Permanent Neonatal Diabetes MellitusPhase 4SuResponsSURNCT02624830
Long-Term Sulfonylurea Response in ABCC8 Neonatal Diabetes (SuResponsSUR)
A Phase 4 study testing Sulfonylurea in people with Permanent Neonatal Diabetes Mellitus, run by Haukeland University Hospital at 1 site in Norway.
Trial summary
The purpose of this study is to investigate long term response of sulfonylurea and glucose control in children with diabetes due to mutations in ABCC8 that have been switched from insulin injections to sulfonylurea tablets. Read more about this study
- Who is it for?
- Ages 9 to 95 years
- Conditions the study is for
- Permanent Neonatal Diabetes Mellitus
- What is being tested?
- Sulfonylurea
- Type of treatment
- Pill or oral medicine, Injection or infusion
- Could I receive a placebo?
- No, everyone receives an active treatment
- How many people
- 30 participants
- Where
- 1 siteNorway
- Study dates
- 15 Feb 2019to Feb 2020
- 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 9 to 95 years
- All sexes
- No healthy volunteers
- Child, Adult, Older adult
Who may be able to join
- Permanent diabetes due to a mutation in ABCC8 (SUR1)
- Patients successfully transferred from insulin to sulfonylurea
- Transferred to sulfonylurea treatment before November 1, 2006 (ie 9 years off insulin)
- Willing and able to provide informed consent (parents if younger than 16 years of age)
Who cannot join
- Permanent diabetes not due to a mutation in ABCC8 (SUR1)
- Patients not successfully transferred from insulin to sulfonylurea
- Transferred to sulfonylurea treatment after November 1, 2006 (ie les than 9 years off insulin)
- Not willing or able to provide informed consent (parents if younger than 16 years of age)
Trial locations and contacts
1 site in 1 country.
Norway1 site, 1 recruiting
- Recruiting
Haukeland University Hospital
Bergen, 5021
About this study
Official title: Long-term Sulfonylurea Response and Glucose Control After Switching From Insulin in Children With Diabetes Due to ABCC8 (SUR1) Mutations
The purpose of this study is to investigate long term response of sulfonylurea and glucose control in children with diabetes due to mutations in ABCC8 that have been switched from insulin injections to sulfonylurea tablets.
Read the detailed description
Neonatal diabetes mellitus is a rare, monogenic form of diabetes occurring during the first 6-9 months of life characterized by hyperglycemia requiring exogenous insulin therapy. The estimated incidence is 1 per 12000 newborns. Although homozygous or compound heterozygous mutations in the genes IPF1 or GCK were the first genetic causes of this disease to be identified, activating mutations in the KIR6.2 and sulfonylurea receptor 1 (SUR1) subunits of the pancreatic ATP-sensitive K+ channel, coded for by the genes KCNJ11 and ABCC8, have recently been identified as the major causes of both transient and permanent neonatal diabetes. In the normal pancreatic beta-cell, metabolism results in increased cellular ATP, which binds to KIR6.2. The potassium channel subsequently closes and hence depolarizes the membrane initiating insulin release via increased calcium entry. Conversely, increased cellular ADP acts on SUR1 to open the channel and prevent insulin release. Activating mutations in these channels reduces sensitivity to the inhibitory actions of ATP and increases sensitivity to the stimulatory actions of ADP. This causes the ATP-sensitive K+ channel to remain open, even in the presence of glucose, therefore preventing insulin release. Sulfonylureas act by an ATP-independent mechanism to close these channels even when mutations are present. Sulfonylureas result in insulin release and were therefore immediately considered and showed to be a potential treatment option in neonatal diabetes caused by mutations in these channels. The effective replacement of insulin treatment by high-dose sulfonylureas has been shown to be successful in 90% of patients with Kir6.2 mutations and 85% of patients with SUR1 mutations resulting in improved glycemic control.
