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Diabetic peripheral neuropathy.

A K Das1, M V Vijayaraghavan

  • 1Department of Medicine, Jawaharlal Institute of Postgraduate Medical Education and Research, Pondicherry.

The Journal of the Association of Physicians of India
|October 1, 1991
PubMed
Summary

Diabetic neuropathy affects many, potentially caused by sorbitol excess and myoinositol depletion. Reversing intraneuronal edema with aldose reductase inhibitors shows promise for prevention and treatment.

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Area of Science:

  • Neurology
  • Endocrinology
  • Metabolic Disorders

Background:

  • Diabetic neuropathy presents a significant clinical challenge, with peripheral neuropathy affecting approximately 20% of diabetic patients.
  • Current understanding of its aetiopathogenesis involves metabolic factors like sorbitol excess and myoinositol depletion, impacting Na+/K+ ATPase activity and potentially causing intraneuronal edema.
  • Vascular theories, including endoneurial microcapillary pathology and hypoxia, are also considered, with a unifying concept suggesting secondary vascular compromise due to sorbitol-induced edema.

Purpose of the Study:

  • To review current concepts in the aetiopathogenesis of diabetic neuropathy.
  • To discuss proposed research classifications for unifying study results.
  • To evaluate diagnostic methods and potential therapeutic interventions for diabetic neuropathy.

Main Methods:

  • Review of existing literature on diabetic neuropathy aetiopathogenesis, diagnosis, and treatment.
  • Discussion of metabolic and vascular hypotheses.
  • Analysis of diagnostic tools such as quantitative sensory testing, autonomic function testing, and electrodiagnosis.
  • Evaluation of therapeutic strategies including glycemic control, myoinositol supplementation, gangliosides, and aldose reductase inhibitors.

Main Results:

  • Tight glycemic control is objectively documented as beneficial using laboratory parameters.
  • Oral myoinositol supplementation and gangliosides have shown marginal improvement in diabetic neuropathy.
  • Intraneuronal edema is implicated in pathogenesis, with potential reversal by aldose reductase inhibitors.

Conclusions:

  • Aldose reductase inhibitors offer potential for preventing and treating diabetic neuropathy by reversing intraneuronal edema.
  • Further research and standardized classifications are needed to unify findings and advance treatment strategies.
  • A comprehensive approach addressing metabolic and vascular factors is crucial for managing diabetic neuropathy.

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