Diabetes Mellitus, Type 1Phase 4NCT01397513
Effects of Aspirin Treatment on Fibrin Network Formation in Patients With Type 1 Diabetes
A Phase 4 study testing Aspirin in people with Diabetes Mellitus, Type 1, run by Karolinska Institutet at 1 site in Sweden.
Trial summary
The fibrin network is an important component of an arterial thrombus and its structure influences the degradation of the formed clot. A tighter and less permeable fibrin network, which is less susceptible to fibrinolysis, is formed in patients with manifest cardiovascular disease (CVD) or conditions associated with… Read more about this study
- Who is it for?
- Ages 30 to 70 years
- Conditions the study is for
- Diabetes Mellitus, Type 1
- What is being tested?
- Aspirin
- Type of treatment
- Pill or oral medicine
- Could I receive a placebo?
- No, everyone receives an active treatment
- How many people
- 48 participants
- Where
- 1 siteSweden
- Study dates
- Mar 2006to Feb 2011
- Phase
- Phase 4
- 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 30 to 70 years
- All sexes
- No healthy volunteers
- Adult, Older adult
Who may be able to join
- Diabetes mellitus, type 1
- Levels of HbA1C (glycated hemoglobin) <7.4% (NGSP standard)
- Levels of HbA1C >8.4% (NGSP standard)
Who cannot join
- Prior aspirin treatment
- Treatment with anticoagulant drugs
- Ongoing treatment with NSAIDs or other antiplatelet drugs
- A history of macrovascular disease
Trial locations and contacts
1 site in 1 country.
Sweden1 site
Karolinska Institutet, Department of Clinical Sciences, Danderyd Hospital
Stockholm, 18288
About this study
Official title: Effects of Low and High Doses of Aspirin Treatment on Fibrin Network Formation in Patients With Type 1 Diabetes and Possible Influence of the Glycemic Control.
The fibrin network is an important component of an arterial thrombus and its structure influences the degradation of the formed clot. A tighter and less permeable fibrin network, which is less susceptible to fibrinolysis, is formed in patients with manifest cardiovascular disease (CVD) or conditions associated with increased risk of atherothrombotic complications. In a previous study we have shown reduced fibrin network permeability in patients with type 1 diabetes, which may contribute to their increased risk of CVD. Low dose aspirin treatment is standard in management of CVD; however, the effect seems reduced in patients with diabetes. Our previous studies have shown that aspirin treatment alters the fibrin network in non-diabetic individuals and increases the fibrin network permeability. The effect of aspirin on fibrin network formation in patients with diabetes is unclear.
We hypothesized that patients with type 1 diabetes might need higher doses of aspirin than the recommended low dose (75mg) treatment to gain effects on fibrin network permeability, and that the effects of aspirin treatment on fibrin network in these patients are influenced by the glycemic control.
Read the detailed description
Diabetes is associated with increased platelet activation, elevated plasma fibrinogen levels and impaired fibrinolysis, factors which may contribute to the elevated risk of cardiovascular disease (CVD) in these patients. Increased platelet activation in patients with diabetes is reflected by elevated levels of platelet microparticles, which are small circulating procoagulant vesicles shed from the platelet membrane upon activation. CVD in these patients may start as early as in the age of 25-30 years and the course is often aggressive and with poor prognosis. Treatment with a daily low dose of acetylsalicylic acid (aspirin 75 mg) is one of the cornerstones in management of CVD in non-diabetic patients; however, the effect seems reduced in patients with diabetes. The mechanisms behind this treatment failure with aspirin in diabetes patients are unclear. Aspirin is a complex drug with multiple effects. The most well known is acetylation and inhibition of platelet cyclooxygenase (COX), but COX-independent mechanisms may also of importance in protection of cardiovascular complications. One such mechanism is alteration of the fibrin/fibrinogen properties and the fibrin network structure, possibly through acetylation of the lysine residues in the fibrinogen molecule involved in crosslinking of fibrin. The fibrin network structure seems important in development of atherothrombotic events, as individuals at high risk of CVD, including patients with type 1 diabetes, as well as patients with manifest CVD have a tighter and less permeable fibrin network structure. The altered fibrin network in patients with type 1 diabetes may in part be due to increased fibrinogen glycation, which may occur on lysine residues. Treatment with aspirin increases fibrin network permeability in non-diabetic subjects. However, the effect of aspirin on fibrin network permeability in patients with diabetes is unclear. Possible competition between acetylation and glycation on lysine residues in the fibrinogen molecule might contribute to the reduced preventive effect of aspirin in management of CVD in patients with diabetes and higher doses of aspirin might therefore be required in these patients.
