and autonomic neuropathy. In contrast, in type 2 diabetic patients, who represent the vast majority of people with diabetes, the results were variable. Intensive diabetes therapy either had no effect or only partially slowed the progression of polyneuropathy, and the effect on autonomic neuropathy was largely lacking. Moreover, improved glycemic control was achieved at the expense of increased risk of hypoglycemia and weight gain.
2. Only a few small studies have evaluated the effects of intensive diabetes therapy on established polyneuropathy in type 1 diabetic patients. They indicate that improved glycemic control may improve some aspects of diabetic neuropathy, but imperfect study designs and methodology hamper the validity of most of these small trials. At more advanced stages improvement is still possible for some measures of nerve function such as motor NCV, but is less likely for autonomic dysfunction. This may be due to the fact that true normoglycemia could not be achieved in many patients. No large, randomized, controlled trial has been performed specifically to show favorable effects of intensive diabetes therapy on diabetic polyneuropathy.
3. In type 1 diabetic patients with the most advanced stages of peripheral neuropathy, progression of nerve conduction deficits is halted after three to four years of normoglycemia following pancreas transplantation, but no effect is seen in autonomic neuropathy. However, successful pancreas transplantation results in long-term normoglycemia. Hence, the effect on nerve function that can be achieved with this method cannot be extrapolated to the widely used current methods of intensive diabetes therapy, since for various reasons the majority of diabetic patients in whom these methods are used do not achieve sustained normoglycemia.
4. Although observational studies suggested a glycemic threshold for the development and progression of long-term complications in type 1 diabetes, the DCCT data do not support such an assumption. Thus, attempts to achieve optimal glycemic control should not aim at a particular HbA1c threshold within the diabetic range, but should follow “the goal of achieving normal glycemia as early as possible in as many IDDM patients as is safely possible” [158].
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