Uric Acid Concentration, Serum, Quantitative Trait Locus 7metabolicNCT04954560
Effect of Losartan or Eprosartan on Fructose Hyperuricemia
A study testing losartan and eprosartan in people with Uric Acid Concentration, Serum, Quantitative Trait Locus 7, run by Medical University of Lodz.
Trial summary
Hyperuricemia is seen in about 20% of adults in the general population, Chronic hyperuricemia, frequently manifesting as the gout, is a well-known risk factor of joint damage but has been also linked to a variety of other pathologies mostly affecting the cardiovascular system. Read more about this study
- Who is it for?
- Ages 18 years and older
- Conditions the study is for
- Uric Acid Concentration, Serum, Quantitative Trait Locus 7
- What is being tested?
- losartan and eprosartan
- Could I receive a placebo?
- No, everyone receives an active treatment
- How many people
- 16 participants
- Where
- No sites listed yet
- Study dates
- 1 Jan 2008to 1 Jan 2010
- 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 years and older
- All sexes
- No healthy volunteers
- Adult, Older adult
Who may be able to join
- Age 18 years old
- Fulfillment of three or more of the AHA / NHLBI 2005 assessment criteria for the metabolic syndrome:
- abdominal obesity (i.e. handling in women ≥88 cm) male ≥ 102 cm
- concentration of triglycerides in the form ≥150 mg / dl
- concentration of HDL fraction (men <40 mg / dL, women <50 mg / dL)
- blood pressure ≥ 130/85 mmHg
- Correction of fasting glucose ≥100 mg / dL)
- Written and informed consent to participate in the case of
Who cannot join
- Congenital defects in fructose metabolism (hereditary fructose intolerance and idiopathic fructosuria)
- Mental illness, dementia
- Insufficient cooperation with the patient, non-compliance with doctor's recommendations
- Pregnancy
- Bilateral renal artery stenosis or stenosis to a solitary kidney and other contraindications for angiotensin receptor antagonists
- Chronic use of uricosuric drugs, xanthine oxidase inhibitors and AT1 receptor inhibitors
About this study
Official title: Losartan and Eprosartan Induce a Similar Effect on Oral Fructose-induced Rise in Serum Uric Acid Concentration in Patients With Metabolic Syndrome
Hyperuricemia is seen in about 20% of adults in the general population, Chronic hyperuricemia, frequently manifesting as the gout, is a well-known risk factor of joint damage but has been also linked to a variety of other pathologies mostly affecting the cardiovascular system. The close relation between high uric acid concentration and increased risk of cardiovascular disease has been reported for more than a century. Furthermore, many studies reported a strong association between hyperuricemia, arterial hypertension, obesity and cardiovascular diseases even in an absence of typical clinical manifestations of gout.
Several studies showed that the prevalence of hyperuricemia in patients with hypertension is much higher than in the general population and may worsen after the onset of antihypertensive treatment. That may indicate that hyperuricemia may be also caused by antihypertensive drugs. In contrast to diuretics and nonselective beta blockers the agents that block the renin-angiotensin-aldosterone system have had a neutral effect on serum uric acid. Several clinical studies showed that losartan in contrast to other AT1-receptor agonists, may have specific uricosuric properties and thereby can lower uric acid concentration. It has been speculated that uricosuric effect could make losartan particularly useful for the treatment of arterial hypertension associated with hyperuricemia and metabolic syndrome.
Read more
The uricosuric effect of losartan is most likely due to overlapping two different mechanisms regulating the excretion of uric acid. Losartan may increase uric acid tubular secretion in the same way as other inhibitors of the renin-angiotensin-aldosterone system, but in addition it may specifically inhibit post-secretory resorption of uric acid in the proximal tubule. The effect may be due to a specific structure of the losartan molecule. The urateanion transporter is a monoammonium selective transporter, and the losartan molecule is mainly a monoanion at normal pH range (as opposed to dianion e.g. eprosartan) and therefore is a good substrate for the exchanger. However, this concept remains speculative since, e.g. irbesartan which is also a monoanion has no consistent uricosuric effect.
Fructose, in contrast to other carbohydrates causes an increase of serum uric acid concentration, which may facilitate the development of the metabolic syndrome.
