New insights into the mechanisms of diabetic neuropathy.

Abstract

The incidence of diabetes is increasing at epidemic rates. There currently are an estimated 17 million individuals with diabetes in the United States and this number is rapidly increasing [1]. The likelihood of developing diabetes is approximately 40% in persons born after the year 2000 [2] and is more prevalent among African Americans, Hispanics and Native Americans [2]. The personal and national loss of productivity is immense [3]. The American Diabetes Association estimates that diabetes cost the United States an estimated $132 billion in 2002, $92 billion in direct medical expenditures and $40 billion due to lost work time, disability, and premature mortality [4]. The morbidity of diabetes is due to both macrovascular and microvascular complications. A diabetic individual is 2 to 4 times more likely to have accelerated atherogenesis of large vessels leading to myocardial infarction, stroke and peripheral vascular occlusive disease [3]. These macrovascular complications can occur in individuals without diabetes, although it is clear that diabetes exacerbates and accelerates atherogenesis. In contrast, microvascular complications are more unique to the diabetic state and eventually occur in nearly all patients with diabetes. Fifteen years after diagnosis, 90% of patients have evidence of diabetic retinopathy, the cause of approximately 25,000 new cases of blindness per year in the United States [5]. Diabetes is the primary cause of renal failure and accounts for 40% of new cases requiring dialysis in the United States each year [4]. More than half of all individuals with diabetes develop neuropathy [4,6] with a lifetime risk of one or more lower extremity amputations estimated at 15% [7]. The current article will focus on this last complication, diabetic neuropathy (DN), with the goal of introducing new ideas on the pathogenesis and potential treatment of this disabling complication of diabetes. Diabetic Neuropathy (DN)