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Without the White Coat Practical management… Diabetes 2Type 2 diabetes mellitus is defined as a complex disease seen as a functional defect in the function of the pancreas especially beta cells that secretes the insulin. In short the defect is the secretion of insulin and insulin action if not corrected will lead to increased levels of plasma glucose levels. Remember, the target cells will always communicate with the beta cells for the release of insulin. Type 2 diabetes is seen as a defect in beta cell that will eventually lead to impaired insulin secretion. In this case the liver will increase glucose production and the skeletal muscles will decrease its glucose uptake. Every diabetic should remember this in order to be guided about the medications that they take and will not forget that all anti-hyperglycemic agents will act not only in the pancreas, but also in some organs. Those which act directly to the pancreas are called “sulfonylureas” or “glinides, it is the “Metformin” group that acts on the liver, and the “thiazolidinediones” family will act directly to skeletal muscles Practical management will consist of a combined therapy that can reach or fulfill strict therapeutic goals in controlling blood glucose levels to a “low”. This target can be achieved and stimulate insulin response in combination therapy. In the last decades it was insulin resistance that we are fighting for, thus came products that are called insulin sensitizers (metformin or/and thiazolidones), and the newest launching of the “basal(intermediate) insulin” encouraging physicians to consider insulin therapy, instead of insulin secretagogues in the management of type 2 diabetes mellitus. The progressive intensive treatment strategy includes a step wise approach that can address hyperglycemia rather than correcting the underlying pathology. (This may be a good reason why a lot of type 2 treatment fails). New cases of diabetes type 2 in which mono therapy was started requires a shift to a combination therapy after a year just to improve blood glucose control in which some key combinations composed of sulfonylureas and metformin. Remember, that insulin resistance contributes a lot to the metabolic syndrome which may play a crucial role in postprandial hyperglycemia. A good combination should always supplement the action of metformin which in the past few years had shown adequate glycemic control. (whose sole action is in the liver, remember in some studies it had shown to decrease HbA1c levels by 1% similar to glimeride, showing less than 50% confirmed hypoglycemic states.) Exogenous insulin will be well recommended in cases of a beta cell failure to compensate for a defective insulin secretion. In most studies, “intermediate” insulin at bedtime combined with a pre-meal sulfonylurea had shown to be effective in some cases. Treatment strategies shall remain a big challenge to our endocrinologist (diabetologist) and practicing physicians, thus combination therapy is much more favored thus remains on which combined therapy will deliver the best results. It will always be a great emphasis in which insulin secretion (first phase) is targeted, thus correcting defective insulin secretion in both the liver and at the skeletal muscle level. The step wise management of type 2 diabetes starts at the floor level of diet and exercise that gradually step up to the use of an oral form of mono therapy, then comes the oral combination (metformin, sulfonylureas(glinides), glitazones and acarbose) then stepping up to oral combination plus insulin and lastly in the top most part of the heirarchy the use of intensive insulin. It is always wise to check the HbA1c level 2 to 3 times a year to see the effectiveness of the anti-diabetic therapy. |