basic molecular mechanisms remain largely unknown.
Molecular hydrogen is an effective antioxidant that reduces cytotoxic reactive oxygen radicals, especially the hydroxyl radical. In several previous experiments, the use of hydrogen-enriched water, HRW, has been shown to have antioxidant effects. The effects of hydrogen on the prevention of hepatocarcinogenesis in STAM mice were also investigated. The number of tumors was significantly lower in the HRW groups and the tumors were smaller than in the other groups. The results clearly demonstrated that HRW can be an effective treatment for apoptosis, inflammation and hepatocarcinogenesis in NAFLD.
The aim of the study is to verify effectiveness and safety of molecular hydrogen on a group of patients with NAFLD.
- Conditions
- Non-Alcoholic Fatty Liver Disease
- Being tested
- HRW drink, HRW Natural Health Products Inc., Made in Vancouver, Canada, placebo
- Keywords
- Molecular hydrogen, effective antioxidant, oxygen radicals, NAFLD, mitochondria
- Medical subject headings
- Non-alcoholic Fatty Liver Disease
What participants receive
What participants receive. In a randomised study each person is assigned to one group by chance.
HRW drink, HRW Natural Health Products Inc., Made in Vancouver, CanadaDietary supplement
The cohort will consist of 17 patients with NAFLD. Name of the product that will be the source of molecular hydrogen: HRW drink, HRW Natural Health Products Inc., Made in Vancouver, Canada. It is a nutritional supplement that is a source of molecular hydrogen.
All study participants will drink one tablet dissolved in 0.33 l of tap water every 8 hours.
They did this for 8 weeks. Blood analysis at study entry and after 8 weeks (end of study).
placeboDietary supplement
13 probands in the control group who will receive placebo. All study participants will drink one placebo tablet dissolved in 0.33 l of tap water every 8 hours.
They did this for 8 weeks. Blood analysis at study entry and after 8 weeks (end of study)
| Study group | Role | What they receive |
|---|---|---|
| patients with NAFLD | Active comparator | 17 patients will receive molecular hydrogen Receives: Dietary Supplement: HRW drink, HRW Natural Health Products Inc., Made in Vancouver, Canada |
| probands in the control group | Placebo comparator | 13 probands in the control group who will receive placebo. Receives: Dietary Supplement: placebo |
What is being measured
The primary outcome is the main question the study is designed to answer.
Changes in body parameters: Weight in kilograms, height in meters, waist circumference in centimeters
The following parameters will be measured for each proband before (time 0) and after the study (time 8 weeks):
- weight and height will be combined to report BMI in kg/m^2, waist circumference in cm.
Measured: 8 weeks
Changes in blood parameters ALT
ALT (alaninaminotransferase) ukat/L
Measured: 8 weeks
Changes in blood parameters AST
AST (aspartataminotransferase) ukat/L
Measured: 8 weeks
Changes in blood parameters ALP
ALP (alkaline phosphatase) ukat/L
Measured: 8 weeks
Changes in blood parameters GMT
GMT (gamaglutamyltransferase) ukat/L
Measured: 8 weeks
Changes in blood parameters Albumin
Albumin (g/L)
Measured: 8 weeks
Changes in blood parameters Cholinesterase
Cholinesterase (ukat/L)
Measured: 8 weeks
Changes in blood parameters Bilirubin
Bilirubin total (umol/L)
Measured: 8 weeks
Changes in blood parameters Glucose
Glucose (mmol/L)
Measured: 8 weeks
Changes in blood parameters Cholesterol
Cholesterol (mmol/L)
Measured: 8 weeks
Changes in blood parameters Triacylglycerol
Triacylglycerol (mmol/L)
Measured: 8 weeks
Changes in blood parameters Insulin
Insulin (mIU/L)
Measured: 8 weeks
