Bulimia NervosaNCT02179814
Neural Response to Catecholamine Depletion in Subjects Suffering From Bulimia Nervosa in Their Past and Healthy Controls
A study testing AMPT/ Demser and Diphenhydramine in people with Bulimia Nervosa and Eating Disorders, run by University of Bern at 1 site in Switzerland.
Trial summary
Bulimia nervosa is a severe psychiatric disorder characterized by recurrent binge eating episodes followed by inappropriate compensatory behavior to prevent weight gain such as self-induced vomiting. With this project, the investigators want to investigate the role of the neurotransmitter dopamine in bulimia nervosa. Read more about this study
- Who is it for?
- Ages 18 to 60 years, women onlyHealthy volunteers can take part
- Conditions the study is for
- Bulimia Nervosa, Eating Disorders, Dopamine
- What is being tested?
- AMPT/ Demser and Diphenhydramine
- Could I receive a placebo?
- Yes, some participants may receive a placebo
- How many people
- 60 participants
- Where
- 1 siteSwitzerland
- Study dates
- 20 Feb 2012to May 2022
- 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 60 years
- Women only
- Healthy volunteers accepted
- Adult
Who may be able to join
- female
- age: 18-60
- caucasian ethnicity
- right handedness
- normal or corrected to normal vision and hearing performance
- remitted bulimic participants: have met the DSM IV criteria for bulimia nervosa in the past
- remitted bulimic participants: have been asymptomatic for at least1 month
- signed written informed consent
Who cannot join
- healthy volunteers: any lifetime psychiatric diagnosis
- healthy volunteers: any lifetime psychiatric diagnosis in first-degree relatives
- no or impaired understanding of the tasks or the risks of the study
- medical or neurological illnesses likely to affect physiology or anatomy
- suicidal ideation or suicide attempts within the last 8 weeks
- current use of psychotropic drugs
Show all 17Show fewer
- history of drug including alcohol and nicotine (not more than 10 cigarettes per day) abuse within 1 year or a lifetime history of alcohol or drug dependence (DSM IV criteria) longer than 2 years
- asthma
- glaucoma
- pyloroduodenal obstruction (gastrointestinal stenosis)
- current pregnancy
- current breast feeding
- cardiac pacemaker
- heart or brain surgery
- metallic implants and alien objects in the body
- tattoos on head, neck or shoulders as well as permanent make-up
- claustrophobia
Trial locations and contacts
1 site in 1 country.
Switzerland1 site
University Hospital of Psychiatry, University of Bern
Bern, 3000
About this study
Official title: Neuronal Correlates of Catecholamine Depletion in Patients With Bulimia Nervosa Off Medication and Healthy Controls
Bulimia nervosa is a severe psychiatric disorder characterized by recurrent binge eating episodes followed by inappropriate compensatory behavior to prevent weight gain such as self-induced vomiting. With this project, the investigators want to investigate the role of the neurotransmitter dopamine in bulimia nervosa. Dopamine is reported to have an important influence on the neural reward system and is involved in the processing of gains and losses. The reward system is functionally connected to the individual perception of rewards in the environment. A previous study revealed that under catecholamine depletion including dopamine depletion women suffering from bulimia nervosa in their past reported mild bulimic symptoms and their reward processing became dysfunctional: their ability to use rewarding stimuli for task solving was diminished.
The aim of this study is to investigate the role of reduced dopamine availability in the development or maintaining of bulimia nervosa and in the dysfunctional processing of rewarding stimuli and negative visual information. Therefore, the investigators hypothesize that catecholamine depletion achieved by oral administration of alpha-methyl-paratyrosine (AMPT) will induce mild bulimic symptoms in females suffering from bulimia nervosa in their past. In addition, they will reveal dysfunctions in reward and emotional processing under catecholamine depletion. Using functional magnetic resonance imaging, the investigators propose that a reduced activation of the nucleus accumbens, a neural structure of the reward system, will be the neural correlate of this dysfunctional reward processing. Furthermore, the amygdala, a neural structure that is involved in emotional processing, will show a higher activation under catecholamine depletion. Genetic factors additionally have an influence on the dopaminergic system. Therefore, the investigators hypothesize that genetic factors, for example the COMT val-158-met polymorphism may have an effect on the behavioral and neural response to catecholamine depletion. In sum, this investigation may help to understand which changes in reward and emotional processing may lead to a reoccurrence of bulimic symptoms.
