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2024 (English)In: Diabetes/Metabolism Research Reviews, ISSN 1520-7552, E-ISSN 1520-7560, Vol. 40, no 5, article id e3825Article in journal (Refereed) Published
Abstract [en]
AIMS: We have evaluated long-term weighted mean HbA1c (wHbA1c), HbA1c variability, diabetes duration, and lipid profiles in relation to the development of diabetic peripheral neuropathy (DPN), nephropathy, and retinopathy in childhood-onset type 1 diabetes.
MATERIALS AND METHODS: In a longitudinal cohort study, 49 patients (21 women) with childhood-onset type 1 diabetes were investigated with neurophysiological measurements, blood tests, and clinical examinations after a diabetes duration of 7.7 (±3.3) years (baseline) and followed with repeated examinations for 30.6 (±5.2) years. We calculated wHbA1c by integrating the area under all HbA1c values since the diabetes diagnosis. Lipid profiles were analysed in relation to the presence of DPN. Long-term fluctuations of HbA1c variability were computed as the standard deviation of all HbA1c measurements. Data regarding the presence of other diabetes complications were retrieved from medical records.
RESULTS: In this follow-up study, 51% (25/49) of the patients fulfilled electrophysiological criteria for DPN. In nerve conduction studies, there was a deterioration in the amplitudes and conduction velocities for the median, peroneal, and sural nerves over time. Patients with DPN had a longer duration of diabetes, higher wHbA1c, and increased HbA1c variability. The lowest wHbA1c value associated with the development of DPN was 62 mmol/mol (7.8%). The presence of albuminuria and retinopathy was positively correlated with the presence of neuropathy.
CONCLUSIONS: More than half of the patients had developed DPN after 30 years. None of the patients who developed DPN had a wHbA1c of less than 62 mmol/mol (7.8%).
Place, publisher, year, edition, pages
WILEY, 2024
Keywords
HbA1c target, Cohort study, Longitudinal study, Peripheral neuropathy, Type 1 diabetes
National Category
Endocrinology and Diabetes
Identifiers
urn:nbn:se:liu:diva-206494 (URN)10.1002/dmrr.3825 (DOI)001248200100001 ()38878301 (PubMedID)2-s2.0-85196248140 (Scopus ID)
Note
Funding agencies: Linköping University, Sweden, ALF grants (Swedish governmental funding of clinical research), and the Medical Research Council of Southeast Sweden No: RÖ 697211, RÖ-799001, RÖ899391
2024-08-162024-08-162025-08-12Bibliographically approved