Our hypothesis was that glycation and acetylation occur at the same binding sites in the fibrinogen molecule. Thus, poor glycemic control and increased glycation may lead to lower acetylation of the fibrinogen molecule than during good glycemic control in turn leading to an altered fibrin network.
The aims of the present study were to analyse the effects of low (75 mg) and high dose (320 mg) aspirin treatment on fibrin network formation in patients with type 1 diabetes (primary aim), and to investigate the possible influence of the glycemic control (secondary aim). As platelet microparticles may influence the fibrin formation [17, 18] and since aspirin has well-known effects on platelet function, we also measured plasma concentrations of platelet microparticles.
- Conditions
- Diabetes Mellitus, Type 1
- Being tested
- Aspirin
- Keywords
- Fibrin network structure, Aspirin treatment, Platelet microparticles
- Medical subject headings
- Diabetes Mellitus, Type 1
What participants receive
What participants receive. In a randomised study each person is assigned to one group by chance.
AspirinDrug
Also called Trombyl
Tablets, 75 or 320mg once daily for 4 weeks. A 4-week wash-out period separated the two treatment periods.
| Study group | Role | What they receive |
|---|---|---|
| Aspirin 75mg | Active comparator | Not described Receives: Drug: Aspirin |
| Aspirin 320mg | Active comparator | Not described Receives: Drug: Aspirin |
What is being measured
The primary outcome is the main question the study is designed to answer.
Fibrin network permeability
Changes in fibrin network permeability after 4 weeks of treatment with either aspirin 75 or 320mg.
Measured: At the start and end of each 4-week treatment period
Secondary outcomes (2)
Fibrin network permeability
Subgroup analyses comparing the treatment effects of aspirin 75 or 320mg on fibrin network permeability in patients with good and poor glycemic control, respectively.
Measured: At the start and end of each 4-week treatment period
Platelet microparticles
Changes in plasma concentrations of platelet microparticles after 4 weeks of treatment with either aspirin 75 or 320mg.
Measured: At the start and end of each 4-week treatment period
Timeline
From the start of the study to its completion; the mark is today. Estimated dates are the sponsor’s plan.
- First posted19 Jul 2011 (estimated)
- Study startMar 2006
- Primary completionJul 2010
- Study completionFeb 2011
Resources
- Official record on ClinicalTrials.govThe registry entry this page is built from, with its full change history.
- Publications (19)Papers the sponsor has linked to this study.
- Other trials for Diabetes Mellitus, Type 1Studies of the same condition, open and under way.
- More trials run by Karolinska InstitutetThe 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 4
- Primary purpose
- Treatment
- Allocation
- Randomised
- Intervention model
- Crossover
- Masking
- None (open label)
- Enrolment
- 48 participants (actual)
Sponsor and investigators
- Lead sponsor
- Karolinska Institutet
- Sponsor type
- University, hospital or other
- Investigators
- Gun Jörneskog, MD PhD, Principal investigator, Karolinska Institutet, Department of Clinical Sciences, Danderyd Hospital
IDs, dates and publications
- ClinicalTrials.gov ID
- NCT01397513
- Sponsor's protocol ID
- 151:2005/76316
- Other IDs
- 2005/1403-31/2
- Status last verified
- Mar 2006
- First submitted
- 14 Jul 2011
- Last updated
- 19 Jul 2011
- Results posted
- No
- Data monitoring committee
- Yes
Publications
Collet JP, Park D, Lesty C, Soria J, Soria C, Montalescot G, Weisel JW. Influence of fibrin network conformation and fibrin fiber diameter on fibrinolysis speed: dynamic and structural approaches by confocal microscopy. Arterioscler Thromb Vasc Biol. 2000 May;20(5):1354-61. doi: 10.1161/01.atv.20.5.1354.
