The major findings in our study were increased levels of IL-1β, IL-6 and IL-1Ra in epileptic patients and high levels of IL-1β in TLE group. Our results support the existence of a chronic inflammatory state in epileptic patients.

To our knowledge, this is the first study to assess the relationships between TNF-α, IL-10, and NCS of the most distal sensory nerves in patients with prediabetes or type 2 DM. The mechanisms involved in the pathogenesis of DM and diabetic peripheral neuropathy are complex. The pro-inflammatory stage and the high incidence of neuropathy in patients with prediabetes may suggest a possible causative effect; however, the potential role of inflammation in the pathogenesis of peripheral neuropathy needs further clarification.

Autonomic neuropathy is one of the most common complications of diabetes mellitus (DM). The etiology of autonomic impairment is not well-understood, yet. There is need for studies to investigate the cause–effect relationships of inflammation and/or endothelial dysfunction and diabetic autonomic neuropathy. Only a few reports have mentioned autonomic neuropathy in individuals with impaired glucose tolerance (IGT), previously. Furthermore, the association between the plasma markers of endothelial dysfunction (von Willebrand factor (vWF), soluble E-selectin) and autonomic neuropathy in patients with IGT or DM has not been studied before. In this study, we aimed to investigate the correlation between plasma markers of endothelial dysfunction and autonomic neuropathy in patients with IGT or type 2 DM (T2DM).In this case–control study, 25 IGT patients, 25 T2DM patients with autonomic symptoms, and 30 controls were included. Demographical data, HbA1c, vWF, and soluble E-selectin (sE-selectin) levels were analyzed. Sympathetic skin response (SSR) and heart rate variability (HRV) were used as the indicator of autonomic activity.Plasma levels of HbA1c, vWF, and sE-selectin were higher in patients with IGT than the controls; patients with T2DM had higher levels than both the controls and the patients with IGT. SSR measures were similar among the groups. However, higher number of T2DM patients had absent plantar SSR than controls. HRV analysis at rest revealed lower standard deviation of R-R interval, coefficient of variation of R-R interval, low-frequency (LF) power and total power in patients with IGT and T2DM than the controls. In addition, HRV analysis at deep breathing showed lower high-frequency (HF) power in IGT group. LF:HF ratio was lower in both patient groups at rest. No strong correlation was found between the levels of HbA1c, vWF, sE-selectin, HRV, and SSR measures.Our results support that endothelial dysfunction is evident in individuals with IGT or T2DM and HRV is impaired in early stages in the course of T2DM. However, increased levels of biomarkers of endothelial damage do not correlate with HRV or SSR. More studies are needed to clarify the disease pathogenesis and its clinical correlates. Impaired HRV in T2DM could be due to mechanisms other than endothelial dysfunction.

Aim: To determine the association between interleukin-6 (IL-6) and soluble E-selectin (sE-selectin) levels with the electrodiagnostic abnormalities in patients with impaired fasting glucose (IFG) and impaired glucose tolerance (IGT). Methods: Serum HbA1c, C-reactive protein (CRP), erythrocyte sedimentation rate (ESR), fibrinogen, IL-6 and sE-selectin levels were analyzed in 25 IFG patients, 22 IGT patients and 41 controls. Nerve conduction studies (NCS) of sural, dorsal sural (DS), medial dorsal cutaneous and medial plantar sensory nerves were conducted. Results: HbA1c and IL-6 levels were significantly higher in IFG and IGT patients than the controls. IGT patients had higher sE-selectin levels compared to controls and IFG patients. IL-6 levels were significantly correlated with levels of CRP, fibrinogen, ESR and sE-selectin in patients with prediabetes. Both IFG and IGT patients had substantial impairments in very distal sensory NCS. IL-6 levels were positively correlated with HbA1c and negatively correlated with DS NCS in prediabetic patients. Conclusions: Inflammation and endothelial dysfunction might be important in patients with IFG or IGT. Furthermore, our findings strengthen the idea that inflammation (increased levels of IL-6) might be associated with early electrophysiological impairments in patients with prediabetes. NCS of the most distal sensory nerves significantly enhanced the diagnosis of subclinical neuropathy in patients with prediabetes. Subclinical peripheral sensory neuropathy should be investigated in prediabetes to lower the number of future outcomes they are associated with.

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