Role of Inflammation in the Pathogenesis of Diabetic Peripheral Neuropathy

Diabetic peripheral neuropathy (DPN) means the presence of symptoms and/or signs of peripheral nerve damage that occur to people with diabetes, excluding all other causes of neuropathy. Chronic hyperglycaemia leads to increased secretion of tumour necrotic factor-alpha (TNF-α), with the development of micro and macroangiopathy, damage to nerve fibres and local demyelination.

To determine the role of inflammation in the peripheral nerve damage process concerning people suffering from type II diabetes mellitus.

The study included a total of 80 subjects, men and women, divided into two groups: an examined group (n = 50) consisting of subjects with DPN at the age from 30 to 80 years and a control group (n = 30) of healthy subjects aged from 18 to 45. In the investigated group, a neurological examination was performed using the Diabetic Neuropathy Symptoms (DNS) Score and Electroneurography. All the subjects had the blood plasma concentration of TNF-α by ELISA technique.

The average value of TNF-α in the test group was 8.24 ± 2.899 pg/ml, while the control group was 4.36 ± 2.622 pg/ml (p < 0.0001). The average value of TNF-α was correlated with the achieved DNS score in the investigated group (p = 0.005). Concerning the linear association of the concentration of TNF-α with the peripheral nerve velocity in the investigated group, no statistical significance was detected.

Inflammation can play a role in the pathogenesis of diabetic autonomic neuropathy and cranial neuritis.