ESPE Abstracts (2014) 82 P-D-2-1-321

ESPE2014 Poster Category 2 Diabetes (11 abstracts)

Interaction of Pubertal Development and Metabolic Control in 1303 Adolescents with Diabetes Mellitus Type 1

Michaela Hamm a , Bettina Gohlke a , Joachim Wölfle a , Katharina Fink b , Katja Konrad c , Tilman Rohrer d , Sabine Hofer e & Reinhard Holl b


aPediatric Endocrinology and Diabetology, Children’s Hospital, University Bonn, Bonn, Germany; bDepartment of Epidemiology, University Ulm, Ulm, Germany; cPediatric Endocrinology and Diabetology, Children’s Hospital, University Essen, Essen, Germany; dPediatric Endocrinology and Diabetology, Children’s Hospital, University Homburg, Homburg/Saar, Germany; ePediatric Endocrinology and Diabetology, Children’s Hospital, University Innsbruck, Innsbruck, Austria


Background: T1DM may influence growth and pubertal development and vice versa. Delayed pubertal development and reduced final height are known to be associated with inadequate metabolic control. Many factors including insulin resistance during puberty and insufficient adherence may be responsible for increasing HbA1c.

Objective: Is pubertal growth spurt associated with an increase of HbA1c? Are there gender differences in metabolic control during puberty? Is the pubertal growth spurt impaired in patients with T1DM compared to German reference data?

Methods: 1303 complete longitudinal patient data out of a diabetes follow up program could be analysed over a period of 9 years. Inclusion criteria were continuous recording of height and HbA1c every 6 months from the age of 7–16 years in patients with T1DM. Exclusion criteria were celiac disease, eating disorders, steroid or GH therapy, <3 months duration of disease, BMI<3rd or >97th percentile at start of documentation.

Results: HbA1c levels increased continuously from 7.3% at 7 years to 8.4% at 16 years of age. HbA1c levels of boys were lower except for 1.5 years between 13.5 to 15 years. Highest HbA1c increase in boys (Δ HbA1c 0.38 between 12 and 14 years) was associated with maximum growth spurt. In contrast, in girls main HbA1c increase was observed postpubertal (15–16 years). Growth velocity during puberty was impaired. In boys mean peak growth velocity was reduced by 1.1 cm. Growth velocity in girls declined rapidly after maximum growth spurt.

Conclusion: HbA1c increase in puberty is caused by a complex interaction consisting of physiological and psychological reasons. Gender differences could be explained by higher BMI-SDS, greater insulin resistance, higher prevalence of eating disorders und insulin purging in females. In turn worsening of metabolic control reflected by HbA1c increase is associated with reduced growth velocity.

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