Type 2 Diabetes MellitusNCT00194896
Preferred Treatment of Type 1.5 Diabetes
A study testing rosiglitazone and glyburide in people with Type 2 Diabetes Mellitus, run by University of Washington at 1 site in United States.
Trial summary
The purpose of this research was to test whether one treatment was superior over another in the management of type 1.5 diabetes. Specifically we tested recently diagnosed antibody positive type 2 diabetic patients to determine whether treatment with rosiglitazone results in greater preservation of beta cell function… Read more about this study
- Who is it for?
- Ages 35 to 69 years
- Conditions the study is for
- Type 2 Diabetes Mellitus
- What is being tested?
- rosiglitazone and glyburide
- Type of treatment
- Pill or oral medicine
- Could I receive a placebo?
- No, everyone receives an active treatment
- How many people
- 64 participants
- Where
- 1 siteUnited States
- Study dates
- Feb 2000to Dec 2008
- Phase
- Interventional
- Are there results?
- Yes, posted in the registrySummary in the doctors' view
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 35 to 69 years
- All sexes
- No healthy volunteers
- Adult, Older adult
Who may be able to join
- Age at onset of diabetes - 35-69 years old.
- No history of ketonuria or ketoacidosis.
- Not requiring insulin to achieve glycemic control.
- Not receiving more than two oral hypoglycemic agents.
- Not taking a thiazolidinedione agent.
- HbA1c in established patients (on an oral hypoglycemia agent for over 4 months) of greater than 6% and under 10%.
- Fasting c-peptide greater than or equal to 0.8 ng/ml.
- Women must be either post-menopausal or on adequate birth control (i.e. oral contraceptives, tubal ligation, hysterectomy, condoms, or diaphragm) or use abstinence.
Who cannot join
- Patients with history of chronic pancreatitis or other secondary causes of diabetes.
- Patients receiving systemic corticosteroids.
- Patients with severe systemic illness (e.g. recent MI, CHF or cerebral vascular disease).
- Creatinine greater than 1.4 or liver enzymes greater than 2 times the upper limits of normal.
- Not able to adhere to the protocol.
Trial locations and contacts
1 site in 1 country.
United States1 site
DVA Puget Sound Health Care System
Seattle, Washington, 98108
About this study
Official title: Rosiglitazone Intervention Study in Patients With Type 1.5 Diabetes
The purpose of this research was to test whether one treatment was superior over another in the management of type 1.5 diabetes. Specifically we tested recently diagnosed antibody positive type 2 diabetic patients to determine whether treatment with rosiglitazone results in greater preservation of beta cell function compared to treatment with glyburide.
Read the detailed description
Type 1 diabetes and Type 2 diabetes have different underlying pathophysiologic processes. The disease process in classical Type 1 diabetes is an autoimmune destruction of the pancreatic beta cells. In contrast, the disease process in classical Type 2 diabetes is not autoimmune in nature, a decreased sensitivity to insulin action is central to the disease process, and a poorly understood but non-inflammatory beta cell lesion occurs which diminishes insulin secretion. In clinical practice, the diagnosis of Type 1 versus Type 2 diabetes is made phenotypically using variables such as age at onset, apparent abruptness of onset of hyperglycemia, presence of ketosis, degree of obesity (especially central and intra abdominal), prevalence of other autoimmune diseases, and apparent need for insulin replacement. This clinical distinction of Type 1 versus Type 2 diabetes is recognized to be imperfect.
There is also a third group of individuals, who phenotypically are usually like classic Type 2 diabetics but who are positive for one or more of the autoantibodies commonly seen in the Type 1 disease process, namely islet cell antibodies (ICA) and/or insulin autoantibodies (IAA) and/or autoantibodies to glutamic acid decarboxylase (GAD Ab) and/or autoantibodies to the tyrosine phosphatase islet cell autoantibody 512 (IA 2 Ab).