In future, the findings of this study may help to develop individual pharmacological and psychotherapeutical interventions to enhance the outcome of treatment.
Read the detailed description
Background
The Monoamine Deficiency Hypothesis is one of the most solid theories of the neurobiology of mood, anxiety disorder, and addiction. There is increasing evidence that monoamine deficiency also plays an important role in bulimia nervosa. Many indications revealed a disturbance of the catecholamine system in bulimia nervosa. In symptomatic bulimic patients, the concentration of norepinephrine and dopamine in cerebrospinal fluid and peripheral blood was lower than in healthy controls. The neurotransmitter dopamine is thought to be importantly involved in the processing of rewarding stimuli.
One instructive paradigm for investigating the relationship between catecholaminergic function and psychiatric disorders has involved the behavioral response to catecholamine depletion achieved by oral administration of alpha-methyl-paratyrosine (AMPT). This medication is a tyrosine hydroxylase inhibitor and, therefore, it reduces availability of catecholamines in the brain by depleting central norepinephrine and dopamine stores. A relatively large interindividual variation in the response to catecholamine depletion has been consistently observed. Genetic factors may conceivably contribute to this variation. The COMT val-158-met polymorphism was found to play a critical role for the activity of the enzyme catechol-O-methyltransferase (COMT) that metabolizes catecholamines after they have been released into the synaptic cleft. The enzyme activity in individuals homozygous for the val-158 allele is about 40% higher than in homozygotes of the met-158 allele. A high activity of this enzyme is thought to be associated with a higher reduction of catecholamines, particularly of dopamine in the prefrontal cortex.
In a previous study Gregor Hasler and colleagues were the first to use catecholamine depletion to evaluate the roles played by norepinephrine and dopamine in the pathophysiology of bulimia nervosa. The results of this study revealed that under catecholamine depletion remitted bulimic participants showed dysfunctions in motivated behavior in a reward task. In addition this study provided preliminary evidence that COMT val-158-met polymorphism explains some of the variance in the behavioral response to catecholamine depletion. However, in eating disorders, the pathway leading from genetic polymorphism to neural activity to neuropsychological abnormalities to risk of eating disorders remains to be determined.
With this new study the investigators want to investigate the neural substrate of the induced bulimia-associated neuropsychological abnormalities with functional magnetic resonance imaging (fMRI). An additional goal is to examine the effect of the COMT val-158-met polymorphism on neural activity.
In the following the investigators will present their central hypotheses:
- Remitted bulimic participants will reveal impairments in motivated behavior and abnormal neural activation in a reward task following catecholamine depletion.
- Remitted bulimic participants will show increased amygdala activation during encoding of negative pictures under catecholamine depletion.
- Participants with homozygous val-158 alleles of the COMT val-158-met polymorphism will show an increased activation in the ventral striatum during a reward task.
- Participants with at least one met-158 allele of the COMT val-158-met polymorphism will show higher amygdala activation during the encoding of negative emotional visual information.
Objective
This study will further elucidate the etiology and pathophysiology of bulimia nervosa at various levels, ranging from the role of a specific genetic factor to the activity of specific neural networks to neuropsychological abnormalities and clinical symptoms. It may provide important insights into a specific pathogenetic pathway of bulimia nervosa related to the catecholaminergic in particular to the dopaminergic neurotransmitter system. Since a range of drugs targeting this neurotransmitter system are available, this study may directly inform the development of novel therapeutic strategies tailored to individual patients.
Methods
Remitted bulimic and healthy control participants will be enrolled into a double-blind, placebo-controlled cross-over catecholamine/sham depletion study.
The initial assessment comprises physical examinations, a structured psychiatric interview, clinical ratings and neuropsychological testing.
Catecholamine depletion will be induced by administration of AMPT over 24 hours. Sham depletion includes diphenhydramine at the first medication intake time point because AMPT mostly induce mild sedation.
