Role of inflammation in sensory neuropathy in prediabetes or diabetes

Duksal, Tarik; Tiftikçioğlu, Bedile İrem; Bilgin, Sule; Köse, Şükran; Zorlu, Yaşar

doi:10.1111/ane.12474

Cited by 42 publications

(32 citation statements)

References 29 publications

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“…The finding for IL-6 not only corroborates the report from the KORA F4 study (8) but also is in line with other cross-sectional studies investigating DSPN or impaired nerve conduction (5,17). By contrast, associations between higher TNF-a and DSPN or its components have so far been limited to small studies that did not adjust for confounding factors (6,7,9,15,31), whereas no associations were found in studies that considered confounders (5,8). From a mechanistic point of view, it is important to note that IL-6 and TNFa are functionally related: TNF-a activates the transcription factor nuclear factor-kB and thereby induces IL-6 expression.…”

Section: Il-6 Tnf-a and Incident Dspnsupporting

confidence: 88%

Proinflammatory Cytokines Predict the Incidence and Progression of Distal Sensorimotor Polyneuropathy: KORA F4/FF4 Study

et al. 2017

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OBJECTIVEExperimental and epidemiological studies have implicated inflammatory processes in the pathogenesis of distal sensorimotor polyneuropathy (DSPN), but prospective studies are lacking. We hypothesized that biomarkers of inflammation predict the development and progression of DSPN in a population-based cohort. RESEARCH DESIGN AND METHODSThis study was based on participants aged 62-81 years from the Cooperative Health Research in the Region of Augsburg (KORA) F4/FF4 cohort, with a mean follow-up of 6.5 years. The predictive value of systemic levels of eight biomarkers of inflammation was assessed for incident DSPN in 133 incident case subjects and 397 individuals without incident DSPN, and for DSPN progression in 57 patients with prevalent DSPN at both time points. RESULTSHigher hs-CRP, interleukin (IL)-6, tumor necrosis factor (TNF)-a, IL-1 receptor antagonist (IL-1RA), and soluble intercellular adhesion molecule (sICAM-1) and lower adiponectin levels were associated with incident DSPN in age-and sexadjusted analysis; IL-18 and omentin were not. IL-6 (odds ratio 1.31 [95% CI 1.00-1.71]) and TNF-a (odds ratio 1.31 [95% CI 1.03-1.67]) remained associated with incident DSPN after adjusting for known DSPN risk factors. The addition of both cytokines to a clinical risk model improved model fit and reclassification. sICAM-1 and IL-1RA were positively associated with progression of DSPN. CONCLUSIONSSystemic subclinical and vascular inflammation predicted both the onset and progression of DSPN over 6.5 years in an older general population. Thus modulation of inflammatory processes may be relevant to prevent and/or treat diabetic neuropathy.Distal sensorimotor polyneuropathy (DSPN) is the most frequent neurological complication of type 2 diabetes (1). The pathomechanisms leading to the onset and progression of DSPN are not completely understood, which profoundly limits current prevention and treatment. Advanced age and diabetes duration represent the most important known risk factors, but there is increasing evidence that height,

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Section: Il-6 Tnf-a and Incident Dspnsupporting

confidence: 88%

Proinflammatory Cytokines Predict the Incidence and Progression of Distal Sensorimotor Polyneuropathy: KORA F4/FF4 Study

et al. 2017

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“…Again, our result differs from the results of Duksal et al who found no correlations between TNF-α levels and conduction velocities in the studied nerves [47], but who assessed only dorsal sural and medial planter sensory nerves in their study.…”

Section: Discussioncontrasting

confidence: 99%

Tumor necrosis factor alpha in peripheral neuropathy in type 2 diabetes mellitus

Sheikh¹,

Alahmar²,

Salem³

et al. 2019

Egypt J Neurol Psychiatry Neurosurg

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Objective: To compare serum levels of tumor necrosis factor alpha (TNF-α) between type 2 diabetes mellitus patients with and without peripheral neuropathy (PN). Also, to study the relation between peripheral nerves conduction velocity and serum level of TNF-α in those patients. Patients and methods: This study included three groups with 40 patients in each group. Diabetic PN patients (groups I and II) were compared with diabetic patients without PN (group III). Groups I and II differed in the duration of clinical neuropathy with less than 5 years in group I and more than 5 years in group II. All patients were subjected to general and neurological examination, neuropathy symptom score (NSS), neuropathy disability score (NDS), glycosylated hemoglobin (HbA1c), serum level of TNF-α and both sensory and motor nerve conduction study. Results: This study showed raised serum levels of TNF-α in diabetic patients with PN, more with increased duration of neuropathy. TNF-α levels showed statistically significant negative correlation with nerve conduction velocity but positive correlations with each of neuropathy disability score, neuropathy symptom score, and glycosylated hemoglobin. Conclusion: TNF-α might be involved in the pathogenesis of diabetic PN, and its serum level might be used as a biomarker for the severity of diabetic PN.

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“…These markers were further increased in those with painful DN [41], data that are in concert with findings from another study that reported increased IL-2 in participants with neuropathic pain [62]. Duksal et al recently reported that elevated serum levels of IL-6 and IL-10 in patients with prediabetes and T2DM correlated with markers of large nerve fiber sensory and motor axonal damage and with signs of motor nerve demyelination [63]. Since IL-10 is considered an anti-inflammatory cytokine, that negatively regulates TNF-α, one could speculate that the observed increased IL-10 levels in this study could have been a compensatory mechanism.…”

Section: Inflammation and Diabetic Neuropathymentioning

confidence: 58%

Inflammation as a Therapeutic Target for Diabetic Neuropathies

Pop‐Busui

Ang

Holmes³

et al. 2016

Curr Diab Rep

188

126

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Diabetic neuropathies (DNs) are one of the most prevalent chronic complications of diabetes and a major cause of disability, high mortality, and poor quality of life. Given the complex anatomy of the peripheral nervous system and types of fiber dysfunction, DNs have a wide spectrum of clinical manifestations. The treatment of DNs continues to be challenging, likely due to the complex pathogenesis that involves an array of systemic and cellular imbalances in glucose and lipids metabolism. These lead to the activation of various biochemical pathways, including increased oxidative/nitrosative stress, activation of the polyol and protein kinase C pathways, activation of polyADP ribosylation, and activation of genes involved in neuronal damage, cyclooxygenase-2 activation, endothelial dysfunction, altered Na+/K+-ATPase pump function, impaired C-peptide-related signaling pathways, endoplasmic reticulum stress, and low-grade inflammation. This review summarizes current evidence regarding the role of low-grade inflammation as a potential therapeutic target for DNs.

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Role of inflammation in sensory neuropathy in prediabetes or diabetes

Cited by 42 publications

References 29 publications

Proinflammatory Cytokines Predict the Incidence and Progression of Distal Sensorimotor Polyneuropathy: KORA F4/FF4 Study

Proinflammatory Cytokines Predict the Incidence and Progression of Distal Sensorimotor Polyneuropathy: KORA F4/FF4 Study

Tumor necrosis factor alpha in peripheral neuropathy in type 2 diabetes mellitus

Inflammation as a Therapeutic Target for Diabetic Neuropathies

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