These patients, autoantibody positive [Ab(+)] Type 2 or Type 1.5 diabetes, were the focus of our study. Compared to antibody negative Type 2 diabetics, patients with Type 1.5 diabetes have a more rapid decline in beta cell function, fail sulfonylurea therapy and require insulin therapy earlier (4-13).
Hypothesis: Rosiglitazone treatment will ameliorate or slow the underlying disease process in antibody positive Type 2 diabetes.
Patients meeting the inclusion criteria came in for a baseline visit. The nature of the study was explained and informed consent obtained. A fasting blood sample was obtained for autoantibodies, glucose, C peptide of proinsulin molecule (C-peptide), glycosylated hemoglobin (HbA1c), genetic typing, and T lymphocyte (T cell) responses to islet antigens. The beta cell function test was performed. Patients were then randomized to either rosiglitazone or glyburide.
All patients were encouraged to perform self blood glucose monitoring twice per day, before breakfast and before dinner. The treatment goals for all patients was the same: before breakfast and before dinner blood sugar levels between 90-130 milligrams per deciliter (mg/dI) and HbA1c of less then 7% without severe hypoglycemia. Patients unable to reach goal with monotherapy had metformin (initially) or acarbose (secondarily) added, as there is no evidence to suggest that either affect beta-cell function.
The rosiglitazone treatment group commenced therapy with 4 milligram (mg) once per day and increased to twice per day if adequate glycemic control was not achieved. For glyburide, therapy was initiated with 2.5 mg in the morning or the patient was maintained on the dose they had been receiving prior to starting the study. The starting dose was raised by 2.5 mg in the evening and further up to a maximum of 10 mg twice a day if necessary to achieve desired glycemic control.
If adequate control, HbA1c less than 7%, was not achieved on glyburide or rosiglitazone monotherapy, metformin was added and the dose gradually increased as needed and tolerated to a maximum of 1000 mg twice daily. If necessary, acarbose was also used up to a maximum dose of 100 mg thrice daily as needed and tolerated.
After initiation of the study, patients were seen at 1 month and then every 3 months for up to 3 years. Those patients randomized to rosiglitazone had the liver enzyme alanine transaminase (ALT) monitored every 2 months. In addition, telephone contact was utilized to achieve and maintain glycemic goals. Each participant was followed for up to 3 years. Drs. Chiu and Palmer coordinated the study. If the patient and his/her private physician prefer, the treatment protocol was implemented by the patient's private physician.
- Conditions
- Type 2 Diabetes Mellitus
- Being tested
- rosiglitazone, glyburide
- Keywords
- type 2 diabetes mellitus, autoantibodies, islet proteins, rosiglitazone, glyburide, c-peptide
- Medical subject headings
- Diabetes Mellitus, Type 2
What participants receive
What participants receive. In a randomised study each person is assigned to one group by chance.
rosiglitazoneDrug
Also called Avandia
Tablet taken orally at a dosage of 4 mg once per day and increase to twice per day if adequate glycemic control was not achieved. Study drug was taken up to 3 years.
glyburideDrug
Tablet taken orally, initially 2.5 mg in the morning or dose subject received prior to starting the study. Dosage was increased by 2.5 mg in the evening up to a maximum of 10 mg twice a day if necessary to achieve desired glycemic control. Study drug was taken up to 3 years.
| Study group | Role | What they receive |
|---|---|---|
| rosiglitazone | Active comparator | Rosiglitazone is an oral antidiabetic agent which acts primarily by increasing insulin sensitivity. The rosiglitazone treatment group commenced therapy with 4 mg once per day and increase to twice per day if adequate glycemic control was not achieved. Receives: Drug: rosiglitazone |
| glyburide | Active comparator | Glyburide is a sulfonylurea. Glyburide therapy was initiated with 2.5 mg in the morning or the patient was maintained on the dose they had been receiving prior to starting the study. This starting dose was raised by 2.5 in the evening and further up to a maximum of 10 mg twice a day if necessary to achieve desired glycemic control. Receives: Drug: glyburide |
What is being measured
The primary outcome is the main question the study is designed to answer.
