Fabry DiseaseNCT02649660
Lipidomics and Functional Analyses of Platelets in Fabry Disease
An observational study of Fabry Disease, run by Spital Linth at 2 sites in Switzerland.
Trial summary
This study aims to evaluate whether platelets are biochemically and functionally altered in Fabry disease (FD) and therefore possibly implicated in FD manifestations such as cerebrovascular events. Read more about this study
- Who is it for?
- Ages 18 to 65 yearsHealthy volunteers can take part
- Conditions the study is for
- Fabry Disease
- How many people
- 32 participants
- Where
- 2 sitesSwitzerland
- Study dates
- Oct 2015to 31 Dec 2017
- Phase
- Observational
- 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
Study population: Patients with Fabry Disease and healthy volunteers
Who may be able to join
- Healthy Volunteers: without any known cardiovascular, cerebrovascular and renal diseases and without any known conditions affecting platelet function, blood coagulation and lipid metabolism.
- Patients: Genetically confirmed Fabry Disease
- Adult persons (18-65 years old), both female and male
- Informed written consent
Who cannot join
- Failure to meet inclusion criteria
- Pregnancy (as declared by the study participant, no pregnancy test will be performed)
Trial locations and contacts
2 sites in 1 country.
Switzerland2 sites, 2 recruiting
- Recruiting
Spital Linth
Uznach, Canton of St. Gallen, 8730
Pierre-Alexandre Krayenbuehl, MD, +41 55 285 40 62, Pierre-Alexandre.Krayenbuehl@spital-linth.ch
Pierre-Alexandre Krayenbuehl, MD
- Recruiting
University Hospital, Zürich
Zurich, Canton of Zurich, 8091
Albina Nowak, MD, +41 44 255 10 54, albina.nowak@usz.ch
Albina Nowak, MD
About this study
This study aims to evaluate whether platelets are biochemically and functionally altered in Fabry disease (FD) and therefore possibly implicated in FD manifestations such as cerebrovascular events. To test this hypothesis the investigators aim to compare platelet and plasma lipid profiles, as well as platelet function and coagulation parameters of FD patients and healthy controls.
Read the detailed description
Fabry disease (FD) is a severe X-linked inborn error of the lysosomal glycosphingolipid metabolism. FD patients have significantly increased risks for cardiac and cerebrovascular events, which can also occur early and in absence of the typical FD symptoms. However, the pathophysiological mechanisms leading to vascular occlusion and ischemia in FD are largely unclear. Prevention of recurrent cerebrovascular events is usually based on empirical anti-platelet therapy.
Prothrombotic states and partially activated platelets have been reported for FD patients. Platelets contain glycosphingolipids, including globotriaosylceramide (Gb3), and have lysosomal α-galactosidase activity. To investigate whether the lack of or the reduced α-galactosidase enzyme activity present in Fabry disease affects platelet lipid metabolism the investigators plan to perform LC-MS-based lipidomics analyses of platelets and plasma in FD patients and healthy controls. To assess whether platelets are functionally altered in FD, the investigators aim to determine the activation status, activability, aggregability and other parameters along with plasma markers of coagulation using flow cytometry, aggregometry and immunoassays.
- Conditions
- Fabry Disease
- Keywords
- Fabry Disease, Platelets, Lipidomics, Sphingolipids, α-Galactosidase A, Globotriaosylceramide, Gb3, GL-3, CD77, Alpha-galactosidase, Platelet activation, Lysosomal storage disease, LysoGb3, Spingosine-1-Phosphate, Platelet function, CD62P, P-selectin
- Medical subject headings
- Fabry Disease, Lysosomal Storage Diseases
What is being measured
The primary outcome is the main question the study is designed to answer.
Differences in sphingolipid profiles of platelets and plasma between Fabry disease patients and healthy subjects
Determination of sphingolipid concentrations in isolated platelets and plasma by targeted LC-MS (liquid chromatography mass spectrometry)-based lipidomics analysis of globotriaosylceramides (Gb3), globotriaosylspingosines (Lyso-Gb3), globotetraosylceramides (Gb4), lactosylceramides (LacCer), glucosylceramides, ceramides, sphingomyelins, sphingosines and sphingosine-1-phosphates.
Measured: Baseline
Differences in platelet function assessed by aggregometry
Determination of platelet aggregation after agonist stimulation with TRAP (thrombin receptor activator peptide), ADP (adenosine disphosphate) and arachidonic acid by light transmission aggregometry.
