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The aim of the current study was to evaluate the safety and efficacy of initiation protocol for MiniMed ™ 780G system among an Egyptian cohort of young people living with type 1 diabetes (T1D). A prospective single-arm study including 72 participants with T1D. Five days of structured education and training were provided to all users and continuous glucose monitoring (CGM) was initiated on the first day of the training. Users initiated the pump initially in manual mode, with suspend before low feature, for 3 days before shifting to Auto Mode. The mean HbA1c decreased from 8.72 ± 2.01 % to 6.7 ± 0.4 % (p<0.01). Time in range (70–180 mg/dL) substantially improved from 55.24 % ± 10.35 to 81.7 % ± 5.12 % after spending 84 days in auto mode (p<0.001) with 2.03 % of the time spent below 70 mg/dL. Regarding AHCL compatibility, users spent at least 90 % of time in auto mode. Young people with T1D successfully initiated the AHCL system, using a tailored structured on-boarding protocol. Structured stepwise initiation protocol and onboarding steps are important prerequisite for participants' adherence and engagement with the system. Patient education together with optimized pump settings are important predictors of glycemic outcomes. [ABSTRACT FROM AUTHOR]

The MNX1 gene encodes a homeobox transcription factor found to be important for pancreatic beta cell differentiation and development. Mutations of the MNX1 gene that cause permanent neonatal diabetes mellitus (PNDM) are rare and have been reported in only two cases. Both cases presented with hyperglycemia, with one case having isolated PNDM while the other had PNDM and multiple neurologic, skeletal, lung, and urologic congenital anomalies resulting in death in early infancy. We describe the genetic and clinical features of a preterm male infant with a homozygous [c.816C > A p.(Phe272Leu)] MNX1 mutation. Our proband is the first case to present in severe diabetic ketoacidosis (DKA), indicating severe insulin deficiency. Unlike the previously reported female case who had the same mutation and presented with isolated PNDM, our proband had hypospadias and congenital umbilical hernia and showed poor growth on follow up. Our case suggests that MNX1 mutations causing NDM can result in a range of extra‐pancreatic features and a variable phenotype, similar to other transcription factors causing NDM such as GATA6 and GATA4 mutations. We also cannot exclude the possibility of sex‐biased expression of MNX1 gene (which was recently reported for other monogenic/neonatal diabetes genes such as the NEUROD1 and HNF4A in humans) since the two male cases had associated multiple anomalies while the female case had isolated PNDM. Our report further defines the phenotype caused by recessive homozygous MNX1 mutations and explores potential new mechanisms regulating MNX1 gene expression which should be further explored. Our manuscript describes a male newborn with the rare MNX1 mutation with a novel presentation/phenotype of not only hyperglycemia but also severe diabetic ketoacidosis, hypospadias and congenital umbilical hernia. Thus, we expand on the phenotype presentation of MNX1 mutations associated with permanent neonatal diabetes. Since the two males who had MNX1 mutation and diabetes (our case and another previously reported case with a different mutation), had multiple congenital anomalies, whereas the female who had the same mutation as our patient had isolated diabetes, our report also raises the possibility of sex‐biased gene expression, which was recently reported for several monogenic diabetes genes. This is worth exploring further in the future especially as more cases are reported. [ABSTRACT FROM AUTHOR]