Based on previous reports, the investigators expect maximal depletion 30 hours after the first dose AMPT. Blood samples will be taken at that time to measure serum prolactin levels as a proxy of catecholamine synthesis. Behavioral experiments (tasks assessing reward and emotional processing) will be conducted in a MR-scanner. The participants will complete various self-report ratings before the first, during and after medication intake.
- Being tested
- AMPT/ Demser, Diphenhydramine, Placebo
- Keywords
- bulimia nervosa, dopamine, reward, catechol-O-methyltransferase, gene, catecholamines, alpha-methyl-para-tyrosine, magnetic resonance imaging
- Medical subject headings
- Bulimia Nervosa, Feeding and Eating Disorders
What participants receive
What participants receive. In a randomised study each person is assigned to one group by chance.
AMPT/ DemserDrug
alpha-methyl-paratyrosine (AMPT, trade name: Demser) body-weight adjusted dosage (40 mg/kg body weight, maximum 4000mg) at 4 medication intake time points over 24 hours
DiphenhydramineDrug
Also called Benocten (trade name in Switzerland)
Diphenhydramine (25mg) at the first medication intake time point
PlaceboDrug
Placebo at the second, third and fourth medication intake time point
| Study group | Role | What they receive |
|---|---|---|
| AMPT | Experimental | Experimental:
alpha-methyl-paratyrosine (AMPT, trade name: Demser), body-weight adjusted dosage (40 mg/kg body weight, maximum 4000mg) at 4 time points over 24 hours Receives: Drug: AMPT/ Demser |
| Diphenhydramine & placebo | Sham comparator | Diphenhydramine (25mg, trade name in Switzerland: Benocten) at the first medication intake time point, placebo at the second to fourth intake time point (medication intake over 24 hours) Receives: Drug: Diphenhydramine; Drug: Placebo |
What is being measured
The primary outcome is the main question the study is designed to answer.
Number of participants with side effects
Measured: 1 year
Secondary outcomes (3)
Performance differences in behavioral tasks after catecholamine depletion
Measured: 4 years
Differences in neural activation assessed during functional magnetic resonance imaging (fMRI) in the different conditions
Measured: 4 years
Differences in neural activation assessed during functional magnetic resonance imaging (fMRI) and in performance in behavioral tasks in the different conditions between the different genotypes
Measured: 4 years
Timeline
From the start of the study to its completion; the mark is today. Estimated dates are the sponsor’s plan.
- First posted2 Jul 2014 (estimated)
- Study start20 Feb 2012
- Primary completionMay 2019 (estimated)
- Study completionMay 2022 (estimated)
Why it stopped: Conduct of the first analyses
Resources
- Official record on ClinicalTrials.govThe registry entry this page is built from, with its full change history.
- Publications (3)Papers the sponsor has linked to this study.
- Other trials for Bulimia NervosaStudies of the same condition, open and under way.
- More trials run by University of BernThe 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
- Diagnosis
- Allocation
- Randomised
- Intervention model
- Crossover
- Masking
- Double blind
- Who is masked
- Participant, Investigator
- Enrolment
- 60 participants (estimated)
Sponsor and investigators
- Lead sponsor
- University of Bern
- Sponsor type
- University, hospital or other
- Responsible party
- Sponsor
- Investigators
- Gregor Hasler, Prof. Dr. med, Principal investigator, University Hospital of Psychiatry, University of Bern
IDs, dates and publications
- ClinicalTrials.gov ID
- NCT02179814
- Sponsor's protocol ID
- 132/10
- Other IDs
- 2011DR1011, 32003B_138264 / 1
- Status last verified
- Jan 2019
- First submitted
- 25 Jun 2014
- Last updated
- 24 Jan 2019
- Results posted
- No
- Data monitoring committee
- No
Publications
Hasler G, Fromm S, Carlson PJ, Luckenbaugh DA, Waldeck T, Geraci M, Roiser JP, Neumeister A, Meyers N, Charney DS, Drevets WC. Neural response to catecholamine depletion in unmedicated subjects with major depressive disorder in remission and healthy subjects. Arch Gen Psychiatry. 2008 May;65(5):521-31. doi: 10.1001/archpsyc.65.5.521.
