Distal Sensory Peripheral Neuropathy: An Undervalued Determinant of Wellbeing.

Abstract

Peripheral neuropathy (PN) is a significant, frequently debilitating complication of HIV infection and diabetes caused by damage to the sensory and motor peripheral nerves. In persons with HIV infection (PWH), neuropathy is thought to result from highly active antiretroviral therapy (HAART) neurotoxicity, particularly stavudine (d4T), dideoxycytidine (ddC), and didanosine (ddI), effects of HIV, or both [1]. Advanced age, taller height (as a proxy for longer neuronal axons), comorbid diabetes, and treatment with nucleotide reverse transcriptase inhibitors (NRTI), increased PN risk [2]. Among patients with diabetes, neuropathy is likely the culmination of multiple chronic insults to the nervous system, including hyperglycemia, microvascular insufficiency, oxidative stress, and autoimmunity [1,3,4]. Risk increases with advancing age and duration of diabetes, poor glycemic control, high body mass index (BMI), and comorbid conditions such as hypertension. While the prevalence of PN varies according to the types of criteria used for diagnosis, population demographics, stage of disease, and other variables, database reviews and meta-analyses estimate that between 30% and 70% of PWH and 10% and 90% diabetes cases are complicated by PN at any given time [4]. The most common type of PN among patients with HIV or diabetes is distal sensory peripheral neuropathy (DSPN), also called distal symmetric polyneuropathy, characterized by progressive dysfunction of length-dependent sensory peripheral nerves [1,4-9]. Damage to largeand small-fiber neural networks cause a range of symptoms starting in the toes and feet, such as tingling, prickling, and discomfort, that increase over time in a symmetric, bilateral "stocking-glove" distribution involving the legs, hands, and arms. Symptoms may be accompanied by pain, either at disease onset or later in the course, typically described as burning, aching, shooting, or electrical [1].