Diabetic neuropathy: A focus on small fibres

Malik, Rayaz A.

doi:10.1002/dmrr.3255

Cited by 30 publications

(27 citation statements)

References 31 publications

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“…Peripheral neuropathy is the most frequent chronic complication of DM. The prevalence of peripheral neuropathy in DM ranges from 10% at one year after DM diagnosis to more than 50% during progression of the disease [ 4 , 25 , 123 , 124 ], making diabetic peripheral neuropathy (DPN) the most abundant type of peripheral neuropathy worldwide [ 3 , 4 , 125 ] ( Table 1 ). Diabetic neuropathy that is painful develops in approximately 50% of DM patients with neuropathy [ 126 ].…”

Section: Peripheral Amyloid Neuropathiesmentioning

confidence: 99%

Amyloid Proteins and Peripheral Neuropathy

Asiri

Engelsman

Eijkelkamp

et al. 2020

Cells

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Painful peripheral neuropathy affects millions of people worldwide. Peripheral neuropathy develops in patients with various diseases, including rare familial or acquired amyloid polyneuropathies, as well as some common diseases, including type 2 diabetes mellitus and several chronic inflammatory diseases. Intriguingly, these diseases share a histopathological feature—deposits of amyloid-forming proteins in tissues. Amyloid-forming proteins may cause tissue dysregulation and damage, including damage to nerves, and may be a common cause of neuropathy in these, and potentially other, diseases. Here, we will discuss how amyloid proteins contribute to peripheral neuropathy by reviewing the current understanding of pathogenic mechanisms in known inherited and acquired (usually rare) amyloid neuropathies. In addition, we will discuss the potential role of amyloid proteins in peripheral neuropathy in some common diseases, which are not (yet) considered as amyloid neuropathies. We conclude that there are many similarities in the molecular and cell biological defects caused by aggregation of the various amyloid proteins in these different diseases and propose a common pathogenic pathway for “peripheral amyloid neuropathies”.

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Section: Peripheral Amyloid Neuropathiesmentioning

confidence: 99%

Amyloid Proteins and Peripheral Neuropathy

Asiri

Engelsman

Eijkelkamp

et al. 2020

Cells

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“…Diagnosis of diabetic sensorimotor polyneuropathy is challenging and often made during later stages of disease progression in part due to the lack of methodology that can objectively detect its early stages. 1 The inability to accurately detect and stage the loss of peripheral nerves and function early has likely contributed to the failure of many clinical trials seeking a treatment for diabetic peripheral neuropathy. Recently, the quantification of intraepidermal nerve fiber density in skin biopsies or using corneal confocal microscopy to non-invasively examine the corneal sub-epithelial nerves have emerged as promising techniques for the early detection of nerve fiber loss.…”

Section: Introductionmentioning

confidence: 99%

<p>Progressive Loss of Corneal Nerve Fibers and Sensitivity in Rats Modeling Obesity and Type 2 Diabetes Is Reversible with Omega-3 Fatty Acid Intervention: Supporting Cornea Analyses as a Marker for Peripheral Neuropathy and Treatment</p>

Coppey¹,

Davidson²,

Shevalye³

et al. 2020

DMSO

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Purpose: To determine whether cornea nerve fiber density and/or corneal function are valid markers for early detection and treatment of peripheral neuropathy in rats modeling prediabetes and type 2 diabetes. Methods: High-fat feeding combined without or with low-dose streptozotocin was used to create rat models for prediabetes and type 2 diabetes that were longitudinally studied for loss of structure and function of sensory nerves in the cornea and skin as well as nerve conduction velocity and vascular reactivity of epineurial arterioles. There were three time points examined in each of the three conditions with 12 rats per group. The latest time point (24 weeks of high-fat diet with or without 16 weeks of hyperglycemia) was used to examine reversibility of neuro and vascular pathology following 16 weeks of treatment with menhaden oil, a natural source of long-chain omega-3 polyunsaturated fatty acids. The number of rats in the intervention study ranged from 6 to 17. Results: Our longitudinal study demonstrated that vascular and neural dysfunction associated with obesity or type 2 diabetes occur early and are progressive. Decrease in cornea nerve fiber length and function were valid markers of disease in both the pre-diabetic and diabetic rat models and were more sensitive than decrease in intraepidermal nerve fiber density of the skin and thermal nociception of the hindpaw. Late intervention with menhaden oil significantly reversed both vascular and peripheral nerve damage induced by chronic obesity or type 2 diabetes. Conclusion: These studies provide support for examination of corneal structure and function as an early marker of peripheral neuropathy in prediabetes and type 2 diabetes. Furthermore, we demonstrate that omega-3 polyunsaturated fatty acids derived from fish oil are an effective treatment for peripheral neuropathy that occurs with chronic obesity or type 2 diabetes.