PubMed 18458204Grob S, Stern J, Gamper L, Moergeli H, Milos G, Schnyder U, Hasler G. Behavioral responses to catecholamine depletion in unmedicated, remitted subjects with bulimia nervosa and healthy subjects. Biol Psychiatry. 2015 Apr 1;77(7):661-7. doi: 10.1016/j.biopsych.2013.09.013. Epub 2013 Oct 25.
PubMed 24209774Homan P, Grob S, Milos G, Schnyder U, Hasler G. Reduction in total plasma ghrelin levels following catecholamine depletion: relation to bulimic and depressive symptoms. Psychoneuroendocrinology. 2013 Sep;38(9):1545-52. doi: 10.1016/j.psyneuen.2012.12.024. Epub 2013 Jan 16.
PubMed 23333252
Study at a glance
From the registry record, last updated by the sponsor on 24 Jan 2019. Recruitment status is as the sponsor reported it: confirm with the study team.
- Official title
- Neuronal Correlates of Catecholamine Depletion in Patients With Bulimia Nervosa Off Medication and Healthy Controls
- ClinicalTrials.gov ID
- NCT02179814
- Acronym / sponsor ID
- 132/10
- Keywords
- bulimia nervosa, dopamine, reward, catechol-O-methyltransferase, gene, catecholamines, alpha-methyl-para-tyrosine, magnetic resonance imaging
- Study type
- Interventional
- Recruitment status
- SuspendedReason stopped: Conduct of the first analyses
- Enrolment
- 60 participants (estimated)
- Lead sponsor
- University of BernUniversity, hospital or other
- Collaborators
- Insel Gruppe AG, University Hospital Bern, University of Zurich
- Study start
- 20 Feb 2012 (actual)
- Primary completion
- May 2019 (estimated)
- Study completion
- May 2022 (estimated)
- First posted
- 2 Jul 2014 (estimated)
- 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.
Bulimia nervosa is a severe psychiatric disorder characterized by recurrent binge eating episodes followed by inappropriate compensatory behavior to prevent weight gain such as self-induced vomiting. With this project, the investigators want to investigate the role of the neurotransmitter dopamine in bulimia nervosa. Dopamine is reported to have an important influence on the neural reward system and is involved in the processing of gains and losses. The reward system is functionally connected to the individual perception of rewards in the environment. A previous study revealed that under catecholamine depletion including dopamine depletion women suffering from bulimia nervosa in their past reported mild bulimic symptoms and their reward processing became dysfunctional: their ability to use rewarding stimuli for task solving was diminished.
The aim of this study is to investigate the role of reduced dopamine availability in the development or maintaining of bulimia nervosa and in the dysfunctional processing of rewarding stimuli and negative visual information. Therefore, the investigators hypothesize that catecholamine depletion achieved by oral administration of alpha-methyl-paratyrosine (AMPT) will induce mild bulimic symptoms in females suffering from bulimia nervosa in their past. In addition, they will reveal dysfunctions in reward and emotional processing under catecholamine depletion. Using functional magnetic resonance imaging, the investigators propose that a reduced activation of the nucleus accumbens, a neural structure of the reward system, will be the neural correlate of this dysfunctional reward processing. Furthermore, the amygdala, a neural structure that is involved in emotional processing, will show a higher activation under catecholamine depletion. Genetic factors additionally have an influence on the dopaminergic system. Therefore, the investigators hypothesize that genetic factors, for example the COMT val-158-met polymorphism may have an effect on the behavioral and neural response to catecholamine depletion. In sum, this investigation may help to understand which changes in reward and emotional processing may lead to a reoccurrence of bulimic symptoms.
In future, the findings of this study may help to develop individual pharmacological and psychotherapeutical interventions to enhance the outcome of treatment.
Detailed description
Background
The Monoamine Deficiency Hypothesis is one of the most solid theories of the neurobiology of mood, anxiety disorder, and addiction. There is increasing evidence that monoamine deficiency also plays an important role in bulimia nervosa. Many indications revealed a disturbance of the catecholamine system in bulimia nervosa. In symptomatic bulimic patients, the concentration of norepinephrine and dopamine in cerebrospinal fluid and peripheral blood was lower than in healthy controls. The neurotransmitter dopamine is thought to be importantly involved in the processing of rewarding stimuli.