This dramatic effect of sulfonylurea is now standard, world-wide treatment in neonatal diabetes due to a mutation in either KCNJ11 or ABCC8. There is, however, far no information on long-term use of sulfonylurea in patients with KCNJ11 or ABCC8 mutations. The investigators have therefore initiated an international, multicenter, prospective study aiming to include some 75 patients aged from 9 years with a genetic diagnosis of diabetes due to a ABCC8 gene mutation identified by sequencing in Bergen, Norway; Exeter, U.K.; Paris, France or Rome, Italy. Most patients were referred based on membership in the International Society of Pediatric and Adolescent Diabetes. All of the patients attempted transfer from treatment with insulin to a sufficient dose of sulfonylureas. No other selection criteria were applied, and all patients were included when there was outcome data following the attempted transfer. The observation period was at least 9 years after commencing sulfonylureas in all patients. The study is conducted in accordance with the Declaration of Helsinki and informed consent has been obtained from all participating patients, with parental consent given on behalf of children.
- Conditions
- Permanent Neonatal Diabetes Mellitus
- Being tested
- Sulfonylurea
- Medical subject headings
- Diabetes Mellitus, Permanent Neonatal
What participants receive
What participants receive. In a randomised study each person is assigned to one group by chance.
SulfonylureaDrug
Also called Glibenclamide and other forms of sulfonylureas
See Arm description.
| Study group | Role | What they receive |
|---|---|---|
| Drug, Sulfonylurea | Experimental | Sulfonylurea tablets (glibenclamide, other forms of sulfonylureas) were administered at the time of intervention (before November 1, 2006). The patients have been prospectively followed up. Sulfonylurea dose, insulin requirement, death of all causes, episodes of severe hypoglycemia, ketoacidosis, development of discoloured teeth and diarrhea have been recorded. For a small number of subjects, increment of insulin and C-peptide after either an oral or intravenous glucose load and/or response to intravenous glucagon have been tested. Receives: Drug: Sulfonylurea |
What is being measured
The primary outcome is the main question the study is designed to answer.
Sulfonylurea efficacy
Insulin requirement with or without sulfonylurea treatment during the intervention
Measured: Within 13 years from intervention
Metabolic control
Change in HbA1c levels during the intervention
Measured: Within 13 years from intervention
Secondary outcomes (9)
All cause mortality
Death of all causes
Measured: Within 13 years from intervention
Incidence of hypoglycemia
Episodes per year of severe hypoglycemia (ISPAD definitions)
Measured: Within 13 years from intervention
Incidence of ketoacidosis
Episodes per year of severe ketoacidosis (ISPAD definitions)
Measured: Within 13 years from intervention
Development of diarrhea
Chronic diarrhea with no clear cause
Measured: Within 13 years from intervention
Development of discoloured teeth
Discoloured teeth with no clear cause
Measured: Within 13 years from intervention
Insulin secretory response to intravenous glucose
Change in increment of insulin and C-peptide after a standard intravenous glucose tolerance test tested at start of intervention and retested at end of the study
Measured: Within 13 years from intervention
Insulin secretory response to oral glucose
Change in increment of insulin and C-peptide after a standard oral glucose tolerance test tested at start of intervention and retested at end of the study
Measured: Within 13 years from intervention
Sulfonylurea dose
Change in sulfonylurea dose (per kg and day, and absolute dose per day) from start of intervention and up till end of study
Measured: Within 13 years from intervention
Insulin secretory response to a glucagon test
Change in increment of C-peptide and glucose after a standard glucagon test tested at start of intervention and retested at end of the study
Measured: Within 13 years from intervention
Timeline
From the start of the study to its completion; the mark is today. Estimated dates are the sponsor’s plan.
- First posted8 Dec 2015 (estimated)
- Study start15 Feb 2019
- Primary completionFeb 2020 (estimated)
- Study completionFeb 2020 (estimated)
Resources
- Official record on ClinicalTrials.govThe registry entry this page is built from, with its full change history.
- Publications (8)Papers the sponsor has linked to this study.
- Other trials for Permanent Neonatal Diabetes MellitusStudies of the same condition, open and under way.
