Treatment of Diabetic Neuropathy and Neuropathic Pain

Table 1—

Treatment of diabetic neuropathy based on the putative pathogenetic mechanisms

Abnormality Compound Aim of treatment Status of randomized clinical trials
Polyol pathway ↑ Aldose reductase inhibitors Nerve sorbitol ↓
Sorbinil Withdrawn (adverse events)
Tolrestat Withdrawn (adverse events)
Ponalrestat Ineffective
Zopolrestat Withdrawn (marginal effects)
Zenarestat Withdrawn (adverse events)
Lidorestat Withdrawn (adverse events)
Fidarestat Effective in phase II trials
Ranirestat Effective in phase II trial
Epalrestat Marketed in Japan
myo-Inositol ↑ myo-Inositol Nerve myo-inositol ↑ Equivocal
γ-Linolenic acid synthesis ↓ γ-Linolenic acid Essential fatty acids metabolism ↑ Withdrawn (effective: deficits)
Oxidative stress ↑ α-Lipoic acid Oxygen free radicals ↓ Effective in randomized clinical trials (studies ongoing)
Vitamin E Oxygen free radicals ↓ Effective in one randomized clinical trial
Nerve hypoxia ↑ Vasodilators Nerve blood flow ↑
ACE inhibitors Effective in phase II trial
Prostaglandin analogs Effective in phase II trial
PhVEGF165 gene transfer Angiogenesis ↑ Phase III trial ongoing
Protein kinase C ↑ Protein kinase C β inhibitor (ruboxistaurin) Nerve blood flow ↑ Phase III trial ongoing
C-peptide ↓ C-peptide Nerve blood flow ↑ Effective in phase II trials
Neurotrophism ↓ Nerve growth factor (NGF) Nerve regeneration, growth ↑ Ineffective
BDNF Nerve regeneration, growth ↑ Ineffective
Long-chain fatty acid metabolism ↓ Acetyl-L-carnitine Long-chain fatty acid accumulation ↓
Ineffective
Nonenzymatic glycation ↑ Aminoguanidine Advanced glycation end product accumulation ↓ Withdrawn

This Article

  1. Diabetes Care February 2008 vol. 31 no. Supplement 2 S255-S261
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