Changes in blood parameters HOMA index
HOMA index (calculation)
Measured: 8 weeks
Changes in blood parameters Leucocytes
Leucocytes (x10^9/L)
Measured: 8 weeks
Changes in blood parameters Hemoglobin
Hemoglobin (g/L)
Measured: 8 weeks
Changes in blood parameters Platelets
Platelets (x10^9/L)
Measured: 8 weeks
Changes in blood parameters TBARS
TBARS (μmol/L)
Measured: 8 weeks
Changes in blood parameters MDA
MDA (malondialdehyde) (μmol/L)
Measured: 8 weeks
Changes in blood parameters LDH
LDH (lactatdehydrogenase) (mU/mL)
Measured: 8 weeks
Changes in blood parameters MMP-2
MMP-2 (matrix metalloproteinase2) (% of change)
Measured: 8 weeks
Changes in blood parameters MMP-9
MMP-9 (matrix-metalloproteinase 9) (% of change)
Measured: 8 weeks
Changes in blood parameters 8-OHdG
8-OHdG (8-hydroxy-2-deoxyguanosine) (ng/mL)
Measured: 8 weeks
Changes in blood parameters SOD
SOD (superoxiddismutase) (ng/mL)
Measured: 8 weeks
Changes in blood parameters NFkB
NFkB (nuclear factor kappa B) (% of change)
Measured: 8 weeks
Changes in blood parameters TNF alfa
TNF alfa (tumor necrosis factor alpha) (% of change)
Measured: 8 weeks
Changes in blood parameters HSP 60
HSP 60 (heat shock protein 60) (% of change)
Measured: 8 weeks
Changes in blood parameters HSP 70
HSP 70 (heat shock protein 70) (% of change)
Measured: 8 weeks
Changes in blood parameters Alpha tocopherol
Alpha tocopherol (μmol/L)
Measured: 8 weeks
Changes in blood parameters Gama tocopherol
Gama tocopherol (μmol/L)
Measured: 8 weeks
Changes in blood parameters Beta carotene
Beta carotene (μmol/L)
Measured: 8 weeks
Changes in blood parameters Coenzyme Q 10 in platelets
Coenzyme Q 10 in platelets (pmol/10^9 cells)
Measured: 8 weeks
Changes in blood parameters Coenzyme Q 10 in plasma
Coenzyme Q 10 in plasma (μmol/L)
Measured: 8 weeks
Changes in blood parameters Coenzyme Q 10 in whole blood
Coenzyme Q 10 in whole blood (μmol/L)
Measured: 8 weeks
Timeline
From the start of the study to its completion; the mark is today. Estimated dates are the sponsor’s plan.
- First posted13 Apr 2022
- Study start1 May 2020
- Primary completion1 Dec 2020
- Study completion18 Dec 2020
Resources
- Official record on ClinicalTrials.govThe registry entry this page is built from, with its full change history.
- Publications (5)Papers the sponsor has linked to this study.
- Other trials for Non-Alcoholic Fatty Liver DiseaseStudies of the same condition, open and under way.
- 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
- Non-randomised
- Intervention model
- Parallel groups
- Masking
- None (open label)
- Enrolment
- 30 participants (actual)
Sponsor and investigators
- Lead sponsor
- Comenius University
- Sponsor type
- University, hospital or other
- Collaborators
- NWN & Drink HRW
- Responsible party
- Sponsor
IDs, dates and publications
- ClinicalTrials.gov ID
- NCT05325398
- Sponsor's protocol ID
- 09/2020/UNB/IIIrdInternal
- Acronym
- EMoHyNAFLD
- Status last verified
- Apr 2022
- First submitted
- 14 May 2021
- Last updated
- 13 Apr 2022
- Results posted
- No
- Data monitoring committee
- No
- FDA-regulated drug
- No
- FDA-regulated device
- No
- Individual data sharing
- Undecided
Publications
Gvozdjakova A, Klauco F, Kucharska J, Sumbalova Z. Is mitochondrial bioenergetics and coenzyme Q10 the target of a virus causing COVID-19? Bratisl Lek Listy. 2020;121(11):775-778. doi: 10.4149/BLL_2020_126.
PubMed 33164536Gvozdjakova A, Sumbalova Z, Kucharska J, Komlosi M, Rausova Z, Vancova O, Szamosova M, Mojto V. Platelet Mitochondrial Respiration, Endogenous Coenzyme Q10 and Oxidative Stress in Patients with Chronic Kidney Disease. Diagnostics (Basel). 2020 Mar 23;10(3):176. doi: 10.3390/diagnostics10030176.
