Background: Individuals with elevated glycosylated hemoglobin (HbA1c) have a higher rate of microvascular complications, especially peripheral neuropathy. Objective: To find the relation between elevated (HbA1c) and the occurrence of peripheral nerve dysfunction in prediabetic individuals and to find the role of the inflammatory marker as, C-Reactive Protein (CRP), in the development of Diabetic Peripheral Neuropathy (DPN). Methods: Screening was done for 80 pre-diabetic individuals and 40 control subjects presenting to the internal medicine clinics, Mansoura University Hospital; Egypt, from August 2014 to July 2015. The pre-diabetic individuals (HBA1c: 6.0-6.5%) and a control group of 40 subjects with HbA1c < 6%. All subjects underwent neurological examination, nerve conduction study of both peroneal and sural nerves, and measurement of HbA1c and CRP. Results: The sural nerve Sensory Nerve Action Potential (SNAP) amplitude was significantly lower in pre-diabetics than in control group. Compound Muscle Action Potential (CMAP) of the peroneal nerve was lower significantly in pre-diabetics with subclinical neuropathy in comparison to controls. The peroneal and sural nerve amplitudes were significantly correlated to CRP, but not to HbA1c.
Original Research ArticleConclusion: Axonal subclinical neuropathy occurs significantly more in pre-diabetics than in normal (control) individuals. The CRP is significantly correlated with the presence of the axonal subclinical neuropathy which indicates an underlying inflammatory role.
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