PubMed 10807754Collet JP, Allali Y, Lesty C, Tanguy ML, Silvain J, Ankri A, Blanchet B, Dumaine R, Gianetti J, Payot L, Weisel JW, Montalescot G. Altered fibrin architecture is associated with hypofibrinolysis and premature coronary atherothrombosis. Arterioscler Thromb Vasc Biol. 2006 Nov;26(11):2567-73. doi: 10.1161/01.ATV.0000241589.52950.4c. Epub 2006 Aug 17.
PubMed 16917107Rooth E, Wallen NH, Blomback M, He S. Decreased fibrin network permeability and impaired fibrinolysis in the acute and convalescent phase of ischemic stroke. Thromb Res. 2011 Jan;127(1):51-6. doi: 10.1016/j.thromres.2010.09.011. Epub 2010 Oct 14.
PubMed 20950841Colle JP, Mishal Z, Lesty C, Mirshahi M, Peyne J, Baumelou A, Bensman A, Soria J, Soria C. Abnormal fibrin clot architecture in nephrotic patients is related to hypofibrinolysis: influence of plasma biochemical modifications: a possible mechanism for the high thrombotic tendency? Thromb Haemost. 1999 Nov;82(5):1482-9.
PubMed 10595642Jorneskog G, Egberg N, Fagrell B, Fatah K, Hessel B, Johnsson H, Brismar K, Blomback M. Altered properties of the fibrin gel structure in patients with IDDM. Diabetologia. 1996 Dec;39(12):1519-23. doi: 10.1007/s001250050607.
PubMed 8960835Cubbon RM, Gale CP, Rajwani A, Abbas A, Morrell C, Das R, Barth JH, Grant PJ, Kearney MT, Hall AS. Aspirin and mortality in patients with diabetes sustaining acute coronary syndrome. Diabetes Care. 2008 Feb;31(2):363-5. doi: 10.2337/dc07-1745. Epub 2007 Oct 24.
PubMed 17959865Antovic A, Perneby C, Ekman GJ, Wallen HN, Hjemdahl P, Blomback M, He S. Marked increase of fibrin gel permeability with very low dose ASA treatment. Thromb Res. 2005;116(6):509-17. doi: 10.1016/j.thromres.2005.02.007.
PubMed 16181986Williams S, Fatah K, Hjemdahl P, Blomback M. Better increase in fibrin gel porosity by low dose than intermediate dose acetylsalicylic acid. Eur Heart J. 1998 Nov;19(11):1666-72. doi: 10.1053/euhj.1998.1088.
PubMed 9857919Yngen M, Ostenson CG, Hu H, Li N, Hjemdahl P, Wallen NH. Enhanced P-selectin expression and increased soluble CD40 Ligand in patients with Type 1 diabetes mellitus and microangiopathy: evidence for platelet hyperactivity and chronic inflammation. Diabetologia. 2004 Mar;47(3):537-540. doi: 10.1007/s00125-004-1352-4. Epub 2004 Feb 13.
PubMed 14963650Ganda OP, Arkin CF. Hyperfibrinogenemia. An important risk factor for vascular complications in diabetes. Diabetes Care. 1992 Oct;15(10):1245-50. doi: 10.2337/diacare.15.10.1245.
PubMed 1425083Dunn EJ, Philippou H, Ariens RA, Grant PJ. Molecular mechanisms involved in the resistance of fibrin to clot lysis by plasmin in subjects with type 2 diabetes mellitus. Diabetologia. 2006 May;49(5):1071-80. doi: 10.1007/s00125-006-0197-4. Epub 2006 Mar 16.
PubMed 16538489Nomura S, Suzuki M, Katsura K, Xie GL, Miyazaki Y, Miyake T, Kido H, Kagawa H, Fukuhara S. Platelet-derived microparticles may influence the development of atherosclerosis in diabetes mellitus. Atherosclerosis. 1995 Aug;116(2):235-40. doi: 10.1016/0021-9150(95)05551-7.