One instructive paradigm for investigating the relationship between catecholaminergic function and psychiatric disorders has involved the behavioral response to catecholamine depletion achieved by oral administration of alpha-methyl-paratyrosine (AMPT). This medication is a tyrosine hydroxylase inhibitor and, therefore, it reduces availability of catecholamines in the brain by depleting central norepinephrine and dopamine stores. A relatively large interindividual variation in the response to catecholamine depletion has been consistently observed. Genetic factors may conceivably contribute to this variation. The COMT val-158-met polymorphism was found to play a critical role for the activity of the enzyme catechol-O-methyltransferase (COMT) that metabolizes catecholamines after they have been released into the synaptic cleft. The enzyme activity in individuals homozygous for the val-158 allele is about 40% higher than in homozygotes of the met-158 allele. A high activity of this enzyme is thought to be associated with a higher reduction of catecholamines, particularly of dopamine in the prefrontal cortex.
In a previous study Gregor Hasler and colleagues were the first to use catecholamine depletion to evaluate the roles played by norepinephrine and dopamine in the pathophysiology of bulimia nervosa. The results of this study revealed that under catecholamine depletion remitted bulimic participants showed dysfunctions in motivated behavior in a reward task. In addition this study provided preliminary evidence that COMT val-158-met polymorphism explains some of the variance in the behavioral response to catecholamine depletion. However, in eating disorders, the pathway leading from genetic polymorphism to neural activity to neuropsychological abnormalities to risk of eating disorders remains to be determined.
With this new study the investigators want to investigate the neural substrate of the induced bulimia-associated neuropsychological abnormalities with functional magnetic resonance imaging (fMRI). An additional goal is to examine the effect of the COMT val-158-met polymorphism on neural activity.
In the following the investigators will present their central hypotheses:
- Remitted bulimic participants will reveal impairments in motivated behavior and abnormal neural activation in a reward task following catecholamine depletion.
- Remitted bulimic participants will show increased amygdala activation during encoding of negative pictures under catecholamine depletion.
- Participants with homozygous val-158 alleles of the COMT val-158-met polymorphism will show an increased activation in the ventral striatum during a reward task.
- Participants with at least one met-158 allele of the COMT val-158-met polymorphism will show higher amygdala activation during the encoding of negative emotional visual information.
Objective
This study will further elucidate the etiology and pathophysiology of bulimia nervosa at various levels, ranging from the role of a specific genetic factor to the activity of specific neural networks to neuropsychological abnormalities and clinical symptoms. It may provide important insights into a specific pathogenetic pathway of bulimia nervosa related to the catecholaminergic in particular to the dopaminergic neurotransmitter system. Since a range of drugs targeting this neurotransmitter system are available, this study may directly inform the development of novel therapeutic strategies tailored to individual patients.
Methods
Remitted bulimic and healthy control participants will be enrolled into a double-blind, placebo-controlled cross-over catecholamine/sham depletion study.
The initial assessment comprises physical examinations, a structured psychiatric interview, clinical ratings and neuropsychological testing.
Catecholamine depletion will be induced by administration of AMPT over 24 hours. Sham depletion includes diphenhydramine at the first medication intake time point because AMPT mostly induce mild sedation.
Based on previous reports, the investigators expect maximal depletion 30 hours after the first dose AMPT. Blood samples will be taken at that time to measure serum prolactin levels as a proxy of catecholamine synthesis. Behavioral experiments (tasks assessing reward and emotional processing) will be conducted in a MR-scanner. The participants will complete various self-report ratings before the first, during and after medication intake.