PubMed 32210203Gvozdjakova A, Kucharska J, Sumbalova Z, Rausova Z, Chladekova A, Komlosi M, Szamosova M, Mojto V. The importance of coenzyme Q10 and its ratio to cholesterol in the progress of chronic kidney diseases linked to non- -communicable diseases. Bratisl Lek Listy. 2020;121(10):693-699. doi: 10.4149/BLL_2020_113.
PubMed 32955899Gvozdjakova A, Kucharska J, Sumbalova Z, Nemec M, Chladekova A, Vancova O, Rausova Z, Kubalova M, Kuzmiakova Z, Mojto V. Platelets mitochondrial function depends on CoQ10 concentration in winter, not in spring season. Gen Physiol Biophys. 2019 Jul;38(4):325-334. doi: 10.4149/gpb_2019012. Epub 2019 Jun 26.
PubMed 31241044Gvozdjakova A, Sumbalova Z, Kucharska J, Chladekova A, Rausova Z, Vancova O, Komlosi M, Ulicna O, Mojto V. Platelet mitochondrial bioenergetic analysis in patients with nephropathies and non-communicable diseases: a new method. Bratisl Lek Listy. 2019;120(9):630-635. doi: 10.4149/BLL_2019_104.
PubMed 31475544
Study at a glance
From the registry record, last updated by the sponsor on 13 Apr 2022. Recruitment status is as the sponsor reported it: confirm with the study team.
- Official title
- Effect of Molecular Hydrogen in Patients With Non Alcoholic Faty Liver Disease
- ClinicalTrials.gov ID
- NCT05325398
- Acronym / sponsor ID
- EMoHyNAFLD / 09/2020/UNB/IIIrdInternal
- Conditions
- Non-Alcoholic Fatty Liver Disease
- Keywords
- Molecular hydrogen, effective antioxidant, oxygen radicals, NAFLD, mitochondria
- Study type
- Interventional
- Recruitment status
- Completed
- Enrolment
- 30 participants (actual)
- Lead sponsor
- Comenius UniversityUniversity, hospital or other
- Collaborators
- NWN & Drink HRW
- Study start
- 1 May 2020 (actual)
- Primary completion
- 1 Dec 2020 (actual)
- Study completion
- 18 Dec 2020 (actual)
- First posted
- 13 Apr 2022 (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.
Molecular hydrogen H2 acts as antioxidant which selectively reduces cytotoxic harmful reactive oxygen species ROS and concomitantly acts as biological messenger, which mediates several signaling pathways that play cytoprotective role in many human diseases. Due to their small size and high permeability, H2 is easily transportable into subcellular structures as mitochondria.
Detailed description
Non-alcoholic fatty liver disease, NAFLD, is the most common cause of liver disease. According to the forecasts, the non-alcoholic steatohepatitis will be the most common cause of liver transplantation and hepatic mortality in 2030. NAFLD is also a significant risk factor for the development of hepatocellular carcinoma, even in the non-cirrhotic stage of liver disease. The prevention of the progression of NAFLD to NASH (nonalcoholic steatohepatitis) is therefore a key factor in preventing this unfavorable prognosis.
Obesity and its associated comorbidities are among the most widespread and challenging conditions in the confrontation of the medical profession in the 21st century. The main metabolic consequence of obesity is insulin resistance, which is strongly associated with the storage of triacylglycerols in the liver. Hepatic steatosis may be associated with steatohepatitis, a condition that can lead to liver cirrhosis and, in the final stage, liver transplantation.
According to various sources, the incidence of NAFLD in the population is 20-30%, in obese up to 60%, which makes it the most common liver disease. In the USA, it is even 3 times more common than type 2 diabetes mellitus and 5-10 times more common than chronic hepatitis C. The incidence of non-alcoholic steatohepatitis NASH is 2-3% and is now thought to be the cause of up to 80% cryptogenic liver cirrhosis. The risk of developing cirrhosis in patients with simple hepatic steatosis is 1-2% over 8 years.
