Association between HbA 1c and peripheral neuropathy in a 10-year follow-up study of people with normal glucose tolerance, impaired glucose tolerance and Type 2 diabetes.

AIMS: To explore the association between HbA1c and sural nerve function in a group of people with normal glucose tolerance, impaired glucose tolerance or Type 2 diabetes.

METHODS: We conducted a 10-year follow-up study in 87 out of an original 119 participants. At study commencement (2004), 64 men and 55 women (mean age 61.1 years) with normal glucose tolerance (n=39), impaired glucose tolerance (n=29), or Type 2 diabetes (n=51) were enrolled. At the 2014 follow-up (men, n=46, women, n=41; mean age 71.1 years), 36, nine and 42 participants in the normal glucose tolerance, impaired glucose tolerance and Type 2 diabetes categories, respectively, were re-tested. Biometric data and blood samples were collected, with an electrophysiological examination performed on both occasions.

RESULTS: At follow-up, we measured the amplitude of the sural nerve in 74 of the 87 participants. The mean amplitude had decreased from 10.9 μV (2004) to 7.0 μV (2014; P<0.001). A 1% increase in HbA1c was associated with a ~1% average decrease in the amplitude of the sural nerve, irrespective of group classification. Crude and adjusted estimates ranged from -0.84 (95% CI -1.32, -0.37) to -1.25 (95% CI -2.31, -0.18). Although the mean conduction velocity of those measured at both occasions (n=73) decreased from 47.6 m/s to 45.8 m/s (P=0.009), any association with HbA1c level was weak. Results were robust with regard to potential confounders and missing data.

CONCLUSIONS: Our data suggest an association between sural nerve amplitude and HbA1c  at all levels of HbA1c . Decreased amplitude was more pronounced than was diminished conduction velocity, supporting the notion that axonal degeneration is an earlier and more prominent effect of hyperglycaemia than demyelination.