Maddalena Macedoni1, Tinka Hovnik2, Emil Plesnik3, Primoz Kotnik4, Natasa Bratina2, Tadej Battelino4, Urh Groselj5. 1. Department of Pediatrics, Section on Diabetes and Metabolism, V. Buzzi Children's Hospital, University of Milan, Milan, Italy. 2. University Children's Hospital, UMC Ljubljana, Slovenia. 3. Marand d.o.o., Ljubljana, Slovenia. 4. University Children's Hospital, UMC Ljubljana, Slovenia; Faculty of Medicine, University of Ljubljana, Slovenia. 5. University Children's Hospital, UMC Ljubljana, Slovenia. Electronic address: urh.groselj@kclj.si.
Abstract
BACKGROUND AND AIMS: Limited data is available on the factors influencing the lipid profiles and the prevalence of dyslipidemia in children, adolescents and young adults with type 1 diabetes. We aimed at assessing the influences of metabolic control and ApoE genotypes on lipid profiles and the prevalence of dyslipidemia in children, adolescents and young adults with type 1 diabetes. METHODS: Children, adolescents and young adults with type 1 diabetes from our nationwide cohort attending the annual check-up were prospectively included. Data on metabolic control and expanded lipid profiles were collected, and ApoE genotyping performed. Test for homoscedasticity of continuous variables was followed by ANOVA and Welch's ANOVA tests, and Chi-square test was used for categorical variables with Kruskal-Wallis test as a control. RESULTS: 467 patients were included in the data analysis: 226 female (48.4%), mean age 14.71 ± 5.09 years and diabetes duration 6.74 ± 4.54 years. Mean HbA1c was 61 ± 5 mmoL/mol (7.71 ± 1.22%), with no gender-related differences. Females had higher mean total cholesterol (p < 0.001), LDL-C (p = 0.005), HDL-C (p < 0.001), non-HDL-C (p = 0.003), and ApoB levels (p < 0.001). 26.3% of participants had LDL-C levels above the type 1 diabetes LDL-C-goal of 2.6 mmoL/L, and 19.5% had elevated/borderline-elevated lipoprotein(a) (Lp(a)). HbA1c levels were positively related to higher levels of LDL-C (p = 0.0070) and Lp(a) (p = 0.0020). Participants with ApoE4(e3/e4) allele had higher levels of LDL-C (p = 0.010), independently of HbA1c. CONCLUSIONS: Females and subjects with suboptimal metabolic control had more adverse lipid profiles. ApoE4(e3/e4) alleles were associated with significantly higher LDL-C levels, independently of HbA1c.
BACKGROUND AND AIMS: Limited data is available on the factors influencing the lipid profiles and the prevalence of dyslipidemia in children, adolescents and young adults with type 1 diabetes. We aimed at assessing the influences of metabolic control and ApoE genotypes on lipid profiles and the prevalence of dyslipidemia in children, adolescents and young adults with type 1 diabetes. METHODS:Children, adolescents and young adults with type 1 diabetes from our nationwide cohort attending the annual check-up were prospectively included. Data on metabolic control and expanded lipid profiles were collected, and ApoE genotyping performed. Test for homoscedasticity of continuous variables was followed by ANOVA and Welch's ANOVA tests, and Chi-square test was used for categorical variables with Kruskal-Wallis test as a control. RESULTS: 467 patients were included in the data analysis: 226 female (48.4%), mean age 14.71 ± 5.09 years and diabetes duration 6.74 ± 4.54 years. Mean HbA1c was 61 ± 5 mmoL/mol (7.71 ± 1.22%), with no gender-related differences. Females had higher mean total cholesterol (p < 0.001), LDL-C (p = 0.005), HDL-C (p < 0.001), non-HDL-C (p = 0.003), and ApoB levels (p < 0.001). 26.3% of participants had LDL-C levels above the type 1 diabetesLDL-C-goal of 2.6 mmoL/L, and 19.5% had elevated/borderline-elevated lipoprotein(a) (Lp(a)). HbA1c levels were positively related to higher levels of LDL-C (p = 0.0070) and Lp(a) (p = 0.0020). Participants with ApoE4(e3/e4) allele had higher levels of LDL-C (p = 0.010), independently of HbA1c. CONCLUSIONS: Females and subjects with suboptimal metabolic control had more adverse lipid profiles. ApoE4(e3/e4) alleles were associated with significantly higher LDL-C levels, independently of HbA1c.