Endocrine Abstracts

Background and aims: Diabetic neuropathy is a common complication of type 1 diabetes. In this study we investigated the importance of long-term metabolic control for the development of diabetic neuropathy in patients with type 1 diabetes diagnosed in childhood.

Materials and methods: Longitudinal cohort study. Twenty-five patients (9 women 16 men) were studied three times with neurophysiological measurements and clinical examinations. At baseline the patients were 15.7±3.7 yrs. (range 7-22) and had diabetes duration of 7.7±3.3 yrs. (range 4-15). At the first follow up 2007-2009 the patients were 29±3.9 yrs. (range 20-35), and had a diabetes duration of 21.6±4.3 yrs. (range 10-31). At the second follow up 2017-2018, the patients were 38.6±3.7 yrs. (range 31-4) and had a diabetes duration of 31.2±4.7 yrs. (range 20-39). The assessment of neurological symptoms followed a standardized process. A neuropathy impairment assessment (NIA) was used to evaluate the signs of diabetic neuropathy. Nerve conduction tests were carried out according to standard techniques. The presence of clinical diabetic neuropathy was determined by a staged approach according to established criteria. Subclinical neuropathy is defined as an electrophysiological abnormality of nerve function without clinical symptoms or signs.

Results: At the initial examination, all patients were free of clinical or subclinical neuropathy. At the first follow up, ten patients 10/25 (40%) had developed clinical (n=5) or subclinical neuropathy (n=5) and they had significantly higher HbA1c, 77.4±16.2 mmol/mol, than the 15 patients without neuropathy, 60.3±8.6 mmol/mol, P=0.022. At the second follow up fifteen patients15/25 (56%) fulfilled the criteria of clinical (n=9) or subclinical neuropathy (n=6). At the second follow up, HbA1c in the ten patients with diabetic neuropathy decreased from 77.4±16.2 mmol/mol at the first follow up to 64.2±16.5 mmol/mol at the second follow up, P=0.013. The additional group of five patients who developed neuropathy between the first and second follow up reduced their HbA1c from 72.0±10.8 mmol/mol to 57.8±14.1 mmol/mol, P=0.006. Taken together, at the second follow up, the difference in HbA1c levels between the 15 patients with neuropathy, 61.4±10.5 mmol/mol, and the 10 patients without neuropathy, 59.6±13.6 mmol/mol, was no longer significant.

Conclusion: The prevalence of diabetic neuropathy in the patient cohort increased with longer diabetes duration and progressed to clinical neuropathy in several cases despite a better metabolic control at the last follow up. The study indicates that an inadequate glycaemic control at early stages of the disease is a risk factor for developing diabetic neuropathy.