Study design
- Primary purpose
- Diagnosis
- Allocation
- Randomised
- Intervention model
- Crossover
- Masking
- Double blind (participant, investigator)
- Number of arms
- 2
| Arm | Type | Receives |
|---|---|---|
| AMPT | Experimental | Drug: AMPT/ DemserExperimental: alpha-methyl-paratyrosine (AMPT, trade name: Demser), body-weight adjusted dosage (40 mg/kg body weight, maximum 4000mg) at 4 time points over 24 hours |
| Diphenhydramine & placebo | Sham comparator | Drug: Diphenhydramine, Drug: PlaceboDiphenhydramine (25mg, trade name in Switzerland: Benocten) at the first medication intake time point, placebo at the second to fourth intake time point (medication intake over 24 hours) |
Who may qualify
- Ages
- 18 to 60 years
- Sex
- Female only
- Healthy volunteers
- Accepted
- Age groups
- Adult
Key inclusion criteria (8 listed)
- female
- age: 18-60
- caucasian ethnicity
- right handedness
- normal or corrected to normal vision and hearing performance
Key exclusion criteria (17 listed)
- healthy volunteers: any lifetime psychiatric diagnosis
- healthy volunteers: any lifetime psychiatric diagnosis in first-degree relatives
- no or impaired understanding of the tasks or the risks of the study
- medical or neurological illnesses likely to affect physiology or anatomy
- suicidal ideation or suicide attempts within the last 8 weeks
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 |
|---|---|---|
| AMPT/ Demseralpha-methyl-paratyrosine (AMPT, trade name: Demser) body-weight adjusted dosage (40 mg/kg body weight, maximum 4000mg) at 4 medication intake time points over 24 hours | Drug | AMPT |
| DiphenhydramineAlso: Benocten (trade name in Switzerland)Diphenhydramine (25mg) at the first medication intake time point | Drug | Diphenhydramine & placebo |
| PlaceboPlacebo at the second, third and fourth medication intake time point | Drug | Diphenhydramine & placebo |
Primary outcome
Number of participants with side effects
Time frame: 1 year
3 secondary outcomes
Performance differences in behavioral tasks after catecholamine depletion
Time frame: 4 years
Differences in neural activation assessed during functional magnetic resonance imaging (fMRI) in the different conditions
Time frame: 4 years
Differences in neural activation assessed during functional magnetic resonance imaging (fMRI) and in performance in behavioral tasks in the different conditions between the different genotypes
Time frame: 4 years
Results and safety
Results are not available in the source record.
Research links
- Official record on ClinicalTrials.govLast updated by the sponsor 24 Jan 2019.
- Background: PubMed 18458204Hasler G, Fromm S, Carlson PJ, Luckenbaugh DA, Waldeck T, Geraci M, Roiser JP, Neumeister A, Meyers N, Charney DS, Drevets WC. Neural response to catecholamine depletion in unmedicated subjects with major depressive disorder in remission and healthy subjects. Arch Gen Psychiatry. 2008 May;65(5):521-31. doi: 10.1001/archpsyc.65.5.521.
- Background: PubMed 24209774Grob S, Stern J, Gamper L, Moergeli H, Milos G, Schnyder U, Hasler G. Behavioral responses to catecholamine depletion in unmedicated, remitted subjects with bulimia nervosa and healthy subjects. Biol Psychiatry. 2015 Apr 1;77(7):661-7. doi: 10.1016/j.biopsych.2013.09.013. Epub 2013 Oct 25.
- Background: PubMed 23333252Homan P, Grob S, Milos G, Schnyder U, Hasler G. Reduction in total plasma ghrelin levels following catecholamine depletion: relation to bulimic and depressive symptoms. Psychoneuroendocrinology. 2013 Sep;38(9):1545-52. doi: 10.1016/j.psyneuen.2012.12.024. Epub 2013 Jan 16.
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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.
Gregor Hasler, Prof. Dr. med principal investigator
University Hospital of Psychiatry, University of Bern
1 site in 1 country: see every site and its status.
Questions about this trial
What is this clinical trial studying?
A study testing AMPT/ Demser and Diphenhydramine in people with Bulimia Nervosa and Eating Disorders, run by University of Bern at 1 site in Switzerland.
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 17 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: paused, as of the sponsor's last update on 24 Jan 2019. 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 Switzerland. 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?
Results are not available in the source record.
How can a doctor refer a patient or contact the research team?
The record lists no contact. The official record names the sponsor, who can be asked directly. AzTrials does not enrol participants or take referrals.
What does the primary outcome measure?
Number of participants with side effects (time frame: 1 year). 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 NCT02179814, which also lists 3 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 24 Jan 2019.