PubMed 7575778Undas A, Brummel-Ziedins KE, Mann KG. Antithrombotic properties of aspirin and resistance to aspirin: beyond strictly antiplatelet actions. Blood. 2007 Mar 15;109(6):2285-92. doi: 10.1182/blood-2006-01-010645. Epub 2006 Dec 5.
PubMed 17148593Bjornsson TD, Schneider DE, Berger H Jr. Aspirin acetylates fibrinogen and enhances fibrinolysis. Fibrinolytic effect is independent of changes in plasminogen activator levels. J Pharmacol Exp Ther. 1989 Jul;250(1):154-61.
PubMed 2746495Lutjens A, te Velde AA, vd Veen EA, vd Meer J. Glycosylation of human fibrinogen in vivo. Diabetologia. 1985 Feb;28(2):87-9. doi: 10.1007/BF00279921.
PubMed 3920098
Study at a glance
From the registry record, last updated by the sponsor on 19 Jul 2011. Recruitment status is as the sponsor reported it: confirm with the study team.
- Official title
- Effects of Low and High Doses of Aspirin Treatment on Fibrin Network Formation in Patients With Type 1 Diabetes and Possible Influence of the Glycemic Control.
- ClinicalTrials.gov ID
- NCT01397513
- Acronym / sponsor ID
- 151:2005/76316
- Conditions
- Diabetes Mellitus, Type 1
- Keywords
- Fibrin network structure, Aspirin treatment, Platelet microparticles
- Phase
- Phase 4
- Study type
- Interventional
- Recruitment status
- Completed
- Enrolment
- 48 participants (actual)
- Lead sponsor
- Karolinska InstitutetUniversity, hospital or other
- Study start
- Mar 2006
- Primary completion
- Jul 2010 (actual)
- Study completion
- Feb 2011 (actual)
- First posted
- 19 Jul 2011 (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.
The fibrin network is an important component of an arterial thrombus and its structure influences the degradation of the formed clot. A tighter and less permeable fibrin network, which is less susceptible to fibrinolysis, is formed in patients with manifest cardiovascular disease (CVD) or conditions associated with increased risk of atherothrombotic complications. In a previous study we have shown reduced fibrin network permeability in patients with type 1 diabetes, which may contribute to their increased risk of CVD. Low dose aspirin treatment is standard in management of CVD; however, the effect seems reduced in patients with diabetes. Our previous studies have shown that aspirin treatment alters the fibrin network in non-diabetic individuals and increases the fibrin network permeability. The effect of aspirin on fibrin network formation in patients with diabetes is unclear.
We hypothesized that patients with type 1 diabetes might need higher doses of aspirin than the recommended low dose (75mg) treatment to gain effects on fibrin network permeability, and that the effects of aspirin treatment on fibrin network in these patients are influenced by the glycemic control.
Detailed description
Diabetes is associated with increased platelet activation, elevated plasma fibrinogen levels and impaired fibrinolysis, factors which may contribute to the elevated risk of cardiovascular disease (CVD) in these patients. Increased platelet activation in patients with diabetes is reflected by elevated levels of platelet microparticles, which are small circulating procoagulant vesicles shed from the platelet membrane upon activation. CVD in these patients may start as early as in the age of 25-30 years and the course is often aggressive and with poor prognosis. Treatment with a daily low dose of acetylsalicylic acid (aspirin 75 mg) is one of the cornerstones in management of CVD in non-diabetic patients; however, the effect seems reduced in patients with diabetes. The mechanisms behind this treatment failure with aspirin in diabetes patients are unclear. Aspirin is a complex drug with multiple effects. The most well known is acetylation and inhibition of platelet cyclooxygenase (COX), but COX-independent mechanisms may also of importance in protection of cardiovascular complications. One such mechanism is alteration of the fibrin/fibrinogen properties and the fibrin network structure, possibly through acetylation of the lysine residues in the fibrinogen molecule involved in crosslinking of fibrin. The fibrin network structure seems important in development of atherothrombotic events, as individuals at high risk of CVD, including patients with type 1 diabetes, as well as patients with manifest CVD have a tighter and less permeable fibrin network structure. The altered fibrin network in patients with type 1 diabetes may in part be due to increased fibrinogen glycation, which may occur on lysine residues. Treatment with aspirin increases fibrin network permeability in non-diabetic subjects. However, the effect of aspirin on fibrin network permeability in patients with diabetes is unclear. Possible competition between acetylation and glycation on lysine residues in the fibrinogen molecule might contribute to the reduced preventive effect of aspirin in management of CVD in patients with diabetes and higher doses of aspirin might therefore be required in these patients.
