Evaluation of the association between diabetic neuropathy development and oxidative stress, DNA damage, MMP-2, MMP-9, MMP-10, TNF–α, IL-1β, IL-6, vitami̇n d levels in diabetic patients

Diabetic polyneuropathy is one of the microvascular complications of diabetes. A lot of mechanisms such as vascular and metabolic processes have been known to be involved in etiopathogenesis. In this study, we aimed to investigate the association between oxidative stress, DNA damage, MMP-2, MMP-9, MMP-10, TNF–α, IL-1β, IL- 6, Vitamin D levels and the occurence of diabetic polyneuropathy and neuropathic pain. 150 participants were involved in the study. 42 of these were healthy controls and 108 were patients with type II diabetes. Patiens with type II diabetes were grouped according to existence of polyneuropathy. There were 56 patients without polyneuropathy (DPNP(-)) and 52 patients with polyneuropathy (DPNP(+)). Demographical characteristics of all participants were recorded. Vitamin D, TNF–α, IL-1β, IL-6, MMP-2, MMP-9, MMP-10, TAS, TOS, OSI and DNA damage levels were studied in all participants. DN4 questionnaire were performed in diabetic patients to evaluate neuropatic pain. Serum TNF–α, IL-1β, IL-6, MMP-9, MMP-10, TOS, OSI and DNA damage levels were significantly higher (p<0,001), on the other hand serum TAS levels were significantly lower in DPNP(+) patients than DPNP(-) patients (p=0,001). After classification according to neuropathic pain scores, TNF–α, IL-1β, IL-6, MMP-9, MMP-10, TOS, OSI and DNA damage leves were significantly higher (p<0,001), on the other hand serum TAS levels were significantly lower in patients with DN4 score ≥4 than patients with DN4 score <4 (p= 0,002). These results support that neuroinflammation, oxidative stress and DNA damage have important roles in pathogenesis of diabetic polyneuropathy and neuropathic pain. New treatment options should be developed for diabetic polyneuropathy and neuropathic pain in consideration of these mechanisms.