Oxidative StressNCT03395977
Uric Acid Effects on Endothelium and Oxydative Stress
A study testing Febuxostat and Rasburicase in people with Oxidative Stress and Endothelial Function, run by Erasme University Hospital at 1 site in Belgium.
Trial summary
Cardiovascular disease is the leading cause of mortality worldwide. Endothelial dysfunction (ED) is the main mechanism which leads to atherosclerosis, where the balance between pro and antioxidant factors results in a decreased nitric oxide (NO) bioavailability. Read more about this study
- Who is it for?
- Ages 18 to 65 yearsHealthy volunteers can take part
- Conditions the study is for
- Oxidative Stress, Endothelial Function, Cardiovascular System
- What is being tested?
- Febuxostat and Rasburicase
- Type of treatment
- Pill or oral medicine, Injection or infusion
- Could I receive a placebo?
- Yes, some participants may receive a placebo
- How many people
- 53 participants
- Where
- 1 siteBelgium
- Study dates
- 3 Jan 2018to 27 Feb 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 18 to 65 years
- All sexes
- Healthy volunteers accepted
- Adult, Older adult
Who may be able to join
- Age between 18 and 40 years
- Male
- Healthy volunteers
- Non smoker for at least 6 months
- Uric acid level in normal range (normouricemic group)
- Age between 40 and 65 years
Show all 13Show fewer
- Male or female (menopaused)
- Healthy volunteers
- Non smoker for at least 6 months
- Uric acid level in normal range (normouricemic group)
- Age between 40 and 65 years
- History of hypertension for more than 6 months
- Non smoker or smoke stopped for at least for 6 months
Who cannot join
- Any diseases of one of the following systems: cardiovascular, digestive, hormonal, urinary, pulmonary, rheumatic or immune.
- Smoker, alcoholic
- Participants should not take any chronic medicine nor vitamins or other antioxidants.
- A G6PD deficit will be excluded as this is a contraindication to uricase administration (hemolytic anemia).
- Phase 2 :
- Any diseases of one of the following systems: cardiovascular, digestive, hormonal, urinary, pulmonary, rheumatic or immune.
Show all 22Show fewer
- Smoker, alcoholic
- Participants should not take any chronic medicine nor vitamins or other antioxidants.
- A G6PD deficit will be excluded as this is a contraindication to uricase administration (hemolytic anemia).
- Phase 3 :
- Acute coronary syndrome
- Heart failure (LVEJ < 40%)
- Diabetes
- Active smoking
- Gout
- Chronic kidney disease stage superior to 3a
- History of cerebrovascular thrombosis
- Cirrhosis
- Alcohol consumption more than 3 units/day
- Participants should not take any chronic medicine nor vitamins or other antioxidants.
- A G6PD deficit will be excluded as this is a contraindication to uricase administration (hemolytic anemia).
- The populations of phases 2 and 3 will be enrolled and studied together with subgroups analyses of the results for the status of hypertension, of treatment, age and gender.
Trial locations and contacts
1 site in 1 country.
About this study
Official title: Differential Effects of Uric Acid and Xanthine Oxidoreductase on Endothelial Function and Oxydative Stress
Cardiovascular disease is the leading cause of mortality worldwide. Endothelial dysfunction (ED) is the main mechanism which leads to atherosclerosis, where the balance between pro and antioxidant factors results in a decreased nitric oxide (NO) bioavailability. Xanthine OxidoReductase (XOR) is one of the main generators of reactive oxygen species (ROS). Uric acid (UA), a major antioxidant in human plasma and end product of purine metabolism, is associated with cardiovascular diseases since many years; however the precise mechanisms which relate UA to ED are still not well understood.
The purpose of this study is to unravel the XOR and UA pathways involved in ED. Three groups of participants (young (< 40 y) male healthy participants [1] ; male and female helthy participants (40 to 65 y) [2] and patients with primary hypertension [3]) will be exposed to febuxostat (a strong and selective XOR inhibitor), or recombinant uricase (which oxidizes UA into allantoin) to vary UA levels and concomitantly control for confounding changes in XOR activity. Oxidative stress will be estimated by several markers. Endothelial function will be assessed by a laser Doppler imager in the presence of hyperthermia and endothelium stimulators. This study is specifically designed to untie the respective effects of UA and XOR pathways on oxidative stress and endothelial function in humans.
