Neuroprotective potential of insulin pump therapy in type 1 diabetes mellitus — ASN Events
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Neuroprotective potential of insulin pump therapy in type 1 diabetes mellitus (#94)

Natalie Kwai 1 , Ria Arnold 1 , Ann Poynten 2 , Cindy Lin 1 , Matthew Kiernan 3 , Arun Krishnan 1
  1. Translational Neuroscience Facility, School of Medical Sciences, University of New South Wales, Randwick, NSW, Australia
  2. Department of Endocrinology, Prince of Wales Hospital, Randwick, NSW, Australia
  3. Prince of Wales Clinical School, University of New South Wales, Randwick, NSW, Australia

Background: Diabetic peripheral neuropathy(DPN) is a common debilitating complication of diabetes mellitus(DM). While strict glycaemic control through multiple daily insulin injections(MDII) or continuous subcutaneous insulin infusion(CSII) may reduce the risk of DPN development, there have been no studies comparing the neurological effects of MDII and CSII. Previous studies utilizing Nerve excitability testing(NET), a novel technique that provides information on axonal ion channel function have found prominent abnormalities indicative of ion channel dysfunction in type 1 DM patients(T1DM) without clinical neuropathy.

Objectives: To establish if there are differences in NET parameters between T1DM treated with MDII and CSII in the absence of clinical neuropathy.

Methods: 36 T1DM underwent a comprehensive neurological examination to identify the presence of neuropathy. Twenty non-neuropathic T1DM were subsequently recruited and grouped according to insulin delivery method: MDII(n=11, 9M:2F, age 27.3+5.8yrs) or CSII(n=9, 7M:2F, age 28.7+13.6yrs). NET was performed on the median nerve in all patients. Groups were matched for age, gender, HbA1c%, BMI and disease duration. NET was also performed on 20 age-matched normal controls(NC) and independent t tests were carried out between treatment groups and NCs.

Results: T1DMs demonstrated pronounced alteration in numerous excitability parameters reflecting axonal dysfunction compared to NCs. Greater abnormalities in markers of nerve membrane potential were noted in the MDII group compared to NCs, specifically, for superexcitability(p<0.001), subexcitability(p < 0.001) and hyperpolarizing threshold electrotonus at 90-100 ms(p < 0.005). In contrast to the prominent changes noted in MDII patients, there were no significant differences noted between CSII patients and NCs.

Conclusions: T1DM patients treated with MDII exhibited greater alteration in nerve function, when compared to patients treated with CSII. These abnormalities are subclinical and reflect altered membrane potential. Critically, these changes are apparent in the absence of neuropathy and suggest a neuroprotective potential for CSII in T1DM patients.