Measured: Baseline
Secondary outcomes (7)
Differences in expression of the platelet activation marker P-selectin (CD62P) between Fabry disease patients and healthy subjects at baseline and after agonist stimulation
Flow cytometric analysis of platelet surface expression of CD62P in whole blood determined at baseline and after platelet activation with the agonists TRAP (thrombin receptor activator peptide), ADP, and arachidonic acid.
Measured: Baseline
Differences in expression of the platelet activation marker CD63 between Fabry disease patients and healthy subjects at baseline and after agonist stimulation
Flow cytometric analysis of platelet surface expression of CD63 in whole blood determined at baseline and after platelet activation with the agonists TRAP (thrombin receptor activator peptide), ADP, and arachidonic acid.
Measured: Baseline
Differences in plasma levels of the platelet activation marker soluble P-selectin between Fabry disease patients and healthy subjects
Plasma concentrations of soluble P-selectin (soluble CD62P) are determined by ELISA (enzyme-linked immunosorbent assay)
Measured: Baseline
Differences in plasma levels of the platelet activation marker sCD40L between Fabry disease patients and healthy subjects
Plasma concentrations of sCD40L (soluble CD40 ligand) are determined by ELISA (enzyme-linked immunosorbent assay)
Measured: Baseline
Differences in presence of platelet aggregates between Fabry disease patients and healthy subjects
Flow cytometric assessment of platelet-platelet and platelet-leukocyte aggregates
Measured: Baseline
Differences of alpha-galactosidase A enzyme activity in plasma and isolated platelets between Fabry disease patients and healthy subjects
Analysis of the alpha-galactosidase A enzyme activity using a fluorometric enzyme assay with 4-methylumbelliferyl-α-D-galactopyranoside as substrate.
Measured: Baseline
Differences in phospholipid profiles in platelets and plasma between Fabry disease patients and healthy subjects
Determination of phospholipid concentrations in isolated platelets and plasma by targeted LC-MS-based lipidomics analysis of phosphatidylcholines, phosphatidylserines, phosphatidylinositols, and phosphatidylethanolamines.
Measured: Baseline
Timeline
From the start of the study to its completion; the mark is today. Estimated dates are the sponsor’s plan.
- First posted7 Jan 2016 (estimated)
- Study startOct 2015
- Primary completion31 Dec 2017 (estimated)
- Study completion31 Dec 2017 (estimated)
Resources
- Official record on ClinicalTrials.govThe registry entry this page is built from, with its full change history.
- Publications (7)Papers the sponsor has linked to this study.
- Other trials for Fabry 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
- Observational
- Observational model
- Cohort
- Time perspective
- Cross-sectional
- Enrolment
- 32 participants (estimated)
Sponsor and investigators
- Lead sponsor
- Spital Linth
- Sponsor type
- Other government
- Collaborators
- University of Zurich, National University of Singapore
- Responsible party
- Sponsor
- Investigators
- Pierre-Alexandre Krayenbühl, MD, Principal investigator, Spital Linth
IDs, dates and publications
- ClinicalTrials.gov ID
- NCT02649660
- Sponsor's protocol ID
- FabryPlatelets
- Status last verified
- May 2017
- First submitted
- 6 Dec 2015
- Last updated
- 8 May 2017
- Results posted
- No
- Data monitoring committee
- No
Publications
Feldt-Rasmussen U. Fabry disease and early stroke. Stroke Res Treat. 2011;2011:615218. doi: 10.4061/2011/615218. Epub 2011 Jun 23.
PubMed 21776363Tao RV, Sweeley CC, Jamieson GA. Sphingolipid composition of human platelets. J Lipid Res. 1973 Jan;14(1):16-25.
PubMed 4701549Beutler E, Kuhl W, Matsumoto F, Pangalis G. Acid hydrolases in leukocytes and platelets of normal subjects and in patients with Gaucher's and Fabry's disease. J Exp Med. 1976 Apr 1;143(4):975-80. doi: 10.1084/jem.143.4.975.
PubMed 3620Sims K, Politei J, Banikazemi M, Lee P. Stroke in Fabry disease frequently occurs before diagnosis and in the absence of other clinical events: natural history data from the Fabry Registry. Stroke. 2009 Mar;40(3):788-94. doi: 10.1161/STROKEAHA.108.526293. Epub 2009 Jan 15.