Read the detailed description
The study group included 16 patients (15F, 1M, mean age 64.5 ± 9.8 years). The patients selected for the study fulfilled the AHA/NHLBI 2005 criteria of the meta-bolic syndrome [30] and ESC/ESH criteria of arterial hypertension. The exclusion cri-teria included an antihypertensive therapy with the renin-angiotensin-aldosterone axis blocking agent used anytime during last 3 months, current or past therapy with SGLT2 inhibitor, GLP-1 agonist or DPP4-inhibitor, suspected or confirmed secondary form of hypertension, estimated glomerular filtration rate <60 ml/min/1.73 m2, chron-ic liver disease, acute infection, psychiatric disorders, mean serum potassium con-centration at last three measurements <4.0 mmol/l, or aspartate aminotransferase or alanine aminotransferase or creatinine kinase > x1.5 upper range limit were excluded. Seven patients had diabetes mellitus of which 4 were treated with insulin. Twelve pa-tients were receiving metformin. Waist circumference was measured on the initial visit. Plasma lipids and blood glucose were measured in a fasting state during the study.
The study was designed as a randomized, crossover, head-to-head comparative study. Randomization was carried out using MS Excel random number generator. After qualification each patient was randomly assigned to receive either losartan (Lorista, KRKA, Slovenia) or eprosartan (Teveten, Solvay Pharmaceuticals, Austral-ia). The patients were taking all other previously prescribed drugs in unmodified dos-es during the whole course of the study. Each study drug was given in a random or-der as a single morning dose (50 mg of losartan or 600 mg of eprosartan) for two periods each lasting 3 months separated by 2-week wash-out time.
Oral fructose tolerance with the administration of 75 g of fructose was con-ducted 3 times during the study in each patient, i.e. at baseline and after each of the treatment periods. Before the commencement of OFTT, the patients collected the urine for 2 hours for assessment of the urinary excretion of uric acid and creatinine. Other baseline measurements included blood pressure, serum concentration of glu-cose, uric acid, creatinine and plasma lipids (total, HDL- and, LDL-cholesterol and triglycerides). Subsequent blood samples were taken three times during each OFTT, i.e. after 30, 60 and 120 minutes from its start to determine serum uric acid concen-tration. In addition, peripheral blood pressure was measured before the collection of each blood sample. After 120 minutes blood was also taken to assess plasma lipids. The second timed 2-hour urine collection was obtained during OFTT. The same pro-cedures were repeated after each treatment period. The patients took all their pre-scribed medication including the study drug in the morning 120 minutes before the beginning of OFTT Routine automated laboratory tests were used to assess blood and urine pa-rameters. Blood pressure was taken in a sitting position with the aneroid sphygmo-manometer. Blood pressure was measured both at baseline and after 3-month ther-apy with each study drug. The mean from four measurements obtained between 0 and 120 minutes OFTT was taken for the analysis. Blood pressure was measured by a designated single member of the staff. Mean blood pressure (MAP) was calculated for all measurements as diastolic BP + 1/3 of pulse pressure (systolic BP - diastolic BP).
The results are expressed as mean ± SD or median with interquartile range depending on each variable distribution. 95% confidence intervals were calculated for the changes of the parameters caused by the treatment. Statistical significance was defined at p<0.05. The within-group comparisons were analyzed using one-way ANOVA and t-test for normally distributed variables or alternatively with non-parametric Wilcoxon test. The normality of the variable distribution was checked with Shapiro-Wilk test. The Pearson or Spearman correlation coefficient was used to as-sess the relations between variables depending on their distribution. Area under the curve (AUC) of serum uric acid during oral fructose tolerance test was calculated using the trapezoidal rule.
- Being tested
- losartan and eprosartan
- Keywords
- sartan, fructose, metabolic syndrome, uric acid
- Medical subject headings
- Metabolic Syndrome
What participants receive
What participants receive. In a randomised study each person is assigned to one group by chance.
losartan and eprosartanDrug
Also called Lorista, Teveten
. Each study drug was given in a random order as a single morning dose (50 mg of losartan or 600 mg of eprosartan) for two periods each lasting 3 months separated by 2-week wash-out time.
| Study group | Role | What they receive |
|---|---|---|
| losartan | Active comparator | Each study drug was given in a random order as a single morning dose (50 mg of losartan or 600 mg of eprosartan) for two periods each lasting 3 months separated by 2-week wash-out time. Receives: Drug: losartan and eprosartan |
| eprosartan | Active comparator | Each study drug was given in a random order as a single morning dose (50 mg of losartan or 600 mg of eprosartan) for two periods each lasting 3 months separated by 2-week wash-out time. Receives: Drug: losartan and eprosartan |
What is being measured
The primary outcome is the main question the study is designed to answer.
serum uric acid after losartan
serum uric acid after losartan therapy
Measured: 3 months
serum uric acid after eprosartan
serum uric acid after eprosartan therapy
Measured: 3 months
urine uric acid after losartan
urine uric acid after losartan therapy
Measured: 3 months
urine uric acid after eprosartan
urine uric acid after eprosartan therapy
Measured: 3 months
Timeline
From the start of the study to its completion; the mark is today. Estimated dates are the sponsor’s plan.