- More trials run by Haukeland University HospitalThe 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
- Not applicable
- Intervention model
- Single group
- Masking
- None (open label)
- Enrolment
- 30 participants (estimated)
Sponsor and investigators
- Lead sponsor
- Haukeland University Hospital
- Sponsor type
- University, hospital or other
- Collaborators
- University of Bergen, University of Exeter, Royal Devon and Exeter NHS Foundation Trust, Institut National de la Santé Et de la Recherche Médicale, France, Hôpital Necker-Enfants Malades, University of Rome Tor Vergata
- Responsible party
- Sponsor
- Investigators
- Pål Rasmus Njølstad, MD, PhD, Study director, Haukeland University Hospital
IDs, dates and publications
- ClinicalTrials.gov ID
- NCT02624830
- Sponsor's protocol ID
- 167.06b
- Acronym
- SuResponsSUR
- Status last verified
- Feb 2020
- First submitted
- 4 Dec 2015
- Last updated
- 12 Feb 2020
- Results posted
- No
- Data monitoring committee
- No
- FDA-regulated drug
- No
- FDA-regulated device
- No
Publications
Gloyn AL, Pearson ER, Antcliff JF, Proks P, Bruining GJ, Slingerland AS, Howard N, Srinivasan S, Silva JM, Molnes J, Edghill EL, Frayling TM, Temple IK, Mackay D, Shield JP, Sumnik Z, van Rhijn A, Wales JK, Clark P, Gorman S, Aisenberg J, Ellard S, Njolstad PR, Ashcroft FM, Hattersley AT. Activating mutations in the gene encoding the ATP-sensitive potassium-channel subunit Kir6.2 and permanent neonatal diabetes. N Engl J Med. 2004 Apr 29;350(18):1838-49. doi: 10.1056/NEJMoa032922.
PubMed 15115830Sagen JV, Raeder H, Hathout E, Shehadeh N, Gudmundsson K, Baevre H, Abuelo D, Phornphutkul C, Molnes J, Bell GI, Gloyn AL, Hattersley AT, Molven A, Sovik O, Njolstad PR. Permanent neonatal diabetes due to mutations in KCNJ11 encoding Kir6.2: patient characteristics and initial response to sulfonylurea therapy. Diabetes. 2004 Oct;53(10):2713-8. doi: 10.2337/diabetes.53.10.2713.
PubMed 15448106Pearson ER, Flechtner I, Njolstad PR, Malecki MT, Flanagan SE, Larkin B, Ashcroft FM, Klimes I, Codner E, Iotova V, Slingerland AS, Shield J, Robert JJ, Holst JJ, Clark PM, Ellard S, Sovik O, Polak M, Hattersley AT; Neonatal Diabetes International Collaborative Group. Switching from insulin to oral sulfonylureas in patients with diabetes due to Kir6.2 mutations. N Engl J Med. 2006 Aug 3;355(5):467-77. doi: 10.1056/NEJMoa061759.
PubMed 16885550Rafiq M, Flanagan SE, Patch AM, Shields BM, Ellard S, Hattersley AT; Neonatal Diabetes International Collaborative Group. Effective treatment with oral sulfonylureas in patients with diabetes due to sulfonylurea receptor 1 (SUR1) mutations. Diabetes Care. 2008 Feb;31(2):204-9. doi: 10.2337/dc07-1785. Epub 2007 Nov 19.
PubMed 18025408Stoffers DA, Zinkin NT, Stanojevic V, Clarke WL, Habener JF. Pancreatic agenesis attributable to a single nucleotide deletion in the human IPF1 gene coding sequence. Nat Genet. 1997 Jan;15(1):106-10. doi: 10.1038/ng0197-106.
PubMed 8988180Njolstad PR, Sovik O, Cuesta-Munoz A, Bjorkhaug L, Massa O, Barbetti F, Undlien DE, Shiota C, Magnuson MA, Molven A, Matschinsky FM, Bell GI. Neonatal diabetes mellitus due to complete glucokinase deficiency. N Engl J Med. 2001 May 24;344(21):1588-92. doi: 10.1056/NEJM200105243442104. No abstract available.
PubMed 11372010Babenko AP, Polak M, Cave H, Busiah K, Czernichow P, Scharfmann R, Bryan J, Aguilar-Bryan L, Vaxillaire M, Froguel P. Activating mutations in the ABCC8 gene in neonatal diabetes mellitus. N Engl J Med. 2006 Aug 3;355(5):456-66. doi: 10.1056/NEJMoa055068.