Changes in Beta Cell Function Assessed by Fasting and Stimulated C-peptide Measured at 36 Months.
Changes in beta cell function assessed by fasting and stimulated C-peptide measured at 36 months.
Measured: 36 months
Secondary outcomes (1)
Patients Positive for T Cell Responses to Islet Proteins at 36 Months.
Number of participants positive for T cell reactivity to islet proteins at 36 months.
Measured: 36 months
Timeline
From the start of the study to its completion; the mark is today. Estimated dates are the sponsor’s plan.
- First posted19 Sep 2005 (estimated)
- Study startFeb 2000
- Primary completionSep 2008
- Study completionDec 2008
Resources
- Official record on ClinicalTrials.govThe registry entry this page is built from, with its full change history.
- Posted resultsParticipant flow, outcome measures and adverse events reported by the sponsor.
- Publications (35)Papers the sponsor has linked to this study.
- Other trials for Type 2 Diabetes MellitusStudies of the same condition, open and under way.
- More trials run by University of WashingtonThe 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
- Treatment
- Allocation
- Randomised
- Intervention model
- Parallel groups
- Masking
- None (open label)
- Enrolment
- 64 participants (actual)
Sponsor and investigators
- Lead sponsor
- University of Washington
- Sponsor type
- University, hospital or other
- Collaborators
- Seattle Institute for Biomedical and Clinical Research, GlaxoSmithKline
- Responsible party
- Sponsor
- Investigators
- Jerry P Palmer, MD, Principal investigator, Seattle Institute for Biomedical & Clinical Research, University of Washington, DVA Puget Sound Health Care System
IDs, dates and publications
- ClinicalTrials.gov ID
- NCT00194896
- Sponsor's protocol ID
- 16707-D
- Other IDs
- 496539-188;, 16707D
- Status last verified
- Mar 2018
- First submitted
- 14 Sep 2005
- Last updated
- 29 Mar 2018
- Results posted
- Yes, on ClinicalTrials.gov
- Data monitoring committee
- Yes
Publications
Lampeter EF, Homberg M, Quabeck K, Schaefer UW, Wernet P, Bertrams J, Grosse-Wilde H, Gries FA, Kolb H. Transfer of insulin-dependent diabetes between HLA-identical siblings by bone marrow transplantation. Lancet. 1993 May 15;341(8855):1243-4. doi: 10.1016/0140-6736(93)91148-f.
PubMed 8098394DeFronzo RA. Pathogenesis of type 2 (non-insulin dependent) diabetes mellitus: a balanced overview. Diabetologia. 1992 Apr;35(4):389-97. doi: 10.1007/BF00401208. No abstract available.
PubMed 1516769Porte D Jr. Banting lecture 1990. Beta-cells in type II diabetes mellitus. Diabetes. 1991 Feb;40(2):166-80. doi: 10.2337/diab.40.2.166.
PubMed 1991568Zimmet PZ, Tuomi T, Mackay IR, Rowley MJ, Knowles W, Cohen M, Lang DA. Latent autoimmune diabetes mellitus in adults (LADA): the role of antibodies to glutamic acid decarboxylase in diagnosis and prediction of insulin dependency. Diabet Med. 1994 Apr;11(3):299-303. doi: 10.1111/j.1464-5491.1994.tb00275.x.
PubMed 8033530Tuomi T, Groop LC, Zimmet PZ, Rowley MJ, Knowles W, Mackay IR. Antibodies to glutamic acid decarboxylase reveal latent autoimmune diabetes mellitus in adults with a non-insulin-dependent onset of disease. Diabetes. 1993 Feb;42(2):359-62. doi: 10.2337/diab.42.2.359.
