Do Sulphonylureas Preserve Cortical Function During Hypoglycaemia?
Recruitment status was Recruiting
|First Received Date ICMJE||May 10, 2007|
|Last Updated Date||May 10, 2007|
|Start Date ICMJE||May 2007|
|Primary Completion Date||Not Provided|
|Current Primary Outcome Measures ICMJE
||Glucose threshold for development of symptoms and cognitive impairment due to hypoglycaemia [ Time Frame: 1 year ]|
|Original Primary Outcome Measures ICMJE||Same as current|
|Change History||No Changes Posted|
|Current Secondary Outcome Measures ICMJE
||Improvement in counter regulatory hormone response to hypoglycaemia [ Time Frame: 1 year ]|
|Original Secondary Outcome Measures ICMJE||Same as current|
|Current Other Outcome Measures ICMJE||Not Provided|
|Original Other Outcome Measures ICMJE||Not Provided|
|Brief Title ICMJE||Do Sulphonylureas Preserve Cortical Function During Hypoglycaemia?|
|Official Title ICMJE||Not Provided|
To see if using medication called sulphonylureas can help improve symptoms which patients rely on to recognise low blood glucose levels ( hypoglycaemia) and also to see if they can reduce the slowing down in brain function which occurs at hypoglycaemia.
Low blood glucose (hypoglycaemia) is the most common and important side effect of insulin treatment for diabetes. Most episodes are “mild” and lead to symptoms that alert the individual to raise their blood sugar level by consuming sugar or starch (carbohydrate). The body also responds to low blood sugars by producing hormones such as adrenaline and cortisol, which help to restore blood sugar levels to normal. As the brain relies on sugar for fuel, it does not function properly if blood sugar levels drop too low, resulting in confusion and in extreme cases reduced conscious levels.
Repeated hypoglycaemia can blunt the protective symptoms and hormonal responses to hypoglycaemia limiting patients’ ability to recognise and correct hypoglycaemia, putting them at high risk of even more hypoglycaemia (Heller and Cryer, 1991).
Sulphonylureas are tablets used to treat type 2 diabetes that work by stimulating the pancreas to make more insulin. They do this by closing pores called KATP channels which are found on the surface of many cells and control the rate of firing of cells. In the pancreas, closing them causes cells to fire and release insulin. However, in other tissues such as in the brain, these channels have a protective function and they open up during times of lack of fuel, such as lack of oxygen or sugar, preventing the cells from firing and putting them into a resting mode which reduces their energy requirement(Dunn-Meynell, Rawson and Levin 1998). However, if the brain cells responsible for generating symptoms are put into this resting mode, they may not produce symptoms, which may contribute to hypoglycaemia unawareness.
|Study Type ICMJE||Interventional|
|Study Phase||Phase 4|
|Study Design ICMJE||Allocation: Randomized
Endpoint Classification: Efficacy Study
Intervention Model: Single Group Assignment
Primary Purpose: Treatment
|Condition ICMJE||Type 1 Diabetes Mellitus|
|Intervention ICMJE||Drug: Glibenclamide|
|Study Arm (s)||Not Provided|
|Publications *||Not Provided|
* Includes publications given by the data provider as well as publications identified by ClinicalTrials.gov Identifier (NCT Number) in Medline.
|Recruitment Status ICMJE||Recruiting|
|Estimated Enrollment ICMJE||10|
|Completion Date||Not Provided|
|Primary Completion Date||Not Provided|
|Eligibility Criteria ICMJE||
|Ages||18 Years to 75 Years|
|Accepts Healthy Volunteers||No|
|Location Countries ICMJE||United Kingdom|
|NCT Number ICMJE||NCT00472875|
|Other Study ID Numbers ICMJE||07/Q0703/18, JDRF grant number 5-2007-478|
|Has Data Monitoring Committee||No|
|Responsible Party||Not Provided|
|Study Sponsor ICMJE||King's College Hospital NHS Trust|
|Collaborators ICMJE||Not Provided|
|Information Provided By||King's College Hospital NHS Trust|
|Verification Date||May 2007|
ICMJE Data element required by the International Committee of Medical Journal Editors and the World Health Organization ICTRP