Read more
The investigators will test the following hypothesis:
- An extremely low level of uric acid after uricase administration induces endothelial dysfunction and oxydative stress,
- A specific XO inhibitor limits unfavourable effects of the serum UA reduction elicited by uricase administration,
- Endothelial function and oxydative stress are further improved with febuxostat as compared to placebo,
- All these observations are more marked in hypertensives then in older participants than in young healthy subjects.
Read the detailed description
The goals of the research protocol are to clearly untie the respective roles of uric acid (UA) and xanthine oxidoreductase (XOR) pathways on endothelial function and oxidative stress in humans.
UA represents the end-product of purine metabolism due to the loss of uricase 15 million years ago in humans. The selective advantage of this mutation could be the strong antioxidant effect of UA (which represents more than 60% of the antioxidant plasmatic capacity). Many recent epidemiological studies have showed a J-shape association between UA levels and cardiovascular risk. An UA level lower than 3 mg/dl could be damageable due to the loss of the antioxidant properties of UA. In contrast, hyperuricemia is associated with an increased inflammation, insulin resistance, ED, platelet aggregation, left ventricle hypertrophy, arterial vasodilatation impairment, aortic stiffness and intima-media thickness. However, the association between UA and cardiovascular disease remains controversial because whether UA is an independent risk factor for these illnesses is unclear.
Interventional studies:
Because the above-mentioned associations do not prove causation, several authors designed interventional studies with the purpose to modify UA levels and determine if this affected endothelial function and oxidative stress. The main limitation of these studies is that they were unable to untie the effects of the synthesis of UA, of UA itself and of the activity of XOR, on ROS production and endothelial function in humans.
This is because:
- serum UA is a powerful plasmatic antioxidant,
- but transformation of hypoxanthine to xanthine and xanthine to UA by XO generates intracellular ROS,
- moreover, in endothelial cells, UA reduces NO bioavailability by many ways (L-arginine blockade and degradation, increased superoxide anion production, NOS inhibition, reduced NOS genes expression and direct NO scavenging),
- in addition, UA forms crystals in the endothelium wall which create a pro-inflammatory and thrombotic state, increases smooth muscle cells proliferation and also insulin resistance and inflammation in adipocytes,
- finally, and most importantly, XO is inhibited by physiologic levels of UA (which acts as an uncompetitive XO inhibitor).
In summary, the present protocol aims at testing the following hypothesis:
- Experimental serum UA variations are correlated with endothelial function and oxydative stress markers : an extremely low level after uricase administration induces ED and oxydative stress,
- A specific XO inhibitor (FX) limits unfavourable effects of the serum UA reduction elicited by uricase administration, since this will hamper the feedback activation of XO by a low UA level,
- Endothelial function and oxydative stress are further improved with FX as compared to placebo, because the first experimental condition results in a XO blockade,
- All these observations are more marked in hypertensive patients then in older participants than in young healthy subjects.
Data collection
Data collection from the participants will be collected informatically through a case report form. The names and personnal data from the patients will be kept in a secret place or in a password-protected file. All the data will be destroyed at the end of the study (including blood and urine samples).
Statistical analysis
Statistical analysis will be performed using SPSS. Baseline characteristics will be compared using a Student t test. Two-way repeated-measures ANOVAs will be used to detect significant changes between sessions and groups. Statistical significance is assumed when p is <0.05. Sample size is not possible due to the lack of data of the effect of acute hypouricemia. We estimate a minimum of 15 participants in each group.
Specific test will be used for non gaussian variables. Correlation test will be used if necessary according the results of the first test.
Placebo-corrected values and comparisons of the delta will be used too.
Subgroups analyses will be performed for the study of population 2 and 3 (enrolled together).
- Being tested
- Placebos, Febuxostat, Rasburicase
- Keywords
- uric acid, xanthin oxydoreductase, febuxostat, uricase
- Medical subject headings
- Hypertension
What participants receive
What participants receive. In a randomised study each person is assigned to one group by chance.
PlacebosDrug
Also called Placebo
Lactose placebo for pills and saline for perfusion.
FebuxostatDrug
Also called Adenuric
Febuxostat tablet.
