<p>Diabetic neuropathy (DN) is a common microvascular complication of diabetes mellitus. Around 50% of patients suffer from this. It is characterised by progressive nerve damage, leading to pain, numbness and neurological problems. This extensive review discusses the complex pathophysiological processes underlying DN, supported by chronic hyperglycaemia, oxidative stress, inflammation, mitochondrial impairment, and microvascular injury, and the importance of early identification and targeted treatment. The importance of early detection and the application of specific treatment methods has been highlighted as crucial to minimising disease burden. Potential biomarkers, including nerve growth factor (NGF), inflammatory cytokines, methylglyoxal, and exosomal microRNAs, as well as emerging diagnostic tools such as intraepidermal nerve fibre density (IENFD) assessment, high-resolution ultrasound, and quantitative sensory testing (QST), provide increased specificity for early diagnosis. Therapeutically, DN management can include first-line pharmacological agents such as duloxetine, pregabalin, or TCAs. Second line and newer drugs like sodium channel blockers like lacosamide, ALA, cannabinoids and tapentadol are gaining popularity. Also, new disease-modifying strategies include SGLT2 inhibitors and GLP-1 receptor agonists that offer glycemia-independent neuroprotection, whereas medications such as bardoxolone methyl, pentoxifylline, and resveratrol modulate oxidative and inflammatory signalling. Regenerative medicinal interventions such as stem cell and exosome therapy, gene therapy, and CRISPR-based gene editing hold promise for reversing neuropathy. Non-pharmacological modalities such as low-level laser therapy, electroacupuncture, and neuromodulation further broaden the therapeutic repertoire. Thus, early screening and targeted treatments are best for preventing, curing, and reversing disease progression, restoring function, and optimising quality of life in patients with DN.</p>

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Diabetic Neuropathy: Evolving Paradigms in Diagnosis and Therapy

  • Sarthak Manna,
  • Nirvika Paul,
  • Srikanta Guria,
  • Srilagna Chatterjee,
  • Madhusudan Das,
  • Sudakshina Ghosh

摘要

Diabetic neuropathy (DN) is a common microvascular complication of diabetes mellitus. Around 50% of patients suffer from this. It is characterised by progressive nerve damage, leading to pain, numbness and neurological problems. This extensive review discusses the complex pathophysiological processes underlying DN, supported by chronic hyperglycaemia, oxidative stress, inflammation, mitochondrial impairment, and microvascular injury, and the importance of early identification and targeted treatment. The importance of early detection and the application of specific treatment methods has been highlighted as crucial to minimising disease burden. Potential biomarkers, including nerve growth factor (NGF), inflammatory cytokines, methylglyoxal, and exosomal microRNAs, as well as emerging diagnostic tools such as intraepidermal nerve fibre density (IENFD) assessment, high-resolution ultrasound, and quantitative sensory testing (QST), provide increased specificity for early diagnosis. Therapeutically, DN management can include first-line pharmacological agents such as duloxetine, pregabalin, or TCAs. Second line and newer drugs like sodium channel blockers like lacosamide, ALA, cannabinoids and tapentadol are gaining popularity. Also, new disease-modifying strategies include SGLT2 inhibitors and GLP-1 receptor agonists that offer glycemia-independent neuroprotection, whereas medications such as bardoxolone methyl, pentoxifylline, and resveratrol modulate oxidative and inflammatory signalling. Regenerative medicinal interventions such as stem cell and exosome therapy, gene therapy, and CRISPR-based gene editing hold promise for reversing neuropathy. Non-pharmacological modalities such as low-level laser therapy, electroacupuncture, and neuromodulation further broaden the therapeutic repertoire. Thus, early screening and targeted treatments are best for preventing, curing, and reversing disease progression, restoring function, and optimising quality of life in patients with DN.