We retrieved from our patient database a retrospective cohort of 398 children and adolescents diagnosed with type 1 diabetes between January 1997 and December 2018 and followed up in the pediatric diabetes clinic of our tertiary health care center (Cliniques universitaires Saint-Luc, Brussels). The study was approved by the local ethical committee (reference CHE:11/JUI/274) and conducted in accordance with the Declaration of Helsinki. Patients eligible were aged between 1 and 18 years and were diagnosed with new-onset T1DM. T1DM was established according to ISPAD guidelines,3 based on symptoms of insulinopenia, elevated blood glucose (BG), positive anti-islet autoantibodies (i.e. GAD65, IA2, and insulin), and lack of family history of genetic diabetes. Exclusion criteria were diabetes onset before the age of 1 year, presence of severe chronic medical conditions before the diagnosis of T1DM (i.e. autoimmune diseases other than type 1 diabetes, active cancer, kidney, liver, or adrenal insufficiency) and use of medication that may affect insulin secretion and/or glucose homeostasis (i.e. corticosteroids, sulfonylurea, incretins, diazoxide, somatostatin, immunomodulatory drugs). Patients with a PR less than 3 months, above 14 months or ongoing at the time of study were also excluded. All patients performed carbohydrate counting and underwent similar dietary education at diagnosis.
Medical records of each patient were reviewed to collect demographic data at diagnosis [i.e. age, gender, date of diagnosis, height, weight, body mass index (BMI)] as well as quarterly follow-up data until 24 months. This included routine clinical and biological parameters [HbA1C levels (%), insulin doses in total daily dose in IU and IU/kg body weight, IDAA1C and GTAA1C scores, number of severe hypoglycemia] and data from glucose monitoring devices [using either continuous glucose monitoring (CGM) or self-monitoring of blood glucose (SMBG)]. The parameters retrieved from CGM or BG meter were average glucose (mg/dl), glucose variability [glycemic SD (mg/dl)], coefficient of variation of glucose (CV, %)], number of glucose measurements, time spent in hypoglycemia (below 70 mg/dl, % total time), number of severe hypoglycemia, time spent in hyperglycemia (above 180 mg/dl, % total time), and time spent in normoglycemia (70–180 mg/dl; % total time) also called time in range (TIR). Body mass index (BMI) was calculated using the formula = body weight (kg)/[height (m)].2Z scores for height and BMI were assessed using Belgian Flemish reference charts.34 (link) Severe hypoglycemia was defined as an alteration of consciousness (with or without coma or convulsion) requiring external assistance from a tier person to actively administer carbohydrates, intramuscular glucagon, or other corrective measures, as described by ISPAD.35 (link)
Medical records of each patient were reviewed to collect demographic data at diagnosis [i.e. age, gender, date of diagnosis, height, weight, body mass index (BMI)] as well as quarterly follow-up data until 24 months. This included routine clinical and biological parameters [HbA1C levels (%), insulin doses in total daily dose in IU and IU/kg body weight, IDAA1C and GTAA1C scores, number of severe hypoglycemia] and data from glucose monitoring devices [using either continuous glucose monitoring (CGM) or self-monitoring of blood glucose (SMBG)]. The parameters retrieved from CGM or BG meter were average glucose (mg/dl), glucose variability [glycemic SD (mg/dl)], coefficient of variation of glucose (CV, %)], number of glucose measurements, time spent in hypoglycemia (below 70 mg/dl, % total time), number of severe hypoglycemia, time spent in hyperglycemia (above 180 mg/dl, % total time), and time spent in normoglycemia (70–180 mg/dl; % total time) also called time in range (TIR). Body mass index (BMI) was calculated using the formula = body weight (kg)/[height (m)].2Z scores for height and BMI were assessed using Belgian Flemish reference charts.34 (link) Severe hypoglycemia was defined as an alteration of consciousness (with or without coma or convulsion) requiring external assistance from a tier person to actively administer carbohydrates, intramuscular glucagon, or other corrective measures, as described by ISPAD.35 (link)