Insulin resistance, which is defined as an elevated HOMA (homeostasis model assessment) index above 1,4, is found in 70% of patients with NAFLD and plays a major role in the accumulation of triacylglycerols TAG (triacylglyceride) in the liver. Through the rise of hormone-sensitive lipase, hyperinsulinemia leads to the hydrolysis of free fatty acids FFA from visceral adipocytes to the portal vein, through which they enter directly into the liver, where they are esterified to TAG. Reducing the production of apolipoprotein B-100, which is an important part of their secretion from the liver into the circulation in the form of VLDL-lipoproteins, is also a potentiating factor in TAG deposition in the liver. Free oxygen radicals ROS (reactive oxygen species), which are formed due to the oxidative stress, are formed directly in the hepatocyte. However, their formation in visceral adipocytes has also been shown to be involved in liver damage. The main site of ROS are mitochondria. In NAFLD, known mitochondrial dysfunction leads to pathological oxidation of FFA (free fatty acid) in peroxisomes and microsomes, making them another source of ROS. ROS, through damage of the mitochondrial membrane by lipoperoxidation and induction of Fas-ligand expression on the hepatocyte, leads to cell apoptosis.
By activating stellate cells, a larger amount of extracellular matrix is formed - Mallory's hyaline, which is associated with the formation of balloon degeneration of hepatocytes, that is a typical histological feature of NASH.
From the cytokines, TNF-alpha is mainly used. It is formed by hepatocytes due to the increased supply of FFA. The diagnostic process is often random. One of the options for non-invasive measurement of liver fibrosis is transient elastography FibroScan, which is used for direct measurement of liver elasticity or use of noninvasive fibrosis indexes (NFS, Fib-4, APRI etc) as nondirect tools. Initial studies have confirmed that H2 penetrates cell membranes and protects mitochondria and cell nuclei from acute oxidative stress. Several studies have reported the effect of H2 on mitochondrial function. With H2, the investigators protect the potential of the mitochondrial membrane, increase ATP production and reduce organelle swelling. There are at least four possible mechanisms for H2 through which gene expression can be altered through mitochondrial bioenergetics, of which ghrelin is probably the most important. Ghrelin is the hormone responsible for appetite.
It reaches its maximum level during hunger. Obestatin has the opposite effect, which in turn suppresses the feeling of hunger. The role of ghrelin as an energy modulator in H2 intervention may be promoted by interaction with expressed glucose transporters, which increase glucose consumption and modulate oxidative phosphorylation in mitochondria. Exercise led to a significant change in ghrelin levels but had no effect on plasma levels of obestatin.
Molecular hydrogen has been shown to relieve oxidative stress, have an anti-inflammatory effect and improve lipid, glucose and energy production in patients as well as in animal models of hepatic steatosis and atherosclerosis. The basic molecular mechanisms remain largely unknown.
Molecular hydrogen is an effective antioxidant that reduces cytotoxic reactive oxygen radicals, especially the hydroxyl radical. In several previous experiments, the use of hydrogen-enriched water, HRW, has been shown to have antioxidant effects. The effects of hydrogen on the prevention of hepatocarcinogenesis in STAM mice were also investigated. The number of tumors was significantly lower in the HRW groups and the tumors were smaller than in the other groups. The results clearly demonstrated that HRW can be an effective treatment for apoptosis, inflammation and hepatocarcinogenesis in NAFLD.
The aim of the study is to verify effectiveness and safety of molecular hydrogen on a group of patients with NAFLD.
Study design
- Primary purpose
- Treatment
- Allocation
- Non-randomised
- Intervention model
- Parallel groups
- Masking
- None (open label)
- Number of arms
- 2
| Arm | Type | Receives |
|---|---|---|
| patients with NAFLD | Active comparator | Dietary Supplement: HRW drink, HRW Natural Health Products Inc., Made in Vancouver, Canada17 patients will receive molecular hydrogen |
| probands in the control group | Placebo comparator | Dietary Supplement: placebo13 probands in the control group who will receive placebo. |
Who may qualify
- Ages
- 33 to 69 years
- Sex
- All
- Healthy volunteers
- Accepted
- Age groups
- Adult, Older adult
Key inclusion criteria (5 listed)
- People with age 33-69 years
- BMI ≥ 25
- Confirmation of fatty liver by ultrasonographic examination
- Signed informed consent
- Alcohol intake according to the AUDIT questionnaire 5 or less points for men or 4 or less points for women
Key exclusion criteria (6 listed)
- Unsigned informed consent
- BMI < 25
- Presence of severe inflammatory disease with activity (Crohn's disease, ulcerative colitis, active tuberculosis, rheumatoid arthritis, etc.)