PubMed 16885549Bowman P, Mathews F, Barbetti F, Shepherd MH, Sanchez J, Piccini B, Beltrand J, Letourneau-Freiberg LR, Polak M, Greeley SAW, Rawlins E, Babiker T, Thomas NJ, De Franco E, Ellard S, Flanagan SE, Hattersley AT; Neonatal Diabetes International Collaborative Group. Long-term Follow-up of Glycemic and Neurological Outcomes in an International Series of Patients With Sulfonylurea-Treated ABCC8 Permanent Neonatal Diabetes. Diabetes Care. 2021 Jan;44(1):35-42. doi: 10.2337/dc20-1520. Epub 2020 Nov 12.
PubMed 33184150
Study at a glance
From the registry record, last updated by the sponsor on 12 Feb 2020. Recruitment status is as the sponsor reported it: confirm with the study team.
- Official title
- Long-term Sulfonylurea Response and Glucose Control After Switching From Insulin in Children With Diabetes Due to ABCC8 (SUR1) Mutations
- ClinicalTrials.gov ID
- NCT02624830
- Acronym / sponsor ID
- SuResponsSUR / 167.06b
- Conditions
- Permanent Neonatal Diabetes Mellitus
- Phase
- Phase 4
- Study type
- Interventional
- Recruitment status
- Unknown status
- Enrolment
- 30 participants (estimated)
- Lead sponsor
- Haukeland University HospitalUniversity, hospital or other
- Collaborators
- University of Bergen, University of Exeter, Royal Devon and Exeter NHS Foundation Trust, Institut National de la Santé Et de la Recherche Médicale, France, Hôpital Necker-Enfants Malades, University of Rome Tor Vergata
- Study start
- 15 Feb 2019 (actual)
- Primary completion
- Feb 2020 (estimated)
- Study completion
- Feb 2020 (estimated)
- First posted
- 8 Dec 2015 (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 purpose of this study is to investigate long term response of sulfonylurea and glucose control in children with diabetes due to mutations in ABCC8 that have been switched from insulin injections to sulfonylurea tablets.
Detailed description
Neonatal diabetes mellitus is a rare, monogenic form of diabetes occurring during the first 6-9 months of life characterized by hyperglycemia requiring exogenous insulin therapy. The estimated incidence is 1 per 12000 newborns. Although homozygous or compound heterozygous mutations in the genes IPF1 or GCK were the first genetic causes of this disease to be identified, activating mutations in the KIR6.2 and sulfonylurea receptor 1 (SUR1) subunits of the pancreatic ATP-sensitive K+ channel, coded for by the genes KCNJ11 and ABCC8, have recently been identified as the major causes of both transient and permanent neonatal diabetes. In the normal pancreatic beta-cell, metabolism results in increased cellular ATP, which binds to KIR6.2. The potassium channel subsequently closes and hence depolarizes the membrane initiating insulin release via increased calcium entry. Conversely, increased cellular ADP acts on SUR1 to open the channel and prevent insulin release. Activating mutations in these channels reduces sensitivity to the inhibitory actions of ATP and increases sensitivity to the stimulatory actions of ADP. This causes the ATP-sensitive K+ channel to remain open, even in the presence of glucose, therefore preventing insulin release. Sulfonylureas act by an ATP-independent mechanism to close these channels even when mutations are present. Sulfonylureas result in insulin release and were therefore immediately considered and showed to be a potential treatment option in neonatal diabetes caused by mutations in these channels. The effective replacement of insulin treatment by high-dose sulfonylureas has been shown to be successful in 90% of patients with Kir6.2 mutations and 85% of patients with SUR1 mutations resulting in improved glycemic control.
This dramatic effect of sulfonylurea is now standard, world-wide treatment in neonatal diabetes due to a mutation in either KCNJ11 or ABCC8. There is, however, far no information on long-term use of sulfonylurea in patients with KCNJ11 or ABCC8 mutations. The investigators have therefore initiated an international, multicenter, prospective study aiming to include some 75 patients aged from 9 years with a genetic diagnosis of diabetes due to a ABCC8 gene mutation identified by sequencing in Bergen, Norway; Exeter, U.K.; Paris, France or Rome, Italy. Most patients were referred based on membership in the International Society of Pediatric and Adolescent Diabetes. All of the patients attempted transfer from treatment with insulin to a sufficient dose of sulfonylureas. No other selection criteria were applied, and all patients were included when there was outcome data following the attempted transfer. The observation period was at least 9 years after commencing sulfonylureas in all patients. The study is conducted in accordance with the Declaration of Helsinki and informed consent has been obtained from all participating patients, with parental consent given on behalf of children.