Our hypothesis was that glycation and acetylation occur at the same binding sites in the fibrinogen molecule. Thus, poor glycemic control and increased glycation may lead to lower acetylation of the fibrinogen molecule than during good glycemic control in turn leading to an altered fibrin network.
The aims of the present study were to analyse the effects of low (75 mg) and high dose (320 mg) aspirin treatment on fibrin network formation in patients with type 1 diabetes (primary aim), and to investigate the possible influence of the glycemic control (secondary aim). As platelet microparticles may influence the fibrin formation [17, 18] and since aspirin has well-known effects on platelet function, we also measured plasma concentrations of platelet microparticles.
Study design
- Primary purpose
- Treatment
- Allocation
- Randomised
- Intervention model
- Crossover
- Masking
- None (open label)
- Number of arms
- 2
| Arm | Type | Receives |
|---|---|---|
| Aspirin 75mg | Active comparator | Drug: Aspirin |
| Aspirin 320mg | Active comparator | Drug: Aspirin |
Who may qualify
- Ages
- 30 to 70 years
- Sex
- All
- Healthy volunteers
- Not accepted
- Age groups
- Adult, Older adult
Key inclusion criteria (3 listed)
- Diabetes mellitus, type 1
- Levels of HbA1C (glycated hemoglobin) <7.4% (NGSP standard)
- Levels of HbA1C >8.4% (NGSP standard)
Key exclusion criteria (4 listed)
- Prior aspirin treatment
- Treatment with anticoagulant drugs
- Ongoing treatment with NSAIDs or other antiplatelet drugs
- A history of macrovascular disease
Eligibility is decided by the study team after screening; this overview does not establish that a patient qualifies. Full inclusion and exclusion criteria.
Interventions
| Intervention | Type | Arms |
|---|---|---|
| AspirinAlso: TrombylTablets, 75 or 320mg once daily for 4 weeks. A 4-week wash-out period separated the two treatment periods. | Drug | Aspirin 320mg, Aspirin 75mg |
Primary outcome
Fibrin network permeability
Time frame: At the start and end of each 4-week treatment period
Changes in fibrin network permeability after 4 weeks of treatment with either aspirin 75 or 320mg.
2 secondary outcomes
Fibrin network permeability
Time frame: At the start and end of each 4-week treatment period
Platelet microparticles
Time frame: At the start and end of each 4-week treatment period
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 19 Jul 2011.
- Background: PubMed 10807754Collet JP, Park D, Lesty C, Soria J, Soria C, Montalescot G, Weisel JW. Influence of fibrin network conformation and fibrin fiber diameter on fibrinolysis speed: dynamic and structural approaches by confocal microscopy. Arterioscler Thromb Vasc Biol. 2000 May;20(5):1354-61. doi: 10.1161/01.atv.20.5.1354.
- Background: PubMed 16917107Collet JP, Allali Y, Lesty C, Tanguy ML, Silvain J, Ankri A, Blanchet B, Dumaine R, Gianetti J, Payot L, Weisel JW, Montalescot G. Altered fibrin architecture is associated with hypofibrinolysis and premature coronary atherothrombosis. Arterioscler Thromb Vasc Biol. 2006 Nov;26(11):2567-73. doi: 10.1161/01.ATV.0000241589.52950.4c. Epub 2006 Aug 17.
- Background: PubMed 20950841Rooth E, Wallen NH, Blomback M, He S. Decreased fibrin network permeability and impaired fibrinolysis in the acute and convalescent phase of ischemic stroke. Thromb Res. 2011 Jan;127(1):51-6. doi: 10.1016/j.thromres.2010.09.011. Epub 2010 Oct 14.