RasburicaseDrug
Also called Fasturtec
Rasburicase injectable solution.
| Study group | Role | What they receive |
|---|---|---|
| Placebos PO and IV | Placebo comparator | PO : per os IV : intraveinously Receives: Drug: Placebos |
| Febuxostat PO and Placebo IV | Experimental | 240 mg a day for 3 days Receives: Drug: Placebos; Drug: Febuxostat |
| Febuxostat PO And Rasburicase IV | Experimental | Febuxostat : 240 mg a day for 3 days. Uricase : 3 mg once. Receives: Drug: Febuxostat; Drug: Rasburicase |
| Placebo PO And Rasburicase IV | Experimental | Placebo : for 3 days. Uricase : 3 mg once. Receives: Drug: Placebos; Drug: Rasburicase |
What is being measured
The primary outcome is the main question the study is designed to answer.
Cutaneous perfusion by Laser Doppler (perfusion unit)
Perfusion unit (Laser Doppler Imager + iontophoresis of (ACh and SNP and hyperemia with ou without L-NAME). Assessment of endothelial function.
Measured: 24 hours after infusion of Uricase or Placebo
Secondary outcomes (9)
Change in Oxydative stress biomarkers from baseline to 30 min or 24 hours after infusion of Uricase or Placebo
Measured: Baseline, 30 minutes and 24 hours after infusion of Uricase or Placebo
Arterial stiffness
Carotido-femoral and carotido-radial pulse wave velocity and pulse wave analysis
Measured: 24 hours after infusion of Uricase or Placebo
Blood pressure (mmHg)
Beat-to-beat measurements with Finapres and manually
Measured: 24 hours after infusion of Uricase or Placebo
Cardiac output (l-min)
Beat-to-beat measurements with Finapres
Measured: 24 hours after infusion of Uricase or Placebo
Change in enzymes activity
Xanthin oxydase activity
Measured: 30 min and 24 hours after infusion of Uricase or Placebo
Change in enzymes expression
eNOS, NOX, XO we will incubate endothelial cells with plasma or serum from subjects. Then we will measure the sus-mentionned enzymes' expression.
Measured: 30 min and 24 hours after infusion of Uricase or Placebo
Change in proteomic or metabolomic analysis
We will perform proteomics or metabolomics analysis directly on serum from participants and also on lysate of endothelial cells pre-incubated with plasma or serum from participants.
Measured: 30 min and 24 hours after infusion of Uricase or Placebo
Change in renin-angiotensin activity
Measured: Baseline, 30 minutes and 24 hours after infusion of Uricase or Placebo
Change in urinary excretion of sodium
Measured: Baseline, 30 minutes and 24 hours after infusion of Uricase or Placebo
Timeline
From the start of the study to its completion; the mark is today. Estimated dates are the sponsor’s plan.
- First posted10 Jan 2018
- Study start3 Jan 2018
- Primary completion31 Dec 2019
- Study completion27 Feb 2020
Resources
- Official record on ClinicalTrials.govThe registry entry this page is built from, with its full change history.
- Publications (2)Papers the sponsor has linked to this study.
- Other trials for Oxidative StressStudies 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
- Basic science
- Allocation
- Randomised
- Intervention model
- Crossover
- Model description
- This is a prospective, randomized, placebo-controlled, double-blinded and 3 ways cross-over study. Three populations : healthy male subjects under 40 y \[1\] ; healthy male and female participants between 40 and 65 years \[2\] and subjects with hypertension \[3\]. Minimum 15 participants in each group are needed. The populations 2 and 3 will be studied together with subgroups analyses of the results for the status of hypertension, of treatment, age and gender. For 5 subjects in each group, we will perform a fourth session with Placebo PO and Rasburicase IV. That session will be non-randomized and blinded only for the subject.
- Masking
- Double blind
- Who is masked
- Participant, Investigator
- Enrolment
- 53 participants (actual)
Sponsor and investigators
- Lead sponsor
- Erasme University Hospital
- Sponsor type
- University, hospital or other
- Collaborators
- Fonds Erasme, Fonds National de la Recherche Scientifique
- Responsible party
- Principal investigator, Benjamin De Becker, Erasme University Hospital
- Investigators
- Philippe van de Borne, Study director, Erasme University Hospital
IDs, dates and publications
- ClinicalTrials.gov ID
- NCT03395977
- Sponsor's protocol ID
- 30309647
- Status last verified
- Feb 2020
- First submitted
- 29 Dec 2017
- Last updated
- 28 Feb 2020
- Results posted
- No
- Data monitoring committee
- Yes
- FDA-regulated drug
- No
- FDA-regulated device
- No
- Individual data sharing
- No
Publications
De Becker B, Hupkens E, Dewachter L, Coremans C, Delporte C, van Antwerpen P, Franck T, Zouaoui Boudjeltia K, Cullus P, van de Borne P. Acute effects of hypouricemia on endothelium, oxidative stress, and arterial stiffness: A randomized, double-blind, crossover study. Physiol Rep. 2021 Sep;9(17):e15018. doi: 10.14814/phy2.15018.
