OBJECTIVES: The ternary complex is composed of insulin-like growth factor (IGF)-I, IGF binding protein (IGFBP)-3 and acid labile subunit (ALS). Growth hormone (GH) promotes IGFBP-3 proteolysis to release free IGF-I, ALS, and IGFBP-3 fragments. Our aim was to determine whether elevated GH levels during GH stimulation testing would trigger IGFBP-3 proteolysis. DESIGN: This prospective study of 10 short prepubertal children (height standard deviation score -2.37 +/- 0.31) used arginine and GH releasing hormone stimulation to study dynamic changes in the ternary complex moieties. IGFBP-3 was measured in two assays: a radioimmunoassay (RIA) that detects both cleaved and intact IGFBP-3; and an immunochemiluminescence assay (ICMA) that detects only intact IGFBP-3. RESULTS: IGFBP-3 measured by RIA increased by 19% (p < 0.05), while IGFBP-3 measured by ICMA did not significantly increase (6.1%). CONCLUSION: The significant increase in IGFBP-3 measured by RIA, but not ICMA, provides evidence of IGFBP-3 proteolysis during acute GH stimulation.

Atypical or second-generation antipsychotic agents, such as aripiprazole and olanzapine, are increasingly used in the management of schizophrenia and bipolar disorders in children. The atypical antipsychotic agents have been associated with the development of hyperglycemia, ketoacidosis, and diabetes. The mechanism of atypical antipsychotic-mediated hyperglycemia is unclear. Most of the published reports have been on individuals at risk for type 2 diabetes. We present the first known cases of the development of diabetes and positive glutamic acid decarboxylase antibodies (suggestive of autoimmune diabetes) in adolescents while on treatment with atypical antipsychotics. The nature of their clinical presentations and the time course of antipsychotic therapy to clinical diagnosis of diabetes make us speculate that atypical antipsychotics may shorten the time course of the development of autoimmune diabetes in predisposed children.

Vitamin D deficiency is prevalent in pregnant women. This deficiency could be exaggerated in multifetal pregnancies by the increased demand on maternal stores of vitamin D. We present 2 cases in which hypocalcemia and secondary hyperparathyroidism occurred in 2 sets of twins from mothers with vitamin D deficiency. The first mother had gastric bypass surgery and Crohn disease. The second mother had no apparent cause of vitamin D deficiency. Both women had iron deficiency anemia and lived in Northeastern United States. We speculate that in twins, the demand for 25-hydroxyvitamin D by 2 fetuses could deplete the 25-hydroxyvitamin D stores in a mother.