Study design
- Primary purpose
- Treatment
- Allocation
- Not applicable
- Intervention model
- Single group
- Masking
- None (open label)
- Number of arms
- 1
| Arm | Type | Receives |
|---|---|---|
| Drug, Sulfonylurea | Experimental | Drug: SulfonylureaSulfonylurea tablets (glibenclamide, other forms of sulfonylureas) were administered at the time of intervention (before November 1, 2006). The patients have been prospectively followed up. Sulfonylurea dose, insulin requirement, death of all causes, episodes of severe hypoglycemia, ketoacidosis, development of discoloured teeth and diarrhea have been recorded. For a small number of subjects, increment of insulin and C-peptide after either an oral or intravenous glucose load and/or response to intravenous glucagon have been tested. |
Who may qualify
- Ages
- 9 to 95 years
- Sex
- All
- Healthy volunteers
- Not accepted
- Age groups
- Child, Adult, Older adult
Key inclusion criteria (4 listed)
- Permanent diabetes due to a mutation in ABCC8 (SUR1)
- Patients successfully transferred from insulin to sulfonylurea
- Transferred to sulfonylurea treatment before November 1, 2006 (ie 9 years off insulin)
- Willing and able to provide informed consent (parents if younger than 16 years of age)
Key exclusion criteria (4 listed)
- Permanent diabetes not due to a mutation in ABCC8 (SUR1)
- Patients not successfully transferred from insulin to sulfonylurea
- Transferred to sulfonylurea treatment after November 1, 2006 (ie les than 9 years off insulin)
- Not willing or able to provide informed consent (parents if younger than 16 years of age)
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 |
|---|---|---|
| SulfonylureaAlso: Glibenclamide and other forms of sulfonylureasSee Arm description. | Drug | Drug, Sulfonylurea |
Primary outcome
Sulfonylurea efficacy
Time frame: Within 13 years from intervention
Insulin requirement with or without sulfonylurea treatment during the intervention
Metabolic control
Time frame: Within 13 years from intervention
Change in HbA1c levels during the intervention
9 secondary outcomes
All cause mortality
Time frame: Within 13 years from intervention
Incidence of hypoglycemia
Time frame: Within 13 years from intervention
Incidence of ketoacidosis
Time frame: Within 13 years from intervention
Development of diarrhea
Time frame: Within 13 years from intervention
Development of discoloured teeth
Time frame: Within 13 years from intervention
Insulin secretory response to intravenous glucose
Time frame: Within 13 years from intervention
Insulin secretory response to oral glucose
Time frame: Within 13 years from intervention
Sulfonylurea dose
Time frame: Within 13 years from intervention
Insulin secretory response to a glucagon test
Time frame: Within 13 years from intervention
Results and safety
Results are not available in the source record.
Research links
- Official record on ClinicalTrials.govLast updated by the sponsor 12 Feb 2020.
- Background: PubMed 15115830Gloyn AL, Pearson ER, Antcliff JF, Proks P, Bruining GJ, Slingerland AS, Howard N, Srinivasan S, Silva JM, Molnes J, Edghill EL, Frayling TM, Temple IK, Mackay D, Shield JP, Sumnik Z, van Rhijn A, Wales JK, Clark P, Gorman S, Aisenberg J, Ellard S, Njolstad PR, Ashcroft FM, Hattersley AT. Activating mutations in the gene encoding the ATP-sensitive potassium-channel subunit Kir6.2 and permanent neonatal diabetes. N Engl J Med. 2004 Apr 29;350(18):1838-49. doi: 10.1056/NEJMoa032922.