- First posted8 Jul 2021
- Study start1 Jan 2008
- Primary completion1 Jan 2010
- Study completion1 Jan 2010
Resources
- Official record on ClinicalTrials.govThe registry entry this page is built from, with its full change history.
- Publications (1)Papers the sponsor has linked to this study.
- Other trials for Uric Acid Concentration, Serum, Quantitative Trait Locus 7Studies 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
- Randomised
- Intervention model
- Crossover
- Model description
- The study was designed as a randomized, crossover, head-to-head comparative study. Randomization was carried out using MS Excel random number generator. After qualification each patient was randomly assigned to receive either losartan (Lorista, KRKA, Slovenia) or eprosartan (Teveten, Solvay Pharmaceuticals, Austral-ia). The patients were taking all other previously prescribed drugs in unmodified dos-es during the whole course of the study. Each study drug was given in a random or-der as a single morning dose (50 mg of losartan or 600 mg of eprosartan) for two periods each lasting 3 months separated by 2-week wash-out time.
- Masking
- None (open label)
- Enrolment
- 16 participants (actual)
Sponsor and investigators
- Lead sponsor
- Medical University of Lodz
- Sponsor type
- University, hospital or other
- Responsible party
- Principal investigator, Michal Nowicki, Medical University of Lodz
- Investigators
- Ireneusz Staroń, Study chair, Medical University of Lodz
IDs, dates and publications
- ClinicalTrials.gov ID
- NCT04954560
- Sponsor's protocol ID
- RNN/185/07/KE
- Acronym
- metabolic
- Status last verified
- Jun 2021
- First submitted
- 3 Jun 2021
- Last updated
- 8 Jul 2021
- Results posted
- No
- Data monitoring committee
- No
- FDA-regulated drug
- No
- FDA-regulated device
- No
- Individual data sharing
- No
Publications
Masajtis-Zagajewska A, Majer J, Nowicki M. Losartan and Eprosartan Induce a Similar Effect on the Acute Rise in Serum Uric Acid Concentration after an Oral Fructose Load in Patients with Metabolic Syndrome. J Renin Angiotensin Aldosterone Syst. 2021 Aug 25;2021:2214978. doi: 10.1155/2021/2214978. eCollection 2021.
PubMed 34527078
Study at a glance
From the registry record, last updated by the sponsor on 8 Jul 2021. Recruitment status is as the sponsor reported it: confirm with the study team.
- Official title
- Losartan and Eprosartan Induce a Similar Effect on Oral Fructose-induced Rise in Serum Uric Acid Concentration in Patients With Metabolic Syndrome
- ClinicalTrials.gov ID
- NCT04954560
- Acronym / sponsor ID
- metabolic / RNN/185/07/KE
- Keywords
- sartan, fructose, metabolic syndrome, uric acid
- Study type
- Interventional
- Recruitment status
- Completed
- Enrolment
- 16 participants (actual)
- Lead sponsor
- Medical University of LodzUniversity, hospital or other
- Study start
- 1 Jan 2008 (actual)
- Primary completion
- 1 Jan 2010 (actual)
- Study completion
- 1 Jan 2010 (actual)
- First posted
- 8 Jul 2021 (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.
Hyperuricemia is seen in about 20% of adults in the general population, Chronic hyperuricemia, frequently manifesting as the gout, is a well-known risk factor of joint damage but has been also linked to a variety of other pathologies mostly affecting the cardiovascular system. The close relation between high uric acid concentration and increased risk of cardiovascular disease has been reported for more than a century. Furthermore, many studies reported a strong association between hyperuricemia, arterial hypertension, obesity and cardiovascular diseases even in an absence of typical clinical manifestations of gout.
Several studies showed that the prevalence of hyperuricemia in patients with hypertension is much higher than in the general population and may worsen after the onset of antihypertensive treatment. That may indicate that hyperuricemia may be also caused by antihypertensive drugs. In contrast to diuretics and nonselective beta blockers the agents that block the renin-angiotensin-aldosterone system have had a neutral effect on serum uric acid. Several clinical studies showed that losartan in contrast to other AT1-receptor agonists, may have specific uricosuric properties and thereby can lower uric acid concentration. It has been speculated that uricosuric effect could make losartan particularly useful for the treatment of arterial hypertension associated with hyperuricemia and metabolic syndrome.