PubMed 34435469De Becker B, Coremans C, Chaumont M, Delporte C, Van Antwerpen P, Franck T, Rousseau A, Zouaoui Boudjeltia K, Cullus P, van de Borne P. Severe Hypouricemia Impairs Endothelium-Dependent Vasodilatation and Reduces Blood Pressure in Healthy Young Men: A Randomized, Placebo-Controlled, and Crossover Study. J Am Heart Assoc. 2019 Dec 3;8(23):e013130. doi: 10.1161/JAHA.119.013130. Epub 2019 Nov 22.
PubMed 31752638
Study at a glance
From the registry record, last updated by the sponsor on 28 Feb 2020. Recruitment status is as the sponsor reported it: confirm with the study team.
- Official title
- Differential Effects of Uric Acid and Xanthine Oxidoreductase on Endothelial Function and Oxydative Stress
- ClinicalTrials.gov ID
- NCT03395977
- Acronym / sponsor ID
- 30309647
- Keywords
- uric acid, xanthin oxydoreductase, febuxostat, uricase
- Study type
- Interventional
- Recruitment status
- Completed
- Enrolment
- 53 participants (actual)
- Lead sponsor
- Erasme University HospitalUniversity, hospital or other
- Collaborators
- Fonds Erasme, Fonds National de la Recherche Scientifique
- Study start
- 3 Jan 2018 (actual)
- Primary completion
- 31 Dec 2019 (actual)
- Study completion
- 27 Feb 2020 (actual)
- First posted
- 10 Jan 2018 (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.
Cardiovascular disease is the leading cause of mortality worldwide. Endothelial dysfunction (ED) is the main mechanism which leads to atherosclerosis, where the balance between pro and antioxidant factors results in a decreased nitric oxide (NO) bioavailability. Xanthine OxidoReductase (XOR) is one of the main generators of reactive oxygen species (ROS). Uric acid (UA), a major antioxidant in human plasma and end product of purine metabolism, is associated with cardiovascular diseases since many years; however the precise mechanisms which relate UA to ED are still not well understood.
The purpose of this study is to unravel the XOR and UA pathways involved in ED. Three groups of participants (young (< 40 y) male healthy participants [1] ; male and female helthy participants (40 to 65 y) [2] and patients with primary hypertension [3]) will be exposed to febuxostat (a strong and selective XOR inhibitor), or recombinant uricase (which oxidizes UA into allantoin) to vary UA levels and concomitantly control for confounding changes in XOR activity. Oxidative stress will be estimated by several markers. Endothelial function will be assessed by a laser Doppler imager in the presence of hyperthermia and endothelium stimulators. This study is specifically designed to untie the respective effects of UA and XOR pathways on oxidative stress and endothelial function in humans.
The investigators will test the following hypothesis:
- An extremely low level of uric acid after uricase administration induces endothelial dysfunction and oxydative stress,
- A specific XO inhibitor limits unfavourable effects of the serum UA reduction elicited by uricase administration,
- Endothelial function and oxydative stress are further improved with febuxostat as compared to placebo,
- All these observations are more marked in hypertensives then in older participants than in young healthy subjects.
Detailed description
The goals of the research protocol are to clearly untie the respective roles of uric acid (UA) and xanthine oxidoreductase (XOR) pathways on endothelial function and oxidative stress in humans.