- Presence of acute infectious disease (acute hepatitis, peritonitis, cholecystitis, pancreatitis, etc.)
- Presence of active neoplastic disease
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 |
|---|---|---|
| HRW drink, HRW Natural Health Products Inc., Made in Vancouver, CanadaThe cohort will consist of 17 patients with NAFLD. Name of the product that will be the source of molecular hydrogen: HRW drink, HRW Natural Health Products Inc., Made in Vancouver, Canada. It is a nutritional supplement that is a source of molecular hydrogen. All study participants will drink one tablet dissolved in 0.33 l of tap water every 8 hours. They did this for 8 weeks. Blood analysis at study entry and after 8 weeks (end of study). | Dietary supplement | patients with NAFLD |
| placebo13 probands in the control group who will receive placebo. All study participants will drink one placebo tablet dissolved in 0.33 l of tap water every 8 hours. They did this for 8 weeks. Blood analysis at study entry and after 8 weeks (end of study) | Dietary supplement | probands in the control group |
Primary outcome
Changes in body parameters: Weight in kilograms, height in meters, waist circumference in centimeters
Time frame: 8 weeks
The following parameters will be measured for each proband before (time 0) and after the study (time 8 weeks): a) weight and height will be combined to report BMI in kg/m^2, waist circumference in cm.
Changes in blood parameters ALT
Time frame: 8 weeks
ALT (alaninaminotransferase) ukat/L
Changes in blood parameters AST
Time frame: 8 weeks
AST (aspartataminotransferase) ukat/L
Changes in blood parameters ALP
Time frame: 8 weeks
ALP (alkaline phosphatase) ukat/L
Changes in blood parameters GMT
Time frame: 8 weeks
GMT (gamaglutamyltransferase) ukat/L
Changes in blood parameters Albumin
Time frame: 8 weeks
Albumin (g/L)
Changes in blood parameters Cholinesterase
Time frame: 8 weeks
Cholinesterase (ukat/L)
Changes in blood parameters Bilirubin
Time frame: 8 weeks
Bilirubin total (umol/L)
Changes in blood parameters Glucose
Time frame: 8 weeks
Glucose (mmol/L)
Changes in blood parameters Cholesterol
Time frame: 8 weeks
Cholesterol (mmol/L)
Changes in blood parameters Triacylglycerol
Time frame: 8 weeks
Triacylglycerol (mmol/L)
Changes in blood parameters Insulin
Time frame: 8 weeks
Insulin (mIU/L)
Changes in blood parameters HOMA index
Time frame: 8 weeks
HOMA index (calculation)
Changes in blood parameters Leucocytes
Time frame: 8 weeks
Leucocytes (x10^9/L)
Changes in blood parameters Hemoglobin
Time frame: 8 weeks
Hemoglobin (g/L)
Changes in blood parameters Platelets
Time frame: 8 weeks
Platelets (x10^9/L)
Changes in blood parameters TBARS
Time frame: 8 weeks
TBARS (μmol/L)
Changes in blood parameters MDA
Time frame: 8 weeks
MDA (malondialdehyde) (μmol/L)
Changes in blood parameters LDH
Time frame: 8 weeks
LDH (lactatdehydrogenase) (mU/mL)
Changes in blood parameters MMP-2
Time frame: 8 weeks
MMP-2 (matrix metalloproteinase2) (% of change)
Changes in blood parameters MMP-9
Time frame: 8 weeks
MMP-9 (matrix-metalloproteinase 9) (% of change)
Changes in blood parameters 8-OHdG
Time frame: 8 weeks
8-OHdG (8-hydroxy-2-deoxyguanosine) (ng/mL)
Changes in blood parameters SOD
Time frame: 8 weeks
SOD (superoxiddismutase) (ng/mL)
Changes in blood parameters NFkB
Time frame: 8 weeks
NFkB (nuclear factor kappa B) (% of change)
Changes in blood parameters TNF alfa
Time frame: 8 weeks
TNF alfa (tumor necrosis factor alpha) (% of change)
Changes in blood parameters HSP 60
Time frame: 8 weeks
HSP 60 (heat shock protein 60) (% of change)
Changes in blood parameters HSP 70
Time frame: 8 weeks
HSP 70 (heat shock protein 70) (% of change)
Changes in blood parameters Alpha tocopherol
Time frame: 8 weeks
Alpha tocopherol (μmol/L)
Changes in blood parameters Gama tocopherol
Time frame: 8 weeks
Gama tocopherol (μmol/L)
Changes in blood parameters Beta carotene
Time frame: 8 weeks
Beta carotene (μmol/L)
Changes in blood parameters Coenzyme Q 10 in platelets
Time frame: 8 weeks
Coenzyme Q 10 in platelets (pmol/10^9 cells)
Changes in blood parameters Coenzyme Q 10 in plasma
Time frame: 8 weeks
Coenzyme Q 10 in plasma (μmol/L)
Changes in blood parameters Coenzyme Q 10 in whole blood
Time frame: 8 weeks
Coenzyme Q 10 in whole blood (μmol/L)
Results and safety
The study is completed, but results are not available in the source record. That does not mean the treatment did or did not work.
