ABSTRACT
The Danish Paediatric Society presents the first Danish definition of fetal alcohol spectrum disorders (FASD) in a new guideline. FASD is an umbrella term for conditions caused by prenatal alcohol exposure. To varying degrees, fetal alcohol damages manifest as physical defects, characteristic facial features and poor growth, as well as behavioural and cognitive disorders. It requires both somatic and psychological evaluation to identify these damages. Early diagnosis and identification of problems are important for prognosis as professional care has a positive preventive effect on comorbidities.
Subject(s)
Fetal Alcohol Spectrum Disorders , Comorbidity , Denmark , Early Diagnosis , Fetal Alcohol Spectrum Disorders/classification , Fetal Alcohol Spectrum Disorders/diagnosis , Fetal Alcohol Spectrum Disorders/etiology , Fetal Alcohol Spectrum Disorders/pathology , Humans , Practice Guidelines as Topic , Societies, MedicalABSTRACT
OBJECTIVE: To validate the partial remission (PR) definition based on insulin dose-adjusted HbA1c (IDAA1c). SUBJECTS AND METHODS: The IDAA1c was developed using data in 251 children from the European Hvidoere cohort. For validation, 129 children from a Danish cohort were followed from the onset of type 1 diabetes (T1D). Receiver operating characteristic curve (ROC) analysis was used to evaluate the predictive value of IDAA1c and age on partial C-peptide remission (stimulated C-peptide, SCP > 300 pmol/L). RESULTS: PR (IDAA1c ≤ 9) in the Danish and Hvidoere cohorts occurred in 62 vs. 61% (3 months, p = 0.80), 47 vs. 44% (6 months, p = 0.57), 26 vs. 32% (9 months, p = 0.32) and 19 vs. 18% (12 months, p = 0.69). The effect of age on SCP was significantly higher in the Danish cohort compared with the Hvidoere cohort (p < 0.0001), likely due to higher attained Boost SCP, so the sensitivity and specificity of those in PR by IDAA1c ≤ 9, SCP > 300 pmol/L was 0.85 and 0.62 at 6 months and 0.62 vs. 0.38 at 12 months, respectively. IDAA1c with age significantly improved the ROC analyses and the AUC reached 0.89 ± 0.04 (age) vs. 0.94 ± 0.02 (age + IDAA1c) at 6 months (p < 0.0004) and 0.76 ± 0.04 (age) vs. 0.90 ± 0.03 (age + IDAA1c) at 12 months (p < 0.0001). CONCLUSIONS: The diagnostic and prognostic power of the IDAA1c measure is kept but due to the higher Boost stimulation in the Danish cohort, the specificity of the formula is lower with the chosen limits for SCP (300 pmol/L) and IDAA1c ≤9, respectively.
Subject(s)
Diabetes Mellitus, Type 1/diagnosis , Hyperglycemia/prevention & control , Hypoglycemic Agents , Insulin Resistance , Insulin-Secreting Cells/drug effects , Insulin , Prediabetic State/diagnosis , Adolescent , Age Factors , C-Peptide/blood , Child , Child, Preschool , Cohort Studies , Denmark , Diabetes Mellitus, Type 1/blood , Diabetes Mellitus, Type 1/drug therapy , Diabetes Mellitus, Type 1/metabolism , Diagnosis, Differential , Female , Glycated Hemoglobin/analysis , Humans , Hypoglycemic Agents/administration & dosage , Infant , Insulin/administration & dosage , Insulin/metabolism , Insulin Secretion , Insulin-Secreting Cells/metabolism , Male , Prediabetic State/blood , Prediabetic State/drug therapy , Prediabetic State/metabolism , Remission Induction , Sensitivity and SpecificityABSTRACT
The purpose of the present study is to explore the progression of type 1 diabetes (T1D) in Danish children 12 months after diagnosis using Latent Factor Modelling. We include three data blocks of dynamic paraclinical biomarkers, baseline clinical characteristics and genetic profiles of diabetes related SNPs in the analyses. This method identified a model explaining 21.6% of the total variation in the data set. The model consists of two components: (1) A pattern of declining residual ß-cell function positively associated with young age, presence of diabetic ketoacidosis and long duration of disease symptoms (Pâ=â0.0004), and with risk alleles of WFS1, CDKN2A/2B and RNLS (Pâ=â0.006). (2) A second pattern of high ZnT8 autoantibody levels and low postprandial glucagon levels associated with risk alleles of IFIH1, TCF2, TAF5L, IL2RA and PTPN2 and protective alleles of ERBB3 gene (Pâ=â0.0005). These results demonstrate that Latent Factor Modelling can identify associating patterns in clinical prospective data--future functional studies will be needed to clarify the relevance of these patterns.