Correlation analysis between plasma fibrinogen and nerve electrophysiological changes in type 2 diabetic peripheral neuropathy.

Abstract

Introduction: The aim of the study was to investigate the pathogenesis of diabetic peripheral neuropathy (DPN) and the value of fibrinogen (FIB) in the early diagnosis of DPN.

Material and methods: A total of 121 patients with type 2 diabetes mellitus (T2DM) and DPN hospitalized in the Endocrinology Department of the 923 Hospital of the People's Liberation Army of China were randomly selected between May and October 2020 and divided into a T2DM asymptomatic (no peripheral neuropathy-related symptoms) group (66 cases) and a T2DM symptomatic group (55 cases) according to the presence or absence of clinical neurological symptoms and signs. Forty healthy volunteers were selected as a normal control group. In addition to plasma FIB and nerve electrophysiological tests, all included subjects were electrophysiologically tested for nerve conduction velocity (NCV), terminal motor latency (DML), sensory nerve action potential (SNAP) amplitude, and compound muscle action potential (CMAP) amplitude.

Results: Compared with the control group, NCV was slowed down in T2DM patients, DML was prolonged, and the amplitude of CMAP and SNAP were decreased. Compared with asymptomatic T2DM patients, symptomatic patients had slower NCV, longer DML, lower CMAP amplitude of median nerve, ulnar nerve and tibial nerve, and significantly lower SNAP amplitude of median nerve and ulnar nerve. CMAP amplitudes were decreased, and median and ulnar nerve SNAP amplitudes were also significantly decreased ( p < 0.05). The plasma FIB concentration of asymptomatic patients with T2DM was higher than that of the control group, and the plasma FIB concentration of symptomatic patients with T2DM was higher than that of asymptomatic patients with T2DM ( p < 0.01). The NCV and DML of asymptomatic patients with T2DM slowed down and prolonged as the FIB level increased; the NCV of T2DM symptomatic patients also slowed down as FIB increased, and median and ulnar nerve DML increased as FIB increased. There was no correlation between NCV and DML and the plasma FIB level in the control group. SNAP amplitudes of symptomatic and asymptomatic patients with T2DM decreased as plasma FIB increased, while CMAP amplitudes of the tibial nerve and the T2DM symptomatic ulnar nerve decreased as FIB increased in the control group.

Conclusions: FIB may be a contributing factor for diabetic neuropathy and could be used as an indicator in the early screening and diagnosis of peripheral neuropathy in patients with T2DM.