Diabetic Neuropathy: Updated ADA Position Statement
New evidence on diabetic neuropathy has emerged since the ADA’s last position statement published in 2005.
The American Diabetes Association (ADA) released an updated position statement on the prevention, detection, and management of diabetic neuropathies, which represent the most common chronic complications of the disease.1 Distal symmetric polyneuropathy (DSPN) and autonomic neuropathy, especially cardiovascular autonomic neuropathy (CAN), are the forms most often studied and most frequently observed in clinical practice. The position statement was published in Diabetes Care.
Since the previous ADA position statement on diabetic neuropathy was published in 2005, new evidence on the topic has emerged. “In addition, given the complexity of diabetic neuropathy, there was somewhat contradictory information in the literature, and thus our group of experts was convened by the ADA to condense and clarify the evidence on the subject, come to a consensus, and present it for the daily use of practicing physicians,” explained lead researcher Rodica Pop-Busui, MD, PhD, professor of internal medicine in the Division of Metabolism, Endocrinology, and Diabetes, and associate chair of clinical research at the University of Michigan in Ann Arbor.
“The recommendations reinforce much of what clinicians are already doing — or should be doing — in routine clinical practice,” according to Kevin M. Pantalone, DO, staff endocrinologist and director of clinical research at the Cleveland Clinic in Ohio. “It is important to note that the most effective treatment of diabetic neuropathy is prevention.” In addition, screening is critical to enable early detection and intervention.
The first section of the position statement offers the following recommendations regarding prevention of DSPN and CAN. First, glucose control should be optimized as early as possible to prevent or slow the development of DSPN and CAN in patients with type 1 diabetes. Enhanced glucose control in this patient group has been found to substantially decrease the incidence of DSPN — by 60% (95% CI, 38%-74%) in one study, for example — and to reduce the risk of CAN by up to 45%.2,3
Second, in patients with type 2 diabetes, glucose control should be optimized to prevent or delay the progression of DSPN, and a multifactorial approach targeting glycemia and other risk factors should be considered in order to prevent CAN. In studies in this patient group, enhanced glucose control led to only a modest reduction in DSPN risk (relative risk reduction, 5% to 9%), and it has not been shown to consistently decrease the risk of CAN.4,5 “However, a multifactorial intervention, including a lifestyle component, targeting glucose and cardiovascular disease risk factors reduced the risk of CAN by 60% in people with type 2 diabetes,” the researchers wrote.6 One study observed nerve fiber regeneration in patients with type 2 diabetes who participated in an exercise program, while nerve fiber loss occurred in those who followed usual care.7
DSPN accounts for an estimated 75% of diabetic neuropathies and is a major cause of foot ulceration and prerequisite to Charcot neuroarthropathy (CN), which increases the risk of amputation and predicts mortality.8,9 In addition, DSPN contributes to falls and fractures, which may further influence the pathogenesis of CN.10 It is recommended that the initial assessment in DSPN take place at the time of diagnosis in patients with type 2 diabetes and 5 years following diagnosis in patients with type 1 diabetes. Annual assessments are recommended in both groups thereafter.