Objective: Hypoglycemia in the infant is potentially hazardous to the central nervous system(CNS), and any delay in solving the problem may impose irreversible sequelae. The aim of this review is to provide basic knowledge to the pediatrician to adequately deal with a hypoglycemic patient.
Methods: Bibliographic review was performed in the Medline for the last 10 years, and the most pertinent papers were selected.
Results: Even today, there are discrepancies as for the best conduct in the hyperinsulinemic patients. The surgical or clinical approaches have had the support of very important authors. Some state that the best choice is the total pancreatectomy, in which 95% of the pancreas is removed, with all its long-term sequelae, while others emphasize the preservation of the pancreas with drug therapy instead of pancreatectomy.
Conclusions: The doctor who takes care of a hypoglycemic child has to remember that the biggest task is to preserve the CNS integrity, and all the efforts must be made to provide an adequate glucose supply to the brain, otherwise irreversible consequences will ensue.
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http://dx.doi.org/10.2223/jped.533 | DOI Listing |
Glycogen storage disease type III (GSD III) is a rare metabolic disorder characterized by a deficiency of liver and muscle amylo-1,6-glucosidase. This condition presents with severe hepatic symptoms in childhood, mostly hepatomegaly, hypoglycemia in half of patients, while muscular complications may predominate in adulthood. Hepatic fibrosis, cirrhosis and hepatocellular carcinoma (HCC) are common complications in older patients.
View Article and Find Full Text PDFFront Endocrinol (Lausanne)
January 2025
Section on Growth and Development, Eunice Kennedy Shriver National Institute of Child Health and Human Development, National Institute of Health, Bethesda, MD, United States.
Recombinant human IGF-1 is used to treat severe primary IGF-1 deficiency, but this treatment requires twice-daily injection, often does not fully correct the growth deficit, and has important off-target effects. We therefore sought to target IGF-1 to growth plate cartilage by generating fusion proteins combining IGF-1 with single-chain human antibody fragments that target matrilin-3, a cartilage matrix protein. We previously showed that this cartilage-targeting IGF-1 fusion protein (CV1574-1) promoted growth plate function in a GH-deficient (lit) mouse model.
View Article and Find Full Text PDFEndocrinol Metab (Seoul)
January 2025
Division of Endocrinology and Metabolism, Department of Internal Medicine, Seoul National University Bundang Hospital, Seoul National University College of Medicine, Seongnam, Korea.
Gestational diabetes mellitus (GDM) affects over 10% of all pregnancies, both in Korea and worldwide. GDM not only increases the risk of adverse pregnancy outcomes such as preeclampsia, preterm birth, macrosomia, neonatal hypoglycemia, and shoulder dystocia, but it also significantly increases the risk of developing postpartum type 2 diabetes mellitus and cardiovascular disease in the mother. Additionally, GDM is linked to a higher risk of childhood obesity and diabetes in offspring, as well as neurodevelopmental disorders, including autistic spectrum disorder.
View Article and Find Full Text PDFDiabetes Care
January 2025
Department of Medicine, Feinberg School of Medicine, Northwestern University, Chicago, IL.
Objective: Subtypes of gestational diabetes mellitus (GDM) based on insulin sensitivity and secretion have been described. We addressed the hypothesis that GDM subtypes are differentially associated with newborn and child anthropometric and glycemic outcomes.
Research Design And Methods: Newborn and child (age 11-14 years) outcomes were examined in 7,970 and 4,160 mother-offspring dyads, respectively, who participated in the Hyperglycemia and Adverse Pregnancy Outcome Study (HAPO) and Follow-Up Study.
Introduction: This is a report of a child with congenital hyperinsulinism associated with a loss-of-function variant in KCNE1. KCNE1 encodes a human potassium channel accessory (beta) subunit that modulates potassium channel Kv7.1 (encoded by KCNQ1).
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