Abstract Diabetic distal symmetric polyneuropathy (DDSP) is the most common form of diabetic neuropathy. DDSP, foot ulcerations, and lower limb amputation greatly increase mortality, which is 23% 2 years after a foot ulceration and rises to 71% after 10 years. DDSP is seen in patients with both type 1 and type 2 diabetes, but the clinical features and pathophysiology are distinctly different. DDSP also presents in patients with pre‐diabetes and/or obesity alone, indicating that glycaemic control is not the sole contributor to the pathophysiology of DDSP. In the BARI 2D trial, 51% of those with type 2 diabetes had peripheral neuropathy at baseline. In the DCCT/EDIC trials, patients with type 1 diabetes had a 6% prevalence of diabetes on enrolment, which increased to 30% after 13–14 years of follow‐up. In the lower limb, a combination of the components of sensory DDSP coupled with motor and autonomic components leads to an increased incidence of foot ulceration. The ADA 2025 Standard of Care recommends screening for diabetic neuropathy at the time of presentation for patients with type 2 diabetes and 5 years after diagnosis in patients with type 1 diabetes. Diagnostic techniques are discussed in this article. The basic pathological process in DDSP is oxidative and inflammatory stress due to diabetes and its associated metabolic abnormalities as well as microvascular disease. Therapy of symptomatic DDSP is less than satisfactory. Medications utilized for neuropathic pain are discussed as are the therapies to prevent and treat foot ulceration. It is important to recognize that DDSP in patients with diabetes may have other causes: particularly deficiencies of vitamins B12 and D, excessive alcohol intake, hypothyroidism, and paraproteinemias.
Bell et al. (Thu,) studied this question.