The uricosuric effect of losartan is most likely due to overlapping two different mechanisms regulating the excretion of uric acid. Losartan may increase uric acid tubular secretion in the same way as other inhibitors of the renin-angiotensin-aldosterone system, but in addition it may specifically inhibit post-secretory resorption of uric acid in the proximal tubule. The effect may be due to a specific structure of the losartan molecule. The urateanion transporter is a monoammonium selective transporter, and the losartan molecule is mainly a monoanion at normal pH range (as opposed to dianion e.g. eprosartan) and therefore is a good substrate for the exchanger. However, this concept remains speculative since, e.g. irbesartan which is also a monoanion has no consistent uricosuric effect.
Fructose, in contrast to other carbohydrates causes an increase of serum uric acid concentration, which may facilitate the development of the metabolic syndrome.
Detailed description
The study group included 16 patients (15F, 1M, mean age 64.5 ± 9.8 years). The patients selected for the study fulfilled the AHA/NHLBI 2005 criteria of the meta-bolic syndrome [30] and ESC/ESH criteria of arterial hypertension. The exclusion cri-teria included an antihypertensive therapy with the renin-angiotensin-aldosterone axis blocking agent used anytime during last 3 months, current or past therapy with SGLT2 inhibitor, GLP-1 agonist or DPP4-inhibitor, suspected or confirmed secondary form of hypertension, estimated glomerular filtration rate <60 ml/min/1.73 m2, chron-ic liver disease, acute infection, psychiatric disorders, mean serum potassium con-centration at last three measurements <4.0 mmol/l, or aspartate aminotransferase or alanine aminotransferase or creatinine kinase > x1.5 upper range limit were excluded. Seven patients had diabetes mellitus of which 4 were treated with insulin. Twelve pa-tients were receiving metformin. Waist circumference was measured on the initial visit. Plasma lipids and blood glucose were measured in a fasting state during the study.
The study was designed as a randomized, crossover, head-to-head comparative study. Randomization was carried out using MS Excel random number generator. After qualification each patient was randomly assigned to receive either losartan (Lorista, KRKA, Slovenia) or eprosartan (Teveten, Solvay Pharmaceuticals, Austral-ia). The patients were taking all other previously prescribed drugs in unmodified dos-es during the whole course of the study. Each study drug was given in a random or-der as a single morning dose (50 mg of losartan or 600 mg of eprosartan) for two periods each lasting 3 months separated by 2-week wash-out time.
Oral fructose tolerance with the administration of 75 g of fructose was con-ducted 3 times during the study in each patient, i.e. at baseline and after each of the treatment periods. Before the commencement of OFTT, the patients collected the urine for 2 hours for assessment of the urinary excretion of uric acid and creatinine. Other baseline measurements included blood pressure, serum concentration of glu-cose, uric acid, creatinine and plasma lipids (total, HDL- and, LDL-cholesterol and triglycerides). Subsequent blood samples were taken three times during each OFTT, i.e. after 30, 60 and 120 minutes from its start to determine serum uric acid concen-tration. In addition, peripheral blood pressure was measured before the collection of each blood sample. After 120 minutes blood was also taken to assess plasma lipids. The second timed 2-hour urine collection was obtained during OFTT. The same pro-cedures were repeated after each treatment period. The patients took all their pre-scribed medication including the study drug in the morning 120 minutes before the beginning of OFTT Routine automated laboratory tests were used to assess blood and urine pa-rameters. Blood pressure was taken in a sitting position with the aneroid sphygmo-manometer. Blood pressure was measured both at baseline and after 3-month ther-apy with each study drug. The mean from four measurements obtained between 0 and 120 minutes OFTT was taken for the analysis. Blood pressure was measured by a designated single member of the staff. Mean blood pressure (MAP) was calculated for all measurements as diastolic BP + 1/3 of pulse pressure (systolic BP - diastolic BP).
The results are expressed as mean ± SD or median with interquartile range depending on each variable distribution. 95% confidence intervals were calculated for the changes of the parameters caused by the treatment. Statistical significance was defined at p<0.05. The within-group comparisons were analyzed using one-way ANOVA and t-test for normally distributed variables or alternatively with non-parametric Wilcoxon test. The normality of the variable distribution was checked with Shapiro-Wilk test. The Pearson or Spearman correlation coefficient was used to as-sess the relations between variables depending on their distribution. Area under the curve (AUC) of serum uric acid during oral fructose tolerance test was calculated using the trapezoidal rule.
