Peripheral nerve dysfunction and its correlation to interleukin-6 level in obese patients

Abstract

Abstract Background Obesity is now a worldwide health problem that predisposes to development of numerous complications, one of which is peripheral neuropathy (PN). Elevated interleukin-6 (IL-6) cytokine levels associating the chronic inflammatory state in obesity is thought to play a major role in obesity complications. Methods We conducted a Cross-sectional study on 30 obese patients and 10 matched healthy lean controls. All participants were subjected to full history taking, neurological examination, motor and sensory peripheral nerve conduction studies (NCS). Serum IL-6 levels were assessed using a commercially available ELISA. Laboratory investigations such as glycated haemoglobin, thyroid profile, liver and kidney function tests were done to exclude other known causes of PN. Results Radial, Posterior Tibial and Peroneal nerves had statistically significantly lower motor amplitudes in obese groups compared to control group. Sensory amplitudes of Median nerve showed statistically significant lower values in obese group with PN compared to control group. Conduction velocities (CV) of Ulnar nerve (motor and sensory) and sensory Median nerve showed statistically significant lower CVs in the obese group with PN compared to obese group without PN. Motor Ulnar nerve CV showed highly statistically significant higher velocities in the obese group without PN compared to control group. Posterior Tibial nerve distal motor latencies and Sensory nerve peak latencies of Median nerve had statistically significant higher values in obese group with PN compared to obese group without PN while statistically significant lower sensory peak latencies of Radial nerve were found in obese group without PN compared to control group. Regarding serum IL-6 levels, highly statistically significant higher levels were found in either obese groups when compared to the control group while no statistical significant difference was present between both obese groups and no correlation was found between serum IL-6 and NCS parameters in obese group with PN. Conclusion Our study revealed that despite only 6.667% of our non diabetic obese patients complained of symptoms of PN, by NCS 66.67% of patients were found to have electrophysiological evidence of PN while the remaining 33.33% of patients showed no evidence of PN and no correlation was found between serum IL-6 levels and nerve conduction parameters changes in obese patients diagnosed with PN.