Research links
- Official record on ClinicalTrials.govLast updated by the sponsor 13 Apr 2022.
- Background: PubMed 33164536Gvozdjakova A, Klauco F, Kucharska J, Sumbalova Z. Is mitochondrial bioenergetics and coenzyme Q10 the target of a virus causing COVID-19? Bratisl Lek Listy. 2020;121(11):775-778. doi: 10.4149/BLL_2020_126.
- Background: PubMed 32210203Gvozdjakova A, Sumbalova Z, Kucharska J, Komlosi M, Rausova Z, Vancova O, Szamosova M, Mojto V. Platelet Mitochondrial Respiration, Endogenous Coenzyme Q10 and Oxidative Stress in Patients with Chronic Kidney Disease. Diagnostics (Basel). 2020 Mar 23;10(3):176. doi: 10.3390/diagnostics10030176.
- Background: PubMed 32955899Gvozdjakova A, Kucharska J, Sumbalova Z, Rausova Z, Chladekova A, Komlosi M, Szamosova M, Mojto V. The importance of coenzyme Q10 and its ratio to cholesterol in the progress of chronic kidney diseases linked to non- -communicable diseases. Bratisl Lek Listy. 2020;121(10):693-699. doi: 10.4149/BLL_2020_113.
- Background: PubMed 31241044Gvozdjakova A, Kucharska J, Sumbalova Z, Nemec M, Chladekova A, Vancova O, Rausova Z, Kubalova M, Kuzmiakova Z, Mojto V. Platelets mitochondrial function depends on CoQ10 concentration in winter, not in spring season. Gen Physiol Biophys. 2019 Jul;38(4):325-334. doi: 10.4149/gpb_2019012. Epub 2019 Jun 26.
- Background: PubMed 31475544Gvozdjakova A, Sumbalova Z, Kucharska J, Chladekova A, Rausova Z, Vancova O, Komlosi M, Ulicna O, Mojto V. Platelet mitochondrial bioenergetic analysis in patients with nephropathies and non-communicable diseases: a new method. Bratisl Lek Listy. 2019;120(9):630-635. doi: 10.4149/BLL_2019_104.
- Individual participant dataSharing planned: Undecided
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Non-alcoholic Fatty Liver Disease
RecruitingPhase 2
A Study of Efimosfermin Alfa in Participants With Biopsy-confirmed Cirrhosis (Compensated) Due to MASH
Metabolic Dysfunction-Associated Steatohepatitis, Non-alcoholic Fatty Liver Disease
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.
The record lists no contact. Use the official record to reach the sponsor.
1 site in 1 country: see every site and its status.
Questions about this trial
What is this clinical trial studying?
A study testing HRW drink, HRW Natural Health Products Inc., Made in Vancouver, Canada in people with Non-Alcoholic Fatty Liver Disease, run by Comenius University at 1 site in Slovakia.
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 5 inclusion and 6 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: finished, as of the sponsor's last update on 13 Apr 2022. 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 Slovakia. 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.
Are results available for this study?
The study is completed, but results are not available in the source record. That does not mean the treatment did or did not work.
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?
Changes in body parameters: Weight in kilograms, height in meters, waist circumference in centimeters (time frame: 8 weeks). The study lists 33 primary outcomes in all. 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 NCT05325398, which also lists 5 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 Apr 2022.