This study aimed to explore the effect of continuous glucose monitors with remote monitoring on psychosocial outcomes in parents of children with type 1 diabetes. RESEARCH DESIGN AND METHODS Children with type 1 diabetes, aged 2-12 years, along with their parents, were studied in a randomized crossover study. They participated in two 3-month periods using conventional blood glucose monitoring (control) or the Dexcom G5 Mobile continuous glucose monitoring (CGM) system with remote monitoring (intervention). The primary outcome was parental fear of hypoglycemia score assessed by the Hypoglycemia Fear Survey. RESULTS Parental Hypoglycemia Fear Survey scores were lower while the child was using CGM with remote monitoring (P < 0.001). Furthermore, parental health-related quality of life and family functioning, stress, anxiety, and sleep measures also improved significantly after intervention. CONCLUSIONS CGM with remote monitoring was found to improve multiple measures of quality of life, reduce family stress, and improve parental sleep.

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Context: 3b-hydroxysteroid dehydrogenase deficiency (3bHSD) is a rare disorder of sexual development and steroidogenesis. There are two isozymes of 3bHSD, HSD3B1 and HSD3B2. Human mutations are known for the HSD3B2 gene which is expressed in the gonads and the adrenals. Little is known about testis histology, fertility and malignancy risk. Objective: To describe the molecular genetics, the steroid biochemistry, the (immuno-)histochemistry and the clinical implications of a loss-of-function HSD3B2 mutation. Methods: Biochemical, genetic and immunohistochemical investigations on human biomaterials. Results: A 46,XY boy presented at birth with severe undervirilization of the external genitalia. Steroid profiling showed low steroid production for mineralocorticoids, glucocorticoids and sex steroids with typical precursor metabolites for HSD3B2 deficiency. The genetic analysis of the HSD3B2 gene revealed a homozygous c.687del27 deletion. At pubertal age, he showed some virilization of the external genitalia and some sex steroid metabolites appeared likely through conversion of precursors secreted by the testis and converted by unaffected HSD3B1 in peripheral tissues. However, he also developed enlarged breasts through production of estrogens in the periphery. Testis histology in late puberty revealed primarily a Sertoli-cell-only pattern and only few tubules with arrested spermatogenesis, presence of few Leydig cells in stroma, but no neoplastic changes. Conclusions: The testis with HSD3B2 deficiency due to the c.687del27 deletion does not express the defective protein. This patient is unlikely to be fertile and his risk for gonadal malignancy is low. Further studies are needed to obtain firm knowledge on malignancy risk for gonads harboring defects of androgen biosynthesis.