Journal
JOURNAL OF DIABETES INVESTIGATION
Volume 12, Issue 11, Pages 2028-2035Publisher
WILEY
DOI: 10.1111/jdi.13568
Keywords
Bilirubin; Diabetic neuropathies; Oxidative stress
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Funding
- grant for the Creation of Innovation Centers for. Advanced Interdisciplinary Research Areas Program from the Ministry of Education, Culture, Sports, Science and Technology of Japan (Funding program 'Innovation Center for Medical Redox Navigation')
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The study aimed to evaluate sural nerve conduction impairments (SNCI) as an objective DPN marker and the contribution of bilirubin to SNCI. Results showed that SNCI was significantly related to diabetes duration, declined estimated glomerular filtration rate, albuminuria, and total bilirubin. Bilirubin was identified as an independent inverse risk factor for SNCI, even after adjusting for known risk factors and markers for microvascular complications.
Aims/Introduction Diagnosis of diabetic peripheral neuropathy (DPN) depends on subjective findings, certain investigations for DPN risks have not been performed enough. Bilirubin protects against vascular complications by reducing oxidative stress in diabetes, but is not fully tested for DPN. This study aimed to evaluate sural nerve conduction impairments (SNCI) as an objective DPN marker and the contribution of bilirubin to SNCI. Materials and methods Using DPN-Check(R), SNCI was defined as a decline of amplitude potential or conduction velocity below the normal limit in 150 inpatients with diabetes. The correlations between SNCI and conventional DPN diagnosis criteria, the incidence of diabetic retinopathy/nephropathy, biomarkers for atherosclerosis, cardiac function by ultrasonic cardiogram, and bilirubin were statistically tested, followed by the comparison of logistic regression models for SNCI to find confounders with bilirubin. Results The incidence of SNCI was 72.0%. The sensitivity and specificity of SNCI for DPN prediagnosis by simplified criteria were 54.6 and 90.5%, respectively, and similarly corresponded with diabetic retinopathy and nephropathy (sensitivity 57.4 and 50.0%, respectively). SNCI significantly related to diabetes duration, declined estimated glomerular filtration rate, albuminuria and total bilirubin. SNCI incidence was attenuated in the higher bilirubin tertiles (89.8/65.3/54.8%, P < 0.001). Bilirubin was an independent inverse risk factor for SNCI, even after adjustment by known risk factors for DPN and markers for microvascular complications. Conclusions SNCI is a comprehensive marker for diabetic complications. We first showed the independent inverse relationship between bilirubin and SNCI through the independent pathway with other complications, provably reducing oxidative stress, as previously reported.
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