UA represents the end-product of purine metabolism due to the loss of uricase 15 million years ago in humans. The selective advantage of this mutation could be the strong antioxidant effect of UA (which represents more than 60% of the antioxidant plasmatic capacity). Many recent epidemiological studies have showed a J-shape association between UA levels and cardiovascular risk. An UA level lower than 3 mg/dl could be damageable due to the loss of the antioxidant properties of UA. In contrast, hyperuricemia is associated with an increased inflammation, insulin resistance, ED, platelet aggregation, left ventricle hypertrophy, arterial vasodilatation impairment, aortic stiffness and intima-media thickness. However, the association between UA and cardiovascular disease remains controversial because whether UA is an independent risk factor for these illnesses is unclear.
Interventional studies:
Because the above-mentioned associations do not prove causation, several authors designed interventional studies with the purpose to modify UA levels and determine if this affected endothelial function and oxidative stress. The main limitation of these studies is that they were unable to untie the effects of the synthesis of UA, of UA itself and of the activity of XOR, on ROS production and endothelial function in humans.
This is because:
- serum UA is a powerful plasmatic antioxidant,
- but transformation of hypoxanthine to xanthine and xanthine to UA by XO generates intracellular ROS,
- moreover, in endothelial cells, UA reduces NO bioavailability by many ways (L-arginine blockade and degradation, increased superoxide anion production, NOS inhibition, reduced NOS genes expression and direct NO scavenging),
- in addition, UA forms crystals in the endothelium wall which create a pro-inflammatory and thrombotic state, increases smooth muscle cells proliferation and also insulin resistance and inflammation in adipocytes,
- finally, and most importantly, XO is inhibited by physiologic levels of UA (which acts as an uncompetitive XO inhibitor).
In summary, the present protocol aims at testing the following hypothesis:
- Experimental serum UA variations are correlated with endothelial function and oxydative stress markers : an extremely low level after uricase administration induces ED and oxydative stress,
- A specific XO inhibitor (FX) limits unfavourable effects of the serum UA reduction elicited by uricase administration, since this will hamper the feedback activation of XO by a low UA level,
- Endothelial function and oxydative stress are further improved with FX as compared to placebo, because the first experimental condition results in a XO blockade,
- All these observations are more marked in hypertensive patients then in older participants than in young healthy subjects.
Data collection
Data collection from the participants will be collected informatically through a case report form. The names and personnal data from the patients will be kept in a secret place or in a password-protected file. All the data will be destroyed at the end of the study (including blood and urine samples).
Statistical analysis
Statistical analysis will be performed using SPSS. Baseline characteristics will be compared using a Student t test. Two-way repeated-measures ANOVAs will be used to detect significant changes between sessions and groups. Statistical significance is assumed when p is <0.05. Sample size is not possible due to the lack of data of the effect of acute hypouricemia. We estimate a minimum of 15 participants in each group.
Specific test will be used for non gaussian variables. Correlation test will be used if necessary according the results of the first test.
Placebo-corrected values and comparisons of the delta will be used too.
Subgroups analyses will be performed for the study of population 2 and 3 (enrolled together).
Study design
- Primary purpose
- Basic science
- Allocation
- Randomised
- Intervention model
- Crossover
- Masking
- Double blind (participant, investigator)
- Number of arms
- 4
- Model description
- This is a prospective, randomized, placebo-controlled, double-blinded and 3 ways cross-over study. Three populations : healthy male subjects under 40 y [1] ; healthy male and female participants between 40 and 65 years [2] and subjects with hypertension [3]. Minimum 15 participants in each group are needed. The populations 2 and 3 will be studied together with subgroups analyses of the results for the status of hypertension, of treatment, age and gender. For 5 subjects in each group, we will perform a fourth session with Placebo PO and Rasburicase IV. That session will be non-randomized and blinded only for the subject.
| Arm | Type | Receives |
|---|---|---|
| Placebos PO and IV | Placebo comparator | Drug: PlacebosPO : per os IV : intraveinously |
| Febuxostat PO and Placebo IV | Experimental | Drug: Placebos, Drug: Febuxostat240 mg a day for 3 days |
| Febuxostat PO And Rasburicase IV | Experimental | Drug: Febuxostat, Drug: RasburicaseFebuxostat : 240 mg a day for 3 days. Uricase : 3 mg once. |
| Placebo PO And Rasburicase IV | Experimental | Drug: Placebos, Drug: RasburicasePlacebo : for 3 days. Uricase : 3 mg once. |
Who may qualify
- Ages
- 18 to 65 years
- Sex
- All
- Healthy volunteers
- Accepted
- Age groups
- Adult, Older adult
Key inclusion criteria (13 listed)
- Age between 18 and 40 years
- Male
- Healthy volunteers
- Non smoker for at least 6 months
- Uric acid level in normal range (normouricemic group)
Key exclusion criteria (22 listed)
- Any diseases of one of the following systems: cardiovascular, digestive, hormonal, urinary, pulmonary, rheumatic or immune.
