559-P: Signs of Early Change in Peripheral Axons in People with Early-Onset Type 2 Diabetes Mellitus

Abstract

Introduction: The prevalence of early-onset type 2 diabetes (EOT2D; diagnosed with T2DM before 40 years old), has increased sharply in recent years. Peripheral neuropathy (DPN) is a common and debilitating complication associated with T2DM, and it is also common in EOT2D, even among adolescents. Nerve excitability studies (NES) examine nerve axonal ion channel function; and may allow early detection of axonal dysfunction. The aim of this study was to explore the differences in NES outcomes between a cohort with EOT2D and matched healthy controls. Method: Thirteen participants with EOT2D with no clinical evidence of DPN and 14 matched healthy control participants (HC) were included in the study. Nerve conduction studies (NCS) were used to assess amplitude, latency, and conduction velocity in sural (sensory) and peroneal (motor) nerves. Motor and sensory NES were conducted on the median nerve. NES parameters assessed included strength-duration time constant, threshold electrotonus (TE), current-threshold relationship and recovery cycle. HbA1c was measured. Independent sample t-tests were used to compare the group means ± standard deviations. Results: Participants with EOT2D (F:M 5:8, age 34.1±6.7yr, BMI 31.7±5.4kg∙m-2) differed from matched HC (F:M 6:8, age 32.5±5.1yr, BMI 29.6±4.4kg∙m-2) for HbA1c (EOT2D=6.8±1.0%, HC=5.2±0.3%, p<0.0001). There were no significant between-group differences in any NCS parameters, confirming the absence of clinical neuropathy. Minor changes in sensory axon NES were found in TE, which measures internodal conductances. Sensory depolarizing TE (TEd) at 10-20ms was decreased significantly in the EOT2D group (TEd 10-20ms: EOT2D = 60.1±2.9ms, HC = 62.9±3.0ms, p = 0.02). There were no significant changes in motor NES. Conclusion: Participants with EOT2D and no clinical evidence of DPN may demonstrate minor changes in sensory axonal function. Prospective studies are required to determine the clinical significance and progression of these changes. Disclosure Y. Gu: None. A.R. Harmer: None. S.M. Dennis: None. T. Li: None. H.C. Timmins: None. P. Loh: None. N. Garg: None. T. Dharmadasa: None. J. Wong: Advisory Panel; Self; Sanofi. Speaker’s Bureau; Self; AstraZeneca, Merck & Co., Inc. A. Gauld: None. P.A. Munoz: None. S.B. Park: None. Funding Diabetes Australia; Sydney Local Health District