Study design
- Primary purpose
- Treatment
- Allocation
- Randomised
- Intervention model
- Crossover
- Masking
- None (open label)
- Number of arms
- 2
- Model description
- The study was designed as a randomized, crossover, head-to-head comparative study. Randomization was carried out using MS Excel random number generator. After qualification each patient was randomly assigned to receive either losartan (Lorista, KRKA, Slovenia) or eprosartan (Teveten, Solvay Pharmaceuticals, Austral-ia). The patients were taking all other previously prescribed drugs in unmodified dos-es during the whole course of the study. Each study drug was given in a random or-der as a single morning dose (50 mg of losartan or 600 mg of eprosartan) for two periods each lasting 3 months separated by 2-week wash-out time.
| Arm | Type | Receives |
|---|---|---|
| losartan | Active comparator | Drug: losartan and eprosartanEach study drug was given in a random order as a single morning dose (50 mg of losartan or 600 mg of eprosartan) for two periods each lasting 3 months separated by 2-week wash-out time. |
| eprosartan | Active comparator | Drug: losartan and eprosartanEach study drug was given in a random order as a single morning dose (50 mg of losartan or 600 mg of eprosartan) for two periods each lasting 3 months separated by 2-week wash-out time. |
Who may qualify
- Ages
- 18 years and older
- Sex
- All
- Healthy volunteers
- Not accepted
- Age groups
- Adult, Older adult
Key inclusion criteria (8 listed)
- Age 18 years old
- Fulfillment of three or more of the AHA / NHLBI 2005 assessment criteria for the metabolic syndrome:
- abdominal obesity (i.e. handling in women ≥88 cm) male ≥ 102 cm
- concentration of triglycerides in the form ≥150 mg / dl
- concentration of HDL fraction (men <40 mg / dL, women <50 mg / dL)
Key exclusion criteria (6 listed)
- Congenital defects in fructose metabolism (hereditary fructose intolerance and idiopathic fructosuria)
- Mental illness, dementia
- Insufficient cooperation with the patient, non-compliance with doctor's recommendations
- Pregnancy
- Bilateral renal artery stenosis or stenosis to a solitary kidney and other contraindications for angiotensin receptor antagonists
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 |
|---|---|---|
| losartan and eprosartanAlso: Lorista, Teveten. Each study drug was given in a random order as a single morning dose (50 mg of losartan or 600 mg of eprosartan) for two periods each lasting 3 months separated by 2-week wash-out time. | Drug | eprosartan, losartan |
Primary outcome
serum uric acid after losartan
Time frame: 3 months
serum uric acid after losartan therapy
serum uric acid after eprosartan
Time frame: 3 months
serum uric acid after eprosartan therapy
urine uric acid after losartan
Time frame: 3 months
urine uric acid after losartan therapy
urine uric acid after eprosartan
Time frame: 3 months
urine uric acid after eprosartan therapy
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 8 Jul 2021.
- Derived from this study: PubMed 34527078Masajtis-Zagajewska A, Majer J, Nowicki M. Losartan and Eprosartan Induce a Similar Effect on the Acute Rise in Serum Uric Acid Concentration after an Oral Fructose Load in Patients with Metabolic Syndrome. J Renin Angiotensin Aldosterone Syst. 2021 Aug 25;2021:2214978. doi: 10.1155/2021/2214978. eCollection 2021.
- Individual participant dataSharing planned: No
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.
Ireneusz Staroń study chair
Medical University of Lodz
Questions about this trial
What is this clinical trial studying?
A study testing losartan and eprosartan in people with Uric Acid Concentration, Serum, Quantitative Trait Locus 7, run by Medical University of Lodz.
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 8 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 8 Jul 2021. Status can change between updates, so confirm with the study contact before making plans.
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?
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?
serum uric acid after losartan (time frame: 3 months). The study lists 4 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 NCT04954560, which also lists 1 linked publication.
Does a listing mean the treatment is approved or proven to work?
No. A listing means the study is registered. It does not show that the treatment is safe, works, or is approved by a regulator.
How often is this information updated?
AzTrials copies changed records from ClinicalTrials.gov every night and reloads the whole registry every week. The sponsor last updated this record on 8 Jul 2021.