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Effect of Metabolic Control at Onset of Diabetes on Progression of Type 1 Diabetes
This study is not yet open for participant recruitment.
Study NCT00505206   Information provided by National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK)
First Received: July 20, 2007   Last Updated: January 5, 2009   History of Changes
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July 20, 2007
January 5, 2009
 
Insulin secretion (C-peptide production) [ Time Frame: 1 year ] [ Designated as safety issue: No ]
Same as current
Complete list of historical versions of study NCT00505206 on ClinicalTrials.gov Archive Site
  • Insulin secretion (C-peptide production) [ Time Frame: 2 years ] [ Designated as safety issue: No ]
  • HbA1C [ Time Frame: 2 years ] [ Designated as safety issue: No ]
  • Insulin dose [ Time Frame: 2 years ] [ Designated as safety issue: No ]
  • Number of hypoglycemic and hyperglycemic events [ Time Frame: 2 years ] [ Designated as safety issue: Yes ]
  • Number and severity of adverse events [ Time Frame: 2 years ] [ Designated as safety issue: Yes ]
Same as current
 
Effect of Metabolic Control at Onset of Diabetes on Progression of Type 1 Diabetes
Effect of Metabolic Control at Onset of Diabetes on Progression of Type 1 Diabetes

The aim of this study is to determine if early and tight restoration of metabolic control at the onset of Type 1 diabetes (T1DM) will improve insulin secretion (C-peptide production) versus routine diabetes management.

There is evidence that early, intensive diabetes management may preserve C-peptide secretion possibly by allowing decreased islet cell activity or "islet cell rest". Less metabolically active islet cells result in a decreased inflammatory response and decreased autoantigen expression.

This leads to a decrease in the destruction of beta cells and possibly to an increase in beta cell regeneration. In addition, the decreased hyperglycemia which results from intensive management may be less toxic to islet cells and make them less susceptible to cytokine mediated destruction.

A closed-loop system (consisting of an in vivo glucose sensor, implantable insulin pump, and a feedback control algorithm to automatically determine insulin delivery rate) may optimally decrease the number of hours each day that islets are exposed to hyperglycemia. Used at the onset of T1DM, this may effectively decrease early "glucotoxicity" to allow earlier restoration of islet cell function, and perhaps alter islet antigen presentation to the immune system. The experimental therapy consists of a short course (minimum of 4 days) of closed-loop diabetic control at the onset of diabetes followed by continuous real-time glucose monitoring associated with continuous subcutaneous insulin infusion therapy (CSII) for two years.

The standard therapy group will receive intensive management of their diabetes through frequent home glucose monitoring and multiple injections or CSII for two years. The implementation of any such therapy in this group will be determined by their treating diabetologist.

Phase II
Interventional
Treatment, Randomized, Open Label, Active Control, Parallel Assignment, Efficacy Study
Type 1 Diabetes Mellitus
  • Device: CSII and CGM
  • Other: Standard Treatment
  • Experimental: Initial, short course of Continuous Subcutaneous Insulin Infusion therapy (CSII) and followed by real-time continuous glucose monitoring (rtCGM)associated with CSII for two years.
  • Active Comparator: THe standard treatment will consist of multiple daily insulin injections (3-4 insulin injections per day) to maintain normal glycemic control.

*   Includes publications given by the data provider as well as publications identified by National Clinical Trials Identifier (NCT ID) in Medline.
 
Not yet recruiting
108
 
 

Inclusion Criteria:

  1. Age 3-20
  2. Within 1-7 days of diagnosis T1DM based on ADA criteria

Exclusion Criteria:

  1. Complicating medical issues that interfere with study conduct
  2. Use of chronic steroids or any non-insulin pharmaceuticals that affect glycemic control
  3. Current participation in another T1DM treatment study or intervention trial for treatment of diabetic ketoacidosis
  4. Pregnancy, lactation, or intention of pregnancy while on study
Both
3 Years to 20 Years
No
 
 
 
 
NCT00505206
Ellen Leschek, Type 1 Diabetes TrialNet
 
National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK)
 
Principal Investigator: Bruce Buckingham, MD Stanford University
Study Chair: Jay Skyler, MD University of Miami
National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK)
January 2009

 †    Required WHO trial registration data element.
††   WHO trial registration data element that is required only if it exists.