PubMed 19150871Igarashi T, Sakuraba H, Suzuki Y. Activation of platelet function in Fabry's disease. Am J Hematol. 1986 May;22(1):63-7. doi: 10.1002/ajh.2830220110.
PubMed 3006478DeGraba T, Azhar S, Dignat-George F, Brown E, Boutiere B, Altarescu G, McCarron R, Schiffmann R. Profile of endothelial and leukocyte activation in Fabry patients. Ann Neurol. 2000 Feb;47(2):229-33.
PubMed 10665494Vedder AC, Biro E, Aerts JM, Nieuwland R, Sturk G, Hollak CE. Plasma markers of coagulation and endothelial activation in Fabry disease: impact of renal impairment. Nephrol Dial Transplant. 2009 Oct;24(10):3074-81. doi: 10.1093/ndt/gfp263. Epub 2009 Jun 10.
PubMed 19515805
Study at a glance
From the registry record, last updated by the sponsor on 8 May 2017. Recruitment status is as the sponsor reported it: confirm with the study team.
- Official title
- Lipidomics and Functional Analyses of Platelets in Fabry Disease
- ClinicalTrials.gov ID
- NCT02649660
- Acronym / sponsor ID
- FabryPlatelets
- Conditions
- Fabry Disease
- Keywords
- Fabry Disease, Platelets, Lipidomics, Sphingolipids, α-Galactosidase A, Globotriaosylceramide, Gb3, GL-3
- Study type
- Observational
- Recruitment status
- Unknown status
- Enrolment
- 32 participants (estimated)
- Lead sponsor
- Spital LinthOther government
- Collaborators
- University of Zurich, National University of Singapore
- Study start
- Oct 2015
- Primary completion
- 31 Dec 2017 (estimated)
- Study completion
- 31 Dec 2017 (estimated)
- First posted
- 7 Jan 2016 (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.
This study aims to evaluate whether platelets are biochemically and functionally altered in Fabry disease (FD) and therefore possibly implicated in FD manifestations such as cerebrovascular events. To test this hypothesis the investigators aim to compare platelet and plasma lipid profiles, as well as platelet function and coagulation parameters of FD patients and healthy controls.
Detailed description
Fabry disease (FD) is a severe X-linked inborn error of the lysosomal glycosphingolipid metabolism. FD patients have significantly increased risks for cardiac and cerebrovascular events, which can also occur early and in absence of the typical FD symptoms. However, the pathophysiological mechanisms leading to vascular occlusion and ischemia in FD are largely unclear. Prevention of recurrent cerebrovascular events is usually based on empirical anti-platelet therapy.
Prothrombotic states and partially activated platelets have been reported for FD patients. Platelets contain glycosphingolipids, including globotriaosylceramide (Gb3), and have lysosomal α-galactosidase activity. To investigate whether the lack of or the reduced α-galactosidase enzyme activity present in Fabry disease affects platelet lipid metabolism the investigators plan to perform LC-MS-based lipidomics analyses of platelets and plasma in FD patients and healthy controls. To assess whether platelets are functionally altered in FD, the investigators aim to determine the activation status, activability, aggregability and other parameters along with plasma markers of coagulation using flow cytometry, aggregometry and immunoassays.
Study design
- Observational model
- Cohort
- Time perspective
- Cross-sectional
Who may qualify
- Ages
- 18 to 65 years
- Sex
- All
- Healthy volunteers
- Accepted
- Age groups
- Adult, Older adult
- Study population
- Patients with Fabry Disease and healthy volunteers
Key inclusion criteria (4 listed)
- Healthy Volunteers: without any known cardiovascular, cerebrovascular and renal diseases and without any known conditions affecting platelet function, blood coagulation and lipid metabolism.
- Patients: Genetically confirmed Fabry Disease
- Adult persons (18-65 years old), both female and male
- Informed written consent
Key exclusion criteria (2 listed)
- Failure to meet inclusion criteria
- Pregnancy (as declared by the study participant, no pregnancy test will be performed)
Eligibility is decided by the study team after screening; this overview does not establish that a patient qualifies. Full inclusion and exclusion criteria.
Primary outcome
Differences in sphingolipid profiles of platelets and plasma between Fabry disease patients and healthy subjects
Time frame: Baseline
Determination of sphingolipid concentrations in isolated platelets and plasma by targeted LC-MS (liquid chromatography mass spectrometry)-based lipidomics analysis of globotriaosylceramides (Gb3), globotriaosylspingosines (Lyso-Gb3), globotetraosylceramides (Gb4), lactosylceramides (LacCer), glucosylceramides, ceramides, sphingomyelins, sphingosines and sphingosine-1-phosphates.