PubMed 8425674Zimmet PZ. The pathogenesis and prevention of diabetes in adults. Genes, autoimmunity, and demography. Diabetes Care. 1995 Jul;18(7):1050-64. doi: 10.2337/diacare.18.7.1050. No abstract available.
PubMed 7555542Groop LC, Bottazzo GF, Doniach D. Islet cell antibodies identify latent type I diabetes in patients aged 35-75 years at diagnosis. Diabetes. 1986 Feb;35(2):237-41. doi: 10.2337/diab.35.2.237.
PubMed 3510930Groop L, Miettinen A, Groop PH, Meri S, Koskimies S, Bottazzo GF. Organ-specific autoimmunity and HLA-DR antigens as markers for beta-cell destruction in patients with type II diabetes. Diabetes. 1988 Jan;37(1):99-103. doi: 10.2337/diab.37.1.99.
PubMed 3275559Kobayashi T, Tamemoto K, Nakanishi K, Kato N, Okubo M, Kajio H, Sugimoto T, Murase T, Kosaka K. Immunogenetic and clinical characterization of slowly progressive IDDM. Diabetes Care. 1993 May;16(5):780-8. doi: 10.2337/diacare.16.5.780.
PubMed 8098691Kobayashi T. Subtype of insulin-dependent diabetes mellitus (IDDM) in Japan: slowly progressive IDDM--the clinical characteristics and pathogenesis of the syndrome. Diabetes Res Clin Pract. 1994 Oct;24 Suppl:S95-9. doi: 10.1016/0168-8227(94)90234-8.
PubMed 7859641Kobayashi T, Nakanishi K, Sugimoto T, Itoh T, Murase T, Kosaka K, Tsuji K. Maleness as risk factor for slowly progressive IDDM. Diabetes Care. 1989 Jan;12(1):7-11. doi: 10.2337/diacare.12.1.7.
PubMed 2653752Kobayashi T, Itoh T, Kosaka K, Sato K, Tsuji K. Time course of islet cell antibodies and beta-cell function in non-insulin-dependent stage of type I diabetes. Diabetes. 1987 Apr;36(4):510-7. doi: 10.2337/diab.36.4.510.
PubMed 3545950Nakanishi K, Kobayashi T, Sugimoto T, Murase T, Itoh T, Kosaka K. Predictive value of insulin autoantibodies for further progression of beta cell dysfunction in non-insulin-dependent diabetics. Diabetes Res. 1988 Nov;9(3):105-9.
PubMed 3072143Hao W, Li L, Mehta V, Lernmark A, Palmer JP. Functional state of the beta cell affects expression of both forms of glutamic acid decarboxylase. Pancreas. 1994 Sep;9(5):558-62. doi: 10.1097/00006676-199409000-00003.
PubMed 7809009Mehta V, Hao W, Brooks-Worrell BM, Palmer JP. The functional state of the beta cell modulates IL-1 and TNF-induced cytotoxicity. Lymphokine Cytokine Res. 1993 Aug;12(4):255-9.
PubMed 8218598
Study at a glance
From the registry record, last updated by the sponsor on 29 Mar 2018. Recruitment status is as the sponsor reported it: confirm with the study team.
- Official title
- Rosiglitazone Intervention Study in Patients With Type 1.5 Diabetes
- ClinicalTrials.gov ID
- NCT00194896
- Acronym / sponsor ID
- 16707-D
- Conditions
- Type 2 Diabetes Mellitus
- Keywords
- type 2 diabetes mellitus, autoantibodies, islet proteins, rosiglitazone, glyburide, c-peptide
- Study type
- Interventional
- Recruitment status
- Completed
- Enrolment
- 64 participants (actual)
- Lead sponsor
- University of WashingtonUniversity, hospital or other
- Collaborators
- Seattle Institute for Biomedical and Clinical Research, GlaxoSmithKline
- Study start
- Feb 2000
- Primary completion
- Sep 2008 (actual)
- Study completion
- Dec 2008 (actual)
- First posted
- 19 Sep 2005 (estimated)
- Results
- Posted 10 Aug 2011
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 research was to test whether one treatment was superior over another in the management of type 1.5 diabetes. Specifically we tested recently diagnosed antibody positive type 2 diabetic patients to determine whether treatment with rosiglitazone results in greater preservation of beta cell function compared to treatment with glyburide.
