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Deficits in systemic biomarkers of neuroinflammation and growth factors promoting nerve regeneration in patients with type 2 diabetes and polyneuropathy.
BMJ Open Diab. Res. Care 7:e000752 (2019)
Introduction The determinants and mechanisms contributing to diabetic sensorimotor polyneuropathy (DSPN) remain unclear. Since neuroinflammation and altered nerve regeneration have been implicated in the pathogenesis of both DSPN and neuropathic pain, we hypothesized that the corresponding biomarkers could be associated with DSPN in general and could have the potential to discriminate between the painful and painless DSPN entities.Methods In a cross-sectional study using multimarker proximity extension assay technology we assessed 71 serum biomarkers including cytokines, chemokines, growth factors, receptors, and others in patients with type 2 diabetes with DSPN (DSPN+) (n=304) or without DSPN (DSPN-) (n=158) and persons with normal glucose tolerance (NGT) without polyneuropathy (n=354).Results After adjustment for multiple testing and sex, age, body mass index, HbA1c, and smoking, the serum levels of 17 biomarkers (four cytokines, five chemokines, four growth factors, two receptors, two miscellaneous) were lower in DSPN+ than in DSPN- and NGT. In DSPN+, six of these biomarkers were associated with peripheral nerve function. The concentrations of 15 other biomarkers differed between NGT and both DSPN+ and DSPN-, but not between DSPN+ and DSPN-. No differences in biomarker levels were found between patients with painful (n=164) and painless DSPN (n=140).Conclusions Deficits in systemic cytokines, chemokines, and growth factors promoting nerve regeneration in patients with type 2 diabetes are linked to polyneuropathy in general but not specifically to the painful or painless entity.
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Publication type
Article: Journal article
Document type
Scientific Article
Keywords
Biomarkers ; Inflammation And Complications ; Peripheral Neuropathy ; Type 2 Diabetes; Oncostatin-m; Painful; Inflammation; Synaptogenesis; Activation; Neuropathy; Cytokines; Disease
ISSN (print) / ISBN
2052-4897
e-ISSN
2052-4897
Quellenangaben
Volume: 7,
Issue: 1,
Article Number: e000752
Publisher
BMJ Publishing Group
Publishing Place
London
Non-patent literature
Publications
Reviewing status
Peer reviewed