- Background: PubMed 10595642Colle JP, Mishal Z, Lesty C, Mirshahi M, Peyne J, Baumelou A, Bensman A, Soria J, Soria C. Abnormal fibrin clot architecture in nephrotic patients is related to hypofibrinolysis: influence of plasma biochemical modifications: a possible mechanism for the high thrombotic tendency? Thromb Haemost. 1999 Nov;82(5):1482-9.
- Background: PubMed 8960835Jorneskog G, Egberg N, Fagrell B, Fatah K, Hessel B, Johnsson H, Brismar K, Blomback M. Altered properties of the fibrin gel structure in patients with IDDM. Diabetologia. 1996 Dec;39(12):1519-23. doi: 10.1007/s001250050607.
- Background: PubMed 17959865Cubbon RM, Gale CP, Rajwani A, Abbas A, Morrell C, Das R, Barth JH, Grant PJ, Kearney MT, Hall AS. Aspirin and mortality in patients with diabetes sustaining acute coronary syndrome. Diabetes Care. 2008 Feb;31(2):363-5. doi: 10.2337/dc07-1745. Epub 2007 Oct 24.
- Background: PubMed 16181986Antovic A, Perneby C, Ekman GJ, Wallen HN, Hjemdahl P, Blomback M, He S. Marked increase of fibrin gel permeability with very low dose ASA treatment. Thromb Res. 2005;116(6):509-17. doi: 10.1016/j.thromres.2005.02.007.
- Background: PubMed 9857919Williams S, Fatah K, Hjemdahl P, Blomback M. Better increase in fibrin gel porosity by low dose than intermediate dose acetylsalicylic acid. Eur Heart J. 1998 Nov;19(11):1666-72. doi: 10.1053/euhj.1998.1088.
- Background: PubMed 14963650Yngen M, Ostenson CG, Hu H, Li N, Hjemdahl P, Wallen NH. Enhanced P-selectin expression and increased soluble CD40 Ligand in patients with Type 1 diabetes mellitus and microangiopathy: evidence for platelet hyperactivity and chronic inflammation. Diabetologia. 2004 Mar;47(3):537-540. doi: 10.1007/s00125-004-1352-4. Epub 2004 Feb 13.
- Background: PubMed 1425083Ganda OP, Arkin CF. Hyperfibrinogenemia. An important risk factor for vascular complications in diabetes. Diabetes Care. 1992 Oct;15(10):1245-50. doi: 10.2337/diacare.15.10.1245.
- Background: PubMed 16538489Dunn EJ, Philippou H, Ariens RA, Grant PJ. Molecular mechanisms involved in the resistance of fibrin to clot lysis by plasmin in subjects with type 2 diabetes mellitus. Diabetologia. 2006 May;49(5):1071-80. doi: 10.1007/s00125-006-0197-4. Epub 2006 Mar 16.
- Background: PubMed 7575778Nomura S, Suzuki M, Katsura K, Xie GL, Miyazaki Y, Miyake T, Kido H, Kagawa H, Fukuhara S. Platelet-derived microparticles may influence the development of atherosclerosis in diabetes mellitus. Atherosclerosis. 1995 Aug;116(2):235-40. doi: 10.1016/0021-9150(95)05551-7.
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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.
Gun Jörneskog, MD PhD principal investigator
Karolinska Institutet, Department of Clinical Sciences, Danderyd Hospital
1 site in 1 country: see every site and its status.
Questions about this trial
What is this clinical trial studying?
A Phase 4 study testing Aspirin in people with Diabetes Mellitus, Type 1, run by Karolinska Institutet at 1 site in Sweden.
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 3 inclusion and 4 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 19 Jul 2011. 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 Sweden. 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.
What does this phase mean?
Phase 4 studies take place after a treatment is approved, to learn more about its long-term benefits and risks in everyday use.
Not every study follows the same path, and some studies (observational studies, device studies) have no phase.
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?
Fibrin network permeability (time frame: At the start and end of each 4-week treatment period). 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 NCT01397513, which also lists 19 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 19 Jul 2011.