Current Options and Perspectives in the Treatment of Diabetic Neuropathy

Abstract

We aimed to summarise recent advances in the therapy of diabetic neuropathy. Although all therapeutic choices in the treatment of diabetes mellitus itself are based on clear pathophysiological basis, this approach is less present in the treatment of the "forgotten complication", diabetic neuropathy. As part of pathogenetic oriented treatment, the role of glycemic control and cardiovascular risk factors are reviewed. The mode of action of benfotiamine is based on inhibition of key alternative pathways, including the polyol, hexosamine, protein-kinase-C pathways, and inhibition of advanced glycation end products formation, just as on activation of transketolase. Alpha- lipoic-acid is considered as the most potent antioxidant. Other forms of pathogenetic oriented treatment, including actovegin, will be summarised. The anticonvulsants gabapentin and pregabalin, as well as the antidepressant duloxetine represent the most important new drugs among agents for symptomatic relief. Most likely, we should offer combination treatment to our patients much more often, first of all combination of pathogenetic and symptomatic drugs. Finally, the broad spectrum of non-pharmacological treatment will be reviewed.

Risk Factors and Comorbidities in Diabetic Neuropathy: An Update 2015

“…Secondary risk factors are smoking and prediabetes [1,21,60,63]. Platelet activation [79][80][81][82], oxidative stress [65][66][67][68][69][70][71][72][73][74], low vitamin D [83,84], insulin resistance [58], and genetic factors [100][101][102][103][104][105][106] play another supplementary role, but, for the time being, there are limited options for intervention. A suggestion for targeting insulin resistance originates from the study by Pop-Busui et al, showing that reduced incident DSPN is less frequent in T2D patients receiving insulin-sensitizing oral agents (66%) than in those receiving insulinproviding treatment (66% vs. 72%, respectively, p = 0.02) [155].…”

“…Experimental evidence suggests that oxidative stress is connected with DSPN [65][66][67][68]. Numerous studies have reported associations between systemic markers of oxidative stress and DSPN in diabetic patients.…”

Why Not to Use the Handgrip Test in the Assessment of Cardiovascular Autonomic Neuropathy Among Patients with Diabetes Mellitus?

“…Alpha-lipoic acid, the most powerful pathogenetic therapeutic option of diabetic peripheral neuropathy [40][41][42] is also considered as the best choice for the treatment of CAN [43]. Alpha-lipoic acid enhances endoneurial blood flow by preventing the inhibition of nitric oxide synthetase and this way precludes ischaemic damage to nerve tissues [41].…”

“…Alpha-lipoic acid, the most powerful pathogenetic therapeutic option of diabetic peripheral neuropathy [40][41][42] is also considered as the best choice for the treatment of CAN [43]. Alpha-lipoic acid enhances endoneurial blood flow by preventing the inhibition of nitric oxide synthetase and this way precludes ischaemic damage to nerve tissues [41]. Another pathogenetic option is the transketolase activator benfotiamine, inhibiting harmful alternative metabolic pathways, such as advanced glycation end product formation, the hexosamin and the protein-kinase-C pathways [44], as well as the polyol pathway [45].…”

Natural History of Corneal Nerve Morphology in Mild Neuropathy Associated With Type 1 Diabetes: Development of a Potential Measure of Diabetic Peripheral Neuropathy

“…Accurate detection and estimation of progression are needed, especially to test putative treatments, which may alleviate the condition, and/or prevent or delay the development of sequelae. As reviewed in more detail elsewhere, 15,16 based on the pathogenesis of DPN, several potential therapeutic approaches have been developed targeting these mechanisms; however, apart from glucose control and pain management, currently there is no approved treatment for DPN. 15,17 Lack of a sensitive, accurate, and reliable clinical end point has been one of the obstacles in mounting treatment trials for DPN.…”