Detailed description
Type 1 diabetes and Type 2 diabetes have different underlying pathophysiologic processes. The disease process in classical Type 1 diabetes is an autoimmune destruction of the pancreatic beta cells. In contrast, the disease process in classical Type 2 diabetes is not autoimmune in nature, a decreased sensitivity to insulin action is central to the disease process, and a poorly understood but non-inflammatory beta cell lesion occurs which diminishes insulin secretion. In clinical practice, the diagnosis of Type 1 versus Type 2 diabetes is made phenotypically using variables such as age at onset, apparent abruptness of onset of hyperglycemia, presence of ketosis, degree of obesity (especially central and intra abdominal), prevalence of other autoimmune diseases, and apparent need for insulin replacement. This clinical distinction of Type 1 versus Type 2 diabetes is recognized to be imperfect.
There is also a third group of individuals, who phenotypically are usually like classic Type 2 diabetics but who are positive for one or more of the autoantibodies commonly seen in the Type 1 disease process, namely islet cell antibodies (ICA) and/or insulin autoantibodies (IAA) and/or autoantibodies to glutamic acid decarboxylase (GAD Ab) and/or autoantibodies to the tyrosine phosphatase islet cell autoantibody 512 (IA 2 Ab).
These patients, autoantibody positive [Ab(+)] Type 2 or Type 1.5 diabetes, were the focus of our study. Compared to antibody negative Type 2 diabetics, patients with Type 1.5 diabetes have a more rapid decline in beta cell function, fail sulfonylurea therapy and require insulin therapy earlier (4-13).
Hypothesis: Rosiglitazone treatment will ameliorate or slow the underlying disease process in antibody positive Type 2 diabetes.
Patients meeting the inclusion criteria came in for a baseline visit. The nature of the study was explained and informed consent obtained. A fasting blood sample was obtained for autoantibodies, glucose, C peptide of proinsulin molecule (C-peptide), glycosylated hemoglobin (HbA1c), genetic typing, and T lymphocyte (T cell) responses to islet antigens. The beta cell function test was performed. Patients were then randomized to either rosiglitazone or glyburide.
All patients were encouraged to perform self blood glucose monitoring twice per day, before breakfast and before dinner. The treatment goals for all patients was the same: before breakfast and before dinner blood sugar levels between 90-130 milligrams per deciliter (mg/dI) and HbA1c of less then 7% without severe hypoglycemia. Patients unable to reach goal with monotherapy had metformin (initially) or acarbose (secondarily) added, as there is no evidence to suggest that either affect beta-cell function.
The rosiglitazone treatment group commenced therapy with 4 milligram (mg) once per day and increased to twice per day if adequate glycemic control was not achieved. For glyburide, therapy was initiated with 2.5 mg in the morning or the patient was maintained on the dose they had been receiving prior to starting the study. The starting dose was raised by 2.5 mg in the evening and further up to a maximum of 10 mg twice a day if necessary to achieve desired glycemic control.
If adequate control, HbA1c less than 7%, was not achieved on glyburide or rosiglitazone monotherapy, metformin was added and the dose gradually increased as needed and tolerated to a maximum of 1000 mg twice daily. If necessary, acarbose was also used up to a maximum dose of 100 mg thrice daily as needed and tolerated.
After initiation of the study, patients were seen at 1 month and then every 3 months for up to 3 years. Those patients randomized to rosiglitazone had the liver enzyme alanine transaminase (ALT) monitored every 2 months. In addition, telephone contact was utilized to achieve and maintain glycemic goals. Each participant was followed for up to 3 years. Drs. Chiu and Palmer coordinated the study. If the patient and his/her private physician prefer, the treatment protocol was implemented by the patient's private physician.