- Background: PubMed 15448106Sagen JV, Raeder H, Hathout E, Shehadeh N, Gudmundsson K, Baevre H, Abuelo D, Phornphutkul C, Molnes J, Bell GI, Gloyn AL, Hattersley AT, Molven A, Sovik O, Njolstad PR. Permanent neonatal diabetes due to mutations in KCNJ11 encoding Kir6.2: patient characteristics and initial response to sulfonylurea therapy. Diabetes. 2004 Oct;53(10):2713-8. doi: 10.2337/diabetes.53.10.2713.
- Background: PubMed 16885550Pearson ER, Flechtner I, Njolstad PR, Malecki MT, Flanagan SE, Larkin B, Ashcroft FM, Klimes I, Codner E, Iotova V, Slingerland AS, Shield J, Robert JJ, Holst JJ, Clark PM, Ellard S, Sovik O, Polak M, Hattersley AT; Neonatal Diabetes International Collaborative Group. Switching from insulin to oral sulfonylureas in patients with diabetes due to Kir6.2 mutations. N Engl J Med. 2006 Aug 3;355(5):467-77. doi: 10.1056/NEJMoa061759.
- Background: PubMed 18025408Rafiq M, Flanagan SE, Patch AM, Shields BM, Ellard S, Hattersley AT; Neonatal Diabetes International Collaborative Group. Effective treatment with oral sulfonylureas in patients with diabetes due to sulfonylurea receptor 1 (SUR1) mutations. Diabetes Care. 2008 Feb;31(2):204-9. doi: 10.2337/dc07-1785. Epub 2007 Nov 19.
- Background: PubMed 8988180Stoffers DA, Zinkin NT, Stanojevic V, Clarke WL, Habener JF. Pancreatic agenesis attributable to a single nucleotide deletion in the human IPF1 gene coding sequence. Nat Genet. 1997 Jan;15(1):106-10. doi: 10.1038/ng0197-106.
- Background: PubMed 11372010Njolstad PR, Sovik O, Cuesta-Munoz A, Bjorkhaug L, Massa O, Barbetti F, Undlien DE, Shiota C, Magnuson MA, Molven A, Matschinsky FM, Bell GI. Neonatal diabetes mellitus due to complete glucokinase deficiency. N Engl J Med. 2001 May 24;344(21):1588-92. doi: 10.1056/NEJM200105243442104. No abstract available.
- Background: PubMed 16885549Babenko AP, Polak M, Cave H, Busiah K, Czernichow P, Scharfmann R, Bryan J, Aguilar-Bryan L, Vaxillaire M, Froguel P. Activating mutations in the ABCC8 gene in neonatal diabetes mellitus. N Engl J Med. 2006 Aug 3;355(5):456-66. doi: 10.1056/NEJMoa055068.
- Derived from this study: PubMed 33184150Bowman P, Mathews F, Barbetti F, Shepherd MH, Sanchez J, Piccini B, Beltrand J, Letourneau-Freiberg LR, Polak M, Greeley SAW, Rawlins E, Babiker T, Thomas NJ, De Franco E, Ellard S, Flanagan SE, Hattersley AT; Neonatal Diabetes International Collaborative Group. Long-term Follow-up of Glycemic and Neurological Outcomes in an International Series of Patients With Sulfonylurea-Treated ABCC8 Permanent Neonatal Diabetes. Diabetes Care. 2021 Jan;44(1):35-42. doi: 10.2337/dc20-1520. Epub 2020 Nov 12.
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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.
Pål Rasmus Njølstad, MD, PhD study director
Haukeland University 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 Sulfonylurea in people with Permanent Neonatal Diabetes Mellitus, run by Haukeland University Hospital at 1 site in Norway.
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 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: status not confirmed, as of the sponsor's last update on 12 Feb 2020. Status can change between updates, so confirm with the study contact before making plans.
Where is the study taking place?
The record lists 1 site in Norway. 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?
Results are not available in the source record.
How can a doctor refer a patient or contact the research team?
Contact Åsta N Sulen (004748214508, asta.sulen@student.uib.no), or a site near the patient. AzTrials does not enrol participants or take referrals.
What does the primary outcome measure?
Sulfonylurea efficacy (time frame: Within 13 years from intervention). 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 NCT02624830, which also lists 8 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 12 Feb 2020.