Differences in platelet function assessed by aggregometry
Time frame: Baseline
Determination of platelet aggregation after agonist stimulation with TRAP (thrombin receptor activator peptide), ADP (adenosine disphosphate) and arachidonic acid by light transmission aggregometry.
7 secondary outcomes
Differences in expression of the platelet activation marker P-selectin (CD62P) between Fabry disease patients and healthy subjects at baseline and after agonist stimulation
Time frame: Baseline
Differences in expression of the platelet activation marker CD63 between Fabry disease patients and healthy subjects at baseline and after agonist stimulation
Time frame: Baseline
Differences in plasma levels of the platelet activation marker soluble P-selectin between Fabry disease patients and healthy subjects
Time frame: Baseline
Differences in plasma levels of the platelet activation marker sCD40L between Fabry disease patients and healthy subjects
Time frame: Baseline
Differences in presence of platelet aggregates between Fabry disease patients and healthy subjects
Time frame: Baseline
Differences of alpha-galactosidase A enzyme activity in plasma and isolated platelets between Fabry disease patients and healthy subjects
Time frame: Baseline
Differences in phospholipid profiles in platelets and plasma between Fabry disease patients and healthy subjects
Time frame: Baseline
Results and safety
Results are not available in the source record.
Research links
- Official record on ClinicalTrials.govLast updated by the sponsor 8 May 2017.
- Background: PubMed 21776363Feldt-Rasmussen U. Fabry disease and early stroke. Stroke Res Treat. 2011;2011:615218. doi: 10.4061/2011/615218. Epub 2011 Jun 23.
- Background: PubMed 4701549Tao RV, Sweeley CC, Jamieson GA. Sphingolipid composition of human platelets. J Lipid Res. 1973 Jan;14(1):16-25.
- Background: PubMed 3620Beutler E, Kuhl W, Matsumoto F, Pangalis G. Acid hydrolases in leukocytes and platelets of normal subjects and in patients with Gaucher's and Fabry's disease. J Exp Med. 1976 Apr 1;143(4):975-80. doi: 10.1084/jem.143.4.975.
- Results publication: PubMed 19150871Sims K, Politei J, Banikazemi M, Lee P. Stroke in Fabry disease frequently occurs before diagnosis and in the absence of other clinical events: natural history data from the Fabry Registry. Stroke. 2009 Mar;40(3):788-94. doi: 10.1161/STROKEAHA.108.526293. Epub 2009 Jan 15.
- Results publication: PubMed 3006478Igarashi T, Sakuraba H, Suzuki Y. Activation of platelet function in Fabry's disease. Am J Hematol. 1986 May;22(1):63-7. doi: 10.1002/ajh.2830220110.
- Results publication: PubMed 10665494DeGraba T, Azhar S, Dignat-George F, Brown E, Boutiere B, Altarescu G, McCarron R, Schiffmann R. Profile of endothelial and leukocyte activation in Fabry patients. Ann Neurol. 2000 Feb;47(2):229-33.
- Results publication: PubMed 19515805Vedder AC, Biro E, Aerts JM, Nieuwland R, Sturk G, Hollak CE. Plasma markers of coagulation and endothelial activation in Fabry disease: impact of renal impairment. Nephrol Dial Transplant. 2009 Oct;24(10):3074-81. doi: 10.1093/ndt/gfp263. Epub 2009 Jun 10.
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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.
Pierre-Alexandre Krayenbühl, MD principal investigator
Spital Linth
2 sites in 1 country: see every site and its status.
Questions about this trial
What is this clinical trial studying?
An observational study of Fabry Disease, run by Spital Linth at 2 sites 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 4 inclusion and 2 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: status not confirmed, as of the sponsor's last update on 8 May 2017. Status can change between updates, so confirm with the study contact before making plans.
Where is the study taking place?
The record lists 2 sites 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. 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?
Contact Pierre-Alexandre Krayenbühl, MD (+41 55 285 40 62, Pierre-Alexandre.Krayenbuehl@spital-linth.ch), or a site near the patient. AzTrials does not enrol participants or take referrals.
What does the primary outcome measure?
Differences in sphingolipid profiles of platelets and plasma between Fabry disease patients and healthy subjects (time frame: Baseline). The study lists 2 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 NCT02649660, which also lists 7 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 8 May 2017.