1%) We labelled a good improvement particularly in sensory nerve

1%). We labelled a good improvement particularly in sensory nerve conduction; most of the patients had an increment ≥10%. Table I Parameters pre- and post-treatment with variation in the whole samplea Less than 10% of patients retained stable measurements in each of the three parameters and worsening of the measured parameters was not observed in any patient (figure 1). Fig. 1 The percentages of patients that improved, remained stable or worsened in the measured parameters after treatment. MNCMNC= motor nerve conduction; SNC = sensory nerve conduction; VAS = visual analog scale. Fifty patients were used for safety analysis and no adverse event occurred during the study. Discussion

DN is a neuropathic FK506 disorder that is associated with diabetes. This condition is thought to result from diabetic microvascular injury involving small blood vessels that supply the nerves (vasa nervorum). After all, DN is a degenerative pathology with a progressively disabling course, affecting all peripheral nerves: pain fibers, motor neurons, and autonomic nerves.[26] It can therefore affect all organs and systems since all are innervated. Though therapies are available to alleviate the symptoms of DN, few options are available to eliminate the root causes. The immense physical, psychological, and economic costs of DN underline the need for causally

targeted therapies. In fact, causal treatments aim at slowing down pathology progression besides reducing use of analgesics and improving nerve deficits.[27] ALA is a powerful antioxidant and several studies — including the FRAX597 SYDNEY2 trial — have demonstrated an improvement in neuropathic

symptoms and deficits.[9] Results of a meta-analysis[28] provided evidence that treatment with ALA 600 mg/day over 5 weeks is safe and significantly improves both neuropathic symptomatology and neuropathic deficits to a clinically meaningful degree Tyrosine-protein kinase BLK in diabetic patients with symptomatic polyneuropathy. SOD protects nerves from injury in cell culture and in animal models of DN.[29] Direct activity on nerve NCT-501 fibers exposed to oxidative stress and indirect activity targeting vasa nervorum make SOD a powerful adjuvant tool in the treatment of DN. Our diagnostic group aims to detect specific sensory profiles through clinical examination, questionnaires dedicated to neuropathic pain and laboratory tools. A new oral formulation combining ALA and SOD was investigated in this prospective pilot study, through assessment of changes in nerve conduction velocity and patients’ symptomatology. Previous studies reported that one potential limitation of the standard electrophysiological techniques is in detecting therapeutic benefit. Our study stated that the improvement of nerve conduction velocity (objective data) matches the improvement of perceived pain in diabetic patients (subjective data).

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