Study design
- Primary purpose
- Treatment
- Allocation
- Randomised
- Intervention model
- Parallel groups
- Masking
- None (open label)
- Number of arms
- 2
| Arm | Type | Receives |
|---|---|---|
| rosiglitazone | Active comparator | Drug: rosiglitazoneRosiglitazone is an oral antidiabetic agent which acts primarily by increasing insulin sensitivity. The rosiglitazone treatment group commenced therapy with 4 mg once per day and increase to twice per day if adequate glycemic control was not achieved. |
| glyburide | Active comparator | Drug: glyburideGlyburide is a sulfonylurea. Glyburide therapy was initiated with 2.5 mg in the morning or the patient was maintained on the dose they had been receiving prior to starting the study. This starting dose was raised by 2.5 in the evening and further up to a maximum of 10 mg twice a day if necessary to achieve desired glycemic control. |
Who may qualify
- Ages
- 35 to 69 years
- Sex
- All
- Healthy volunteers
- Not accepted
- Age groups
- Adult, Older adult
Key inclusion criteria (8 listed)
- Age at onset of diabetes - 35-69 years old.
- No history of ketonuria or ketoacidosis.
- Not requiring insulin to achieve glycemic control.
- Not receiving more than two oral hypoglycemic agents.
- Not taking a thiazolidinedione agent.
Key exclusion criteria (5 listed)
- Patients with history of chronic pancreatitis or other secondary causes of diabetes.
- Patients receiving systemic corticosteroids.
- Patients with severe systemic illness (e.g. recent MI, CHF or cerebral vascular disease).
- Creatinine greater than 1.4 or liver enzymes greater than 2 times the upper limits of normal.
- Not able to adhere to the protocol.
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 |
|---|---|---|
| rosiglitazoneAlso: AvandiaTablet taken orally at a dosage of 4 mg once per day and increase to twice per day if adequate glycemic control was not achieved. Study drug was taken up to 3 years. | Drug | rosiglitazone |
| glyburideTablet taken orally, initially 2.5 mg in the morning or dose subject received prior to starting the study. Dosage was increased by 2.5 mg in the evening up to a maximum of 10 mg twice a day if necessary to achieve desired glycemic control. Study drug was taken up to 3 years. | Drug | glyburide |
Primary outcome
Changes in Beta Cell Function Assessed by Fasting and Stimulated C-peptide Measured at 36 Months.
Time frame: 36 months
Changes in beta cell function assessed by fasting and stimulated C-peptide measured at 36 months.
1 secondary outcome
Patients Positive for T Cell Responses to Islet Proteins at 36 Months.
Time frame: 36 months
Results and safety
Loading the posted results from ClinicalTrials.gov…
Research links
- Official record on ClinicalTrials.govLast updated by the sponsor 29 Mar 2018.
- Posted resultsParticipant flow, baseline, all outcome measures and adverse events.
- Background: PubMed 8098394Lampeter EF, Homberg M, Quabeck K, Schaefer UW, Wernet P, Bertrams J, Grosse-Wilde H, Gries FA, Kolb H. Transfer of insulin-dependent diabetes between HLA-identical siblings by bone marrow transplantation. Lancet. 1993 May 15;341(8855):1243-4. doi: 10.1016/0140-6736(93)91148-f.
- Background: PubMed 1516769DeFronzo RA. Pathogenesis of type 2 (non-insulin dependent) diabetes mellitus: a balanced overview. Diabetologia. 1992 Apr;35(4):389-97. doi: 10.1007/BF00401208. No abstract available.
- Background: PubMed 1991568Porte D Jr. Banting lecture 1990. Beta-cells in type II diabetes mellitus. Diabetes. 1991 Feb;40(2):166-80. doi: 10.2337/diab.40.2.166.
