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Association of glycemic variability assessed by continuous glucose monitoring with subclinical diabetic polyneuropathy in type 2 diabetes patients

AIMS/INTRODUCTION: Diabetic peripheral neuropathy is a common diabetes‐related microvascular complication. The relationship between peripheral nerve function and glucose variability is unclear. We investigated the association of glucose variability with subclinical diabetic polyneuropathy in a large...

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Detalles Bibliográficos
Autores principales: Pan, Jiemin, Yan, Xinfeng, Li, Fengwen, Zhang, Yinan, Jiang, Lan, Wang, Congrong
Formato: Online Artículo Texto
Lenguaje:English
Publicado: John Wiley and Sons Inc. 2021
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8847148/
https://www.ncbi.nlm.nih.gov/pubmed/34455710
http://dx.doi.org/10.1111/jdi.13652
Descripción
Sumario:AIMS/INTRODUCTION: Diabetic peripheral neuropathy is a common diabetes‐related microvascular complication. The relationship between peripheral nerve function and glucose variability is unclear. We investigated the association of glucose variability with subclinical diabetic polyneuropathy in a large‐scale sample of patients with type 2 diabetes. MATERIALS AND METHODS: We enrolled 509 individuals with type 2 diabetes who were screened for diabetic peripheral neuropathy and monitored using a continuous glucose monitoring system. Multiple glycemic variability parameters, including the mean amplitude of glycemic excursions, glucose standard deviation (SD(gluc)) and glucose coefficient of variation were calculated from 3‐day glucose profiles obtained from continuous glucose monitoring. All participants underwent nerve conduction studies, and the composite Z‐scores for nerve conduction parameters were calculated. RESULTS: Multivariate logistic regression analyses showed that SD(gluc) and the conventional risk factor hemoglobin A1c (HbA1c) were independently associated with abnormal nerve function, and the corresponding odds ratios (95% confidence interval) were 1.198 (1.027–1.397, SD(gluc)) and 1.182 (1.061–1.316, HbA1c), respectively. The composite Z‐score of nerve conduction velocity and response amplitude obviously decreased with greater SD(gluc), and the composite Z‐score of distal latency significantly increased with increasing tertiles of SD(gluc) (all P trend <0.05). After adjusting for age, sex, body mass index, diabetes duration and HbA1c, SD(gluc) was independently associated with nerve conduction velocity (β = −0.124, P = 0.021). CONCLUSIONS: The SD(gluc) is a significant independent contributor to subclinical diabetic polyneuropathy, in addition to conventional risk factors including diabetes duration and HbA1c.