- Smoker, alcoholic
- Participants should not take any chronic medicine nor vitamins or other antioxidants.
- A G6PD deficit will be excluded as this is a contraindication to uricase administration (hemolytic anemia).
- Any diseases of one of the following systems: cardiovascular, digestive, hormonal, urinary, pulmonary, rheumatic or immune.
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 |
|---|---|---|
| PlacebosAlso: PlaceboLactose placebo for pills and saline for perfusion. | Drug | Febuxostat PO and Placebo IV, Placebo PO And Rasburicase IV, Placebos PO and IV |
| FebuxostatAlso: AdenuricFebuxostat tablet. | Drug | Febuxostat PO And Rasburicase IV, Febuxostat PO and Placebo IV |
| RasburicaseAlso: FasturtecRasburicase injectable solution. | Drug | Febuxostat PO And Rasburicase IV, Placebo PO And Rasburicase IV |
Primary outcome
Cutaneous perfusion by Laser Doppler (perfusion unit)
Time frame: 24 hours after infusion of Uricase or Placebo
Perfusion unit (Laser Doppler Imager + iontophoresis of (ACh and SNP and hyperemia with ou without L-NAME). Assessment of endothelial function.
9 secondary outcomes
Change in Oxydative stress biomarkers from baseline to 30 min or 24 hours after infusion of Uricase or Placebo
Time frame: Baseline, 30 minutes and 24 hours after infusion of Uricase or Placebo
Arterial stiffness
Time frame: 24 hours after infusion of Uricase or Placebo
Blood pressure (mmHg)
Time frame: 24 hours after infusion of Uricase or Placebo
Cardiac output (l-min)
Time frame: 24 hours after infusion of Uricase or Placebo
Change in enzymes activity
Time frame: 30 min and 24 hours after infusion of Uricase or Placebo
Change in enzymes expression
Time frame: 30 min and 24 hours after infusion of Uricase or Placebo
Change in proteomic or metabolomic analysis
Time frame: 30 min and 24 hours after infusion of Uricase or Placebo
Change in renin-angiotensin activity
Time frame: Baseline, 30 minutes and 24 hours after infusion of Uricase or Placebo
Change in urinary excretion of sodium
Time frame: Baseline, 30 minutes and 24 hours after infusion of Uricase or Placebo
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 28 Feb 2020.
- Derived from this study: PubMed 34435469De Becker B, Hupkens E, Dewachter L, Coremans C, Delporte C, van Antwerpen P, Franck T, Zouaoui Boudjeltia K, Cullus P, van de Borne P. Acute effects of hypouricemia on endothelium, oxidative stress, and arterial stiffness: A randomized, double-blind, crossover study. Physiol Rep. 2021 Sep;9(17):e15018. doi: 10.14814/phy2.15018.
- Derived from this study: PubMed 31752638De Becker B, Coremans C, Chaumont M, Delporte C, Van Antwerpen P, Franck T, Rousseau A, Zouaoui Boudjeltia K, Cullus P, van de Borne P. Severe Hypouricemia Impairs Endothelium-Dependent Vasodilatation and Reduces Blood Pressure in Healthy Young Men: A Randomized, Placebo-Controlled, and Crossover Study. J Am Heart Assoc. 2019 Dec 3;8(23):e013130. doi: 10.1161/JAHA.119.013130. Epub 2019 Nov 22.
- 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.
Philippe van de Borne study director
Erasme University Hospital
1 site in 1 country: see every site and its status.
Questions about this trial
What is this clinical trial studying?
A study testing Febuxostat and Rasburicase in people with Oxidative Stress and Endothelial Function, run by Erasme University Hospital at 1 site in Belgium.
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 13 inclusion and 22 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 28 Feb 2020. 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 Belgium. 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?
Cutaneous perfusion by Laser Doppler (perfusion unit) (time frame: 24 hours after infusion of Uricase or Placebo). 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 NCT03395977, which also lists 2 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 28 Feb 2020.