View clinical trials related to Hyperglycemia.
Filter by:In patients suffering from aneurysmal subarachnoid hemorrhage (aSAH), hyperglycemia is considered an adverse prognostic factor. Glycated hemoglobin (or HbA1c) can be measured to estimate the average plasma glucose concentration over prolonged periods of time, thus determination of glycated hemoglobin at admission after aSAH serves as an approximation of blood glucose levels in the weeks preceding aneurysm rupture. In this patient registry admission HbA1c, clinical course and neurological outcome after 6 month are recorded, to determine whether elevated blood glucose levels prior to aneurysm rupture influence the clinical course and patient outcome after aSAH.
The purpose of this study is to investigate how millet incorporation into different baked product types influences glycemic response and satiety.
We hypothesize that stress hyperglycemia is an indicator that a patient will develop type 2 diabetes mellitus in the future. Subjects who are not diabetic are enrolled and blood glucose readings reviewed during their intensive care unit stay. All subjects are consented and have a HbA1C level drawn to determine if they have diabetes mellitus or not. They are then followed up in 1 year and the HbA1C repeated to determine if they have developed diabetes mellitus over the course.
The study was designed to investigate the optimal management of hyperglycemia developed during pasireotide treatment in participants with Cushing's disease or Acromegaly, which was not manageable with metformin. This was a Phase IV, multi-center, randomized, open-label study. Eligible patients started pasireotide subcutaneously (s.c.) for Cushing's disease and pasireotide LAR (long-acting release) for Acromegaly. Participants being treated with pasireotide s.c or LAR at screening were eligible as long as they met protocol criteria during the screening period. If previously normo-glycemic participants experienced an increase in their fasting blood glucose and met the criteria for diabetes while on pasireotide, they started anti-diabetic treatment using metformin. If they continued to have elevated blood glucose above target on metformin within the first 16 weeks, they were randomized in a 1:1 ratio to receive treatment with incretin based therapy or insulin for approximately 16 weeks. Participants who continued to receive clinical benefit after completing the Core Phase could enter an optional Extension Phase if pasireotide was not commercially available in their country or a local access program was not available to provide drug. Patients continued in the Extension Phase until the last participant randomized in the Core Phase completed 16 weeks of treatment post-randomization.
Most critically ill patients are confronted with hyperglycaemia, which is associated with an increased mortality and morbidity risk. Normalising these elevated blood glucose levels by intensive insulin therapy may improve patient outcome, but is associated with an increased risk of hypoglycaemia. The LOGIC-2 study hypothesises that the LOGIC-Insulin computerised software algorithm will allow better (less hyperglycaemia) and safer (less hypoglycaemia) blood glucose control in critically ill patients than nurse-directed blood glucose control.
This is a clinical study of a drug named dopamine and how it affects our bodies ability to make and secrete insulin. Insulin is a hormone made in the pancreas that helps our body regulate sugar levels. We think that this drug decreases the amount of insulin our body makes and causes our sugar levels to be high. When you are critically ill there can be many adverse effects if you have sugar levels that are too high.
The purpose of this study is to investigate if daily consumption of barley beta-glucans effect lipid and glucose metabolism and alter intestinal microbiota composition in participants with metabolic syndrome or with high risk for metabolic syndrome development. It is assumed that 4-week intervention with beta-glucans will improve some clinical signs of metabolic syndrome and alter composition of intestinal microbiota. Variation in microbiota composition will be investigated with emphasis on Bacteroidetes and Firmicutes ratio. Furthermore it is presupposed that consumption of beta-glucans will stimulate growth of beneficial intestinal bacteria from genus Lactobacillus and Bifidobacteria and consequently effect production of short chain fatty acids in population with metabolic syndrome. Moreover it is presupposed that 4-week consumption of beta-glucans will have influence on glucose metabolism and will consequently improve insulin resistance within people with metabolic syndrome or high risk for metabolic syndrome development. It is assumed that 4-week consumption of beta-glucans will improve specific plasma lipid content in population with metabolic syndrome.
Glucocorticoids therapy exposes the patient to an increased risk for diabetes morbidity. However, there is no proven preventive therapy. GLP-1-RA has shown to improve glucose metabolism in healthy volunteers treated with glucocorticoids. We assume that GLP-1-RA will improve glucose metabolism in patients with high risk for diabetes morbidity, treated with glucocorticoids.
There are no guidelines for the management of glucocorticoid- (henceforth steroid) induced elevated blood sugars (henceforth hyperglycemia). Oncology ward patients have particularly high rates of hyperglycemia and are frequently exposed to high dose steroid therapy. A prior study by Muthala et al. (unpublished data) found a relationship between insulin requirements needed to maintain normal blood sugars, patient weight, and mg of steroid administered. In this pilot study, through an endocrine consult team, a weight-based, steroid dose-based insulin protocol will be implemented for the management of hyperglycemia in lymphoma patients requiring high dose steroid therapy, with the goal of reducing hyperglycemia incidence.
Consumption of carbohydrate containing foods or sugary drinks brings about changes to the blood glucose levels. After a meal or drink, blood glucose levels rise until it reaches a peak concentration usually after 30 minutes. When the body senses the increase in blood glucose, a hormonal process involving insulin takes place to ensure that the glucose is taken up from the blood for storage and where it is needed for energy in the body. This process then brings about a decrease in the concentration of glucose until it reaches approximately the starting concentration. The original concentration of glucose is attained approximately 2 hours after eating or drinking a carbohydrate food or sugary drink respectively. Different carbohydrates and sugary drinks have different effects on blood glucose response depending on the amount as well as the type of carbohydrate. Those that give rise to a high glucose response compared to a reference carbohydrate (usually glucose) are said to be high glycaemic index (GI) foods and those with a lower glucose response compared to a reference carbohydrate (usually glucose) are said to be low glycaemic index (GI) foods.(1) Research has shown that diets that give rise to a high glucose response are associated with a number of abnormalities like increased metabolic syndrome (2). Metabolic syndrome mostly comprises of insulin resistance and glucose intolerance which gives an increased risk of type 2 diabetes. (3) It also gives rise to other conditions like high blood pressure (arterial hypertension), elevated blood insulin levels (hyper-insulinemia), elevated amounts of fat in the liver (fatty hepatosis) and elevated amounts of lipids in the blood (dyslipidemia). After type 2 diabetes become clinically apparent, the risk of cardiovascular disease also rises. (4) Research has also shown that foods/drinks which raise blood glucose levels gradually (low GI) rather than rapidly (high GI) have health benefits which include reducing the risk of metabolic syndrome (5). In vitro studies have shown that polyphenols found in fruits, vegetables and plant based foods have a positive effect on carbohydrate metabolism and can lower the blood glucose levels. (6) This research will determine whether the presence of polyphenols in the diet has any lowering effect on the blood glucose levels and hence the glycaemic index of foods. This will be determined by asking volunteers to consume polyphenol rich drink/food together with white bread and determine the glycaemic response. The GI of bread will be determined initially as a reference. Analysis will be done by measuring blood glucose response to white bread alone as reference and then to white bread with test sample containing polyphenols and then determine GI and see how the GI of bread will be affected. Other analyses to be done are plasma insulin, glucagon, gastric inhibitory polypeptide (GIP) and glucagon like peptides-1 (GLP-1) as they all relate to glycaemic response. Study hypothesis is that glucose metabolism will be affected. NOTE: 1. Only healthy participants undertook the study (Hence metabolic syndrome participants not part of the study) 2. Only glucose and insulin were analysed in the plasma (hence GIP, GLP-1 and glucagon not part of end points)