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“…It should also be emphasized that each neurological modality assesses different aspects of diabetic neuropathy, since other tests assess small fiber integrity and other tests large fiber integrity. Sudomotor dysfunction as a result of small fibers damage develops early in the course of DM before large fiber damage and sensory loss (9,10,36,37). SWF assesses large fiber function, the Ipswich touch test both small and large fiber function, pinprick and temperature tests assess small fiber function and vibration tests assess large fiber function.…”

Section: Discussionmentioning

confidence: 99%

“…The use of SWM has been shown to predict future development of DFU ( 33 , 40 ) and according to current guidelines is recommended for identification of people with loss of protective sensation and at risk for DFU ( 7 , 8 ). Nevertheless, it should be emphasized that SWM detects advanced large fiber neuropathy and the current recommendation for the assessment of DPN using SWM testing may need to be reconsidered ( 36 , 37 ). A systematic review and meta-analysis demonstrated that in 3 prospective studies, SWM had a sensitivity 0.66–0.91, a specificity 0.34–0.86, a +PV 0.18–0.39, a −PV of 0.94–0.94, a +LR of 1.4–4.7, and a −LR of 0.3–0.5 ( 33 ).…”

Section: Discussionmentioning

confidence: 99%

Dryness of Foot Skin Assessed by the Visual Indicator Test and Risk of Diabetic Foot Ulceration: A Prospective Observational Study

et al. 2020

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Research Question: Previous cross-sectional studies have shown an association between sudomotor dysfunction and diabetic foot ulceration (DFU). The aim of this prospective multicenter study was to determine the role of dryness of foot skin and of established neurological modalities in the prediction of risk for foot ulceration in a cohort of individuals with diabetes mellitus (DM). Design: The study was conducted from 2012 to 2017. A total of 308 subjects with DM without history of DFU or critical limb ischemia completed the study. Diabetic neuropathy was assessed using the neuropathy symptom score (NSS) and neuropathy disability score (NDS). In a subset of participants, vibration perception threshold (VPT) was evaluated. Dryness of foot skin was assessed by the visual indicator plaster method (IPM). The diagnostic performance of the above neurological modalities for prediction of DFU was tested by receiver operating characteristic curve (ROC) analysis. Results: During the 6-year follow-up, 55 patients (annual ulceration incidence 2.97%) developed DFU. Multivariate Cox-regression analysis after controlling for the effect of age, gender, and DM duration demonstrated that the risk (hazard ratio, 95% confidence intervals) of DFU increased significantly with either abnormal IPM (3.319, 1.460-7.545, p = 0.004) or high (≥6) NDS (2.782, 1.546-5.007, p = 0.001) or high (≥25 volts) VPT (2.587, 1.277-5.242, p = 0.008). ROC analysis showed that all neurological modalities could discriminate participants who developed DFU (p < 0.001). IPM testing showed high sensitivity (0.86) and low specificity (0.49), while high vs. low NDS and VPT showed low sensitivity (0.40 and 0.39, respectively) and high specificity (0.87 and 0.89, respectively) for identification of patients at risk for DFU. Panagoulias et al. Skin Dryness and Foot Ulceration Conclusion: Dryness of foot skin assessed by the IPM predicts the development of DFU. IPM testing has high sensitivity, whereas high NDS and VPT have high specificity in identifying subjects at risk for DFU. The IPM can be included in the screening methods for identification of the foot at risk.

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Diabetic neuropathy: A focus on small fibres

Cited by 30 publications

References 31 publications

Amyloid Proteins and Peripheral Neuropathy

Amyloid Proteins and Peripheral Neuropathy

<p>Progressive Loss of Corneal Nerve Fibers and Sensitivity in Rats Modeling Obesity and Type 2 Diabetes Is Reversible with Omega-3 Fatty Acid Intervention: Supporting Cornea Analyses as a Marker for Peripheral Neuropathy and Treatment</p>

Dryness of Foot Skin Assessed by the Visual Indicator Test and Risk of Diabetic Foot Ulceration: A Prospective Observational Study

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