Diabetes is a common cause of polyneuropathy. Cardiac arrhythmias and markedly increased mortality rate have been demonstrated in patients with diabetic neuropathy and also demonstrated that abnormally prolonged QT dispersion interval (QTd) is associated with a higher risk of ventricular arrhythmias and sudden death. We investigated the efficacy and tolerability of L-carnitine (LC) in the treatment of diabetic neuropathy and ventricular dispersion, mainly by evaluating the effects of treatment on electrophysiological parameters. Materials and methods: We recruited 30 patients with type I or type II diabetes (mean age: 60 ± 9 years, range: 36-75; 18 males, 12 females) meeting clinical and neurophysiological criteria for diabetic neuropathy. All of the patients were given LC 2 g/day for 10 months. Blood glucose regulation was maintained by diet, oral antidiabetic, or insulin. To determine the nerve functions electrophysiologically, superficial electrode distal latency, amplitude, nerve conduction velocity in median and ulnar nerves in the upper extremities and peroneal, tibial and sural nerves in the lower extremities and F response in motor nerves were studied. Resting 12-lead electrocardiograms were recorded for measurements of QTd, corrected QTd (QTcd), JT dispersion (JTd), and corrected JT dispersion (JTcd). Results: After 10 months of treatment, median, ulnar, and tibial nerves' motor nerve conduction velocities (P < 0.05) and M-wave amplitudes (P < 0.05) increased; distal latencies and the F-wave latencies (P < 0.05) decreased; ulnar, sural, and median sensory nerve action potential amplitude (P < 0.01) and nerve conduction velocities (P < 0.05) increased; distal latencies (P < 0.05) decreased; and , QTd, QTcd, JTd, and JTcd (P < 0.05) decreased significantly when compared to basal values. The greatest changes in sensory nerve action potential amplitude and ventricular dispersion parameters were observed in the sensory sural nerve and QTcd, respectively. LC was well tolerated over the study period. Conclusion: LC, well tolerated by diabetic patients, may improve peripheral neuropathy and ventricular dispersion and may be useful in preventing the increased incidence of arrhythmias and sudden death observed in such patients. Larger clinical trials are needed to confirm these data before changes to clinical practice can be advocated.

Diabetes is a common cause of polyneuropathy. Cardiac arrhythmias and markedly increased mortality rate have been demonstrated in patients with diabetic neuropathy and also demonstrated that abnormally prolonged QT dispersion interval (QTd) is associated with a higher risk of ventricular arrhythmias and sudden death. We investigated the efficacy and tolerability of L-carnitine (LC) in the treatment of diabetic neuropathy and ventricular dispersion, mainly by evaluating the effects of treatment on electrophysiological parameters. Materials and methods: We recruited 30 patients with type I or type II diabetes (mean age: 60 ± 9 years, range: 36-75; 18 males, 12 females) meeting clinical and neurophysiological criteria for diabetic neuropathy. All of the patients were given LC 2 g/day for 10 months. Blood glucose regulation was maintained by diet, oral antidiabetic, or insulin. To determine the nerve functions electrophysiologically, superficial electrode distal latency, amplitude, nerve conduction velocity in median and ulnar nerves in the upper extremities and peroneal, tibial and sural nerves in the lower extremities and F response in motor nerves were studied. Resting 12-lead electrocardiograms were recorded for measurements of QTd, corrected QTd (QTcd), JT dispersion (JTd), and corrected JT dispersion (JTcd). Results: After 10 months of treatment, median, ulnar, and tibial nerves' motor nerve conduction velocities (P < 0.05) and M-wave amplitudes (P < 0.05) increased; distal latencies and the F-wave latencies (P < 0.05) decreased; ulnar, sural, and median sensory nerve action potential amplitude (P < 0.01) and nerve conduction velocities (P < 0.05) increased; distal latencies (P < 0.05) decreased; and , QTd, QTcd, JTd, and JTcd (P < 0.05) decreased significantly when compared to basal values. The greatest changes in sensory nerve action potential amplitude and ventricular dispersion parameters were observed in the sensory sural nerve and QTcd, respectively. LC was well tolerated over the study period. Conclusion: LC, well tolerated by diabetic patients, may improve peripheral neuropathy and ventricular dispersion and may be useful in preventing the increased incidence of arrhythmias and sudden death observed in such patients. Larger clinical trials are needed to confirm these data before changes to clinical practice can be advocated.