Continuous glucose monitoring, oral glucose tolerance, and insulin - glucose parameters in adolescents with simple obesity.

In obese adolescents pancreatic beta-cells may not be able to cope with insulin resistance leading to hyperglycemia and type2 diabetes (T2DM To assess oral glucose tolerance, 72-h continuous blood glucose concentrations (CGM) and calculate homeostatic model assessment (HOMA), and the quantitative insulin sensitivity check index (QUICKI) in 13 adolescents with simple obesity (BMI SDS=4 ± 1.06). OGTT performed in 13 obese adolescents (13.47 ± 3 years) revealed 3 cases (23%) with impaired fasting glucose (IFG: fasting glucose >5.6 mmol/L), 4 cases (30%) with impaired glucose tolerance (IGT: 2h blood glucose >7.8 <11.1 mmol/L), and none with diabetes. Using the continuous glucose monitoring system ( CGMS), IFG was detected in 4 cases, the maximum serum blood glucose (BG : 2h or more after meal) was >7.8 and <11.1 mmol/L (IGT) in 9 children (69%) and >11.1 mmol/L (diabetes) in one case (7.6%). Five cases had a minimum BG recorded of <2.7 mmol/L (hypoglycemia). No glycemic abnormality was detected using HbA1C (5.7 ± 0.3%). 11/13 patients had HOMA values >2.6 and QUICKI values <0.35 denoting insulin resistance. Beta cell mass percent (B %) = 200 ± 94.8% and insulin sensitivity values (IS)=50.4 ± 45.5% denoted insulin resistance with hyper-insulinaemia and preserved beta cell mass. In obese adolescents, CGMS is superior to OGTT and HbA1C in detecting glycemic abnormalities, which appears to be secondary to insulin resistance.

Clinical, biochemical and radiological manifestations of severe vitamin d deficiency in adolescents versus children: response to therapy.

OBJECTIVES: to compare clinical, biochemical and radiological manifestations of severe vitamin D deficiency (VDD - serum 25 OH - vitamin D level <10 ng/ml) in adolescents and children and to investigate the effects of an intramuscular injection (IM) of vitamin D3 megadose. DESIGN: in this prospective study 36 adolescents and 45 children with severe VDD were studied. An IM dose (10,000 IU/kg, max 600,000 IU) of cholecalciferol was injected and parameters of calcium homeostasis were measured at intervals of 3 months. RESULTS: at presentation, infants and young children (age 1.9 ± 0.5 years) with severe VDD had enlarged wrist joints (42/45), cranial bossing (39/45), wide anterior fontanel (27/45), Harrison's sulcus (11/45) , chest rosaries (27/45), bow legs (29/45), delayed teething (40/45), delayed motor milestones (36/45), short stature (length/height SDS <-2)(12/45), craniotabes (4/45) and hypocalcemic tetany ( 11/45). The most frequent biochemical abnormality was high alkaline phosphatase (ALP) (45/45), followed by low phosphate (PO4) (36/45) and low calcium (Ca) (8/45). Adolescents with severe VDD presented with pain in weight bearing joints, back, thighs, knees, and calves (30/36) difficulty walking and/or climbing stairs and/or running (8/36), muscle cramps and/or facial twitches and/or carpopedal spasms (2/36) and genu valgum (2/36). Biochemical serum abnormalities included high ALP (31/36), low phosphate (10/36) and low Ca (4/36). Variable radiological manifestations due to VDD were detected in all children (45/45) and in some of adolescents (19/35). Two different radiological patterns have been recognized in adolescents. Three months after injecting a mega dose of cholecalciferol all biochemical abnormalities were corrected with significant improvement of symptoms related to VDD had been reported in all children (45/45) and in the majority (33/36) of adolescents with VDD. 3-6 months after the injection, complete healing of the radiological evidence of VDD was achieved in all rachitic children and the majority of adolescents (16/19). CONCLUSION: it appears that adolescents adapt better to severe VDD compared to infants, with less severe clinical, biochemical and radiological manifestations. An IM mega dose of cholecalciferol is effective therapy for treatment of VDD in children and adolescents for 3 months but not for 6 months.;

International network on endocrine complications in thalassaemia (I-CET): an opportunity to grow.

Most of the endocrine complications in thalassaemia are attributable to iron overload which may be the result of economic circumstances (expense of the chelation therapy), late onset of chelation therapy or poor compliance with the iron chelation therapy. The major difficulties reported by hematologists or pediatric endocrinologists experienced in thalassaemias or thalassaemia syndromes in following growth disorders and endocrine complications were: lack of familiarity with medical treatment of endocrine complications (40%), interpretation of endocrine tests (30%), costs (65%), absence of paediatric endocrinologist for consultation on growth disorders and endocrine complications (27%), facilities (27%), other (e.g. lack of collaboration and on-time consultation between thalassaemic Centers supervised by hematologists and endocrinologists) (17%). Because any progress we make in research into growth disorders and endocrine complications in thalassaemia should be passed on to all those suffering from it, guaranteeing them the same therapeutic benefits and the same quality of life, on the 8th of May, 2009 in Ferrara (Italy), the International Network on Endocrine Complications in Thalassemia (I-CET) was founded. The I-CET group is planning to conduct, in Ferrara in May 2012, a workshop, "MRI and Endocrine Complications in Thalassaemia", and in Doha (Qatar) in September 2012, a 3-day intensive course entitled, "Growth disorders and Endocrine Complications in Thalassaemia", to provide interested pediatricians, physicians and hematologists from all over the world with an in-depth approach to the diagnosis and management of growth and endocrine disorders in thalassaemic patients.