J-F Lemay1, S Lanzinger2,3, D Pacaud1, P L Plener4, A Fürst-Burger5, T Biester6, D Hilgard7, E Lilienthal8, A Galler9, G Berger10, R W Holl2,3. 1. Department of Paediatrics, Alberta Children's Hospital/Cumming School of Medicine (University of Calgary), Calgary, Canada. 2. University of Ulm, Institute of Epidemiology and Medical Biometry, Central Institute for Biomedical Technology, Ulm, Germany. 3. German Centre for Diabetes Research (DZD), Munich, Germany. 4. Department of Child and Adolescent Psychiatry and Psychotherapy, University of Ulm, Ulm, Germany. 5. Pediatric/Diabetes Clinic, Braunschweig, Germany. 6. AUF DER BULT, Diabetes Centre for Children and Adolescents, Hannover, Germany. 7. Department of Paediatrics, Gemeinschaftskrankenhaus Herdecke, Herdecke, Germany. 8. RUHR-University, Diabetology, Bochum, Germany. 9. Charité - University Medicine of Berlin, Pediatric Endocrinology and Diabetology, Berlin, Germany. 10. Medical University Vienna, Dept. of Pediatric and Adolescent Medicine, Vienna, Austria.
Abstract
BACKGROUND: A paucity of reports in the literature exists concerning the co-existence between autism spectrum disorder (ASD) and type 1 diabetes (T1D). OBJECTIVE: To compare clinical characteristics, diabetes management and metabolic control in youth with T1D and ASD (T1D-ASD) with youth without ASD (T1D-non ASD). METHODS: Using the German/Austrian diabetes patient follow-up registry, this study analyzed aggregated data from the last available year of observation for each patient with T1D, ages 1-20 with consistent data on insulin regimen and glycated hemoglobin (A1C), between January, 2005 and March, 2017. RESULTS: From 61 749 patients, 150 (0.24%) were identified as T1D-ASD. Non-adjusted comparisons showed similar results for mean age at onset and duration of diabetes, but not for gender (male: T1D-ASD: 85.3%; T1D-non ASD: 52.8%; P < .001). Unadjusted comparisons showed no difference for severe hypoglycemia, diabetic ketoacidosis, insulin doses, insulin pump therapy, and body mass index. A statistical difference was observed for A1C (P-value .01) and in the number of blood glucose (SMBG) tests/day (median [interquartile range]: T1D-ASD 6.0 [4.4-7.0]; T1D-non ASD 5.0 [4.4-7.0]; P-value < .001). After adjusting for age, gender, duration of diabetes, and year of observation, only SMBG remained significant (P-value .003). T1D-ASD used psycho-stimulants (15.3% vs 2.2%; P-value < .001), antipsychotics (10.7% vs 0.6%; P-value < .001), and antidepressive medications (3.6% vs 0.7%; P-value < .001) more frequently. CONCLUSION: Metabolic control was similar in the T1D-ASD group compared to T1D-non ASD despite their comorbidity. Awareness of ASD remains important in T1D treatment, as both conditions require long-term multi-disciplinary medical follow-up for optimal outcomes.
BACKGROUND: A paucity of reports in the literature exists concerning the co-existence between autism spectrum disorder (ASD) and type 1 diabetes (T1D). OBJECTIVE: To compare clinical characteristics, diabetes management and metabolic control in youth with T1D and ASD (T1D-ASD) with youth without ASD (T1D-non ASD). METHODS: Using the German/Austrian diabetespatient follow-up registry, this study analyzed aggregated data from the last available year of observation for each patient with T1D, ages 1-20 with consistent data on insulin regimen and glycated hemoglobin (A1C), between January, 2005 and March, 2017. RESULTS: From 61 749 patients, 150 (0.24%) were identified as T1D-ASD. Non-adjusted comparisons showed similar results for mean age at onset and duration of diabetes, but not for gender (male: T1D-ASD: 85.3%; T1D-non ASD: 52.8%; P < .001). Unadjusted comparisons showed no difference for severe hypoglycemia, diabetic ketoacidosis, insulin doses, insulin pump therapy, and body mass index. A statistical difference was observed for A1C (P-value .01) and in the number of blood glucose (SMBG) tests/day (median [interquartile range]: T1D-ASD 6.0 [4.4-7.0]; T1D-non ASD 5.0 [4.4-7.0]; P-value < .001). After adjusting for age, gender, duration of diabetes, and year of observation, only SMBG remained significant (P-value .003). T1D-ASD used psycho-stimulants (15.3% vs 2.2%; P-value < .001), antipsychotics (10.7% vs 0.6%; P-value < .001), and antidepressive medications (3.6% vs 0.7%; P-value < .001) more frequently. CONCLUSION: Metabolic control was similar in the T1D-ASD group compared to T1D-non ASD despite their comorbidity. Awareness of ASD remains important in T1D treatment, as both conditions require long-term multi-disciplinary medical follow-up for optimal outcomes.
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