- Background: PubMed 8033530Zimmet PZ, Tuomi T, Mackay IR, Rowley MJ, Knowles W, Cohen M, Lang DA. Latent autoimmune diabetes mellitus in adults (LADA): the role of antibodies to glutamic acid decarboxylase in diagnosis and prediction of insulin dependency. Diabet Med. 1994 Apr;11(3):299-303. doi: 10.1111/j.1464-5491.1994.tb00275.x.
- Background: PubMed 8425674Tuomi T, Groop LC, Zimmet PZ, Rowley MJ, Knowles W, Mackay IR. Antibodies to glutamic acid decarboxylase reveal latent autoimmune diabetes mellitus in adults with a non-insulin-dependent onset of disease. Diabetes. 1993 Feb;42(2):359-62. doi: 10.2337/diab.42.2.359.
- Background: PubMed 7555542Zimmet PZ. The pathogenesis and prevention of diabetes in adults. Genes, autoimmunity, and demography. Diabetes Care. 1995 Jul;18(7):1050-64. doi: 10.2337/diacare.18.7.1050. No abstract available.
- Background: PubMed 3510930Groop LC, Bottazzo GF, Doniach D. Islet cell antibodies identify latent type I diabetes in patients aged 35-75 years at diagnosis. Diabetes. 1986 Feb;35(2):237-41. doi: 10.2337/diab.35.2.237.
- Background: PubMed 3275559Groop L, Miettinen A, Groop PH, Meri S, Koskimies S, Bottazzo GF. Organ-specific autoimmunity and HLA-DR antigens as markers for beta-cell destruction in patients with type II diabetes. Diabetes. 1988 Jan;37(1):99-103. doi: 10.2337/diab.37.1.99.
- Background: PubMed 8098691Kobayashi T, Tamemoto K, Nakanishi K, Kato N, Okubo M, Kajio H, Sugimoto T, Murase T, Kosaka K. Immunogenetic and clinical characterization of slowly progressive IDDM. Diabetes Care. 1993 May;16(5):780-8. doi: 10.2337/diacare.16.5.780.
- Background: PubMed 7859641Kobayashi T. Subtype of insulin-dependent diabetes mellitus (IDDM) in Japan: slowly progressive IDDM--the clinical characteristics and pathogenesis of the syndrome. Diabetes Res Clin Pract. 1994 Oct;24 Suppl:S95-9. doi: 10.1016/0168-8227(94)90234-8.
- Background: PubMed 2653752Kobayashi T, Nakanishi K, Sugimoto T, Itoh T, Murase T, Kosaka K, Tsuji K. Maleness as risk factor for slowly progressive IDDM. Diabetes Care. 1989 Jan;12(1):7-11. doi: 10.2337/diacare.12.1.7.
- Background: PubMed 3545950Kobayashi T, Itoh T, Kosaka K, Sato K, Tsuji K. Time course of islet cell antibodies and beta-cell function in non-insulin-dependent stage of type I diabetes. Diabetes. 1987 Apr;36(4):510-7. doi: 10.2337/diab.36.4.510.
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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.
Jerry P Palmer, MD principal investigator
Seattle Institute for Biomedical & Clinical Research, University of Washington, DVA Puget Sound Health Care System
1 site in 1 country: see every site and its status.
Questions about this trial
What is this clinical trial studying?
A study testing rosiglitazone and glyburide in people with Type 2 Diabetes Mellitus, run by University of Washington at 1 site in United States.
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 5 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 29 Mar 2018. 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 United States. 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?
Yes. Results are posted in the registry (first posted 10 Aug 2011). A summary is in the For doctors view, and the full results are on ClinicalTrials.gov.
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?
Changes in Beta Cell Function Assessed by Fasting and Stimulated C-peptide Measured at 36 Months. (time frame: 36 months). 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 NCT00194896, which also lists 35 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 29 Mar 2018.