Birth asphyxia-induced brain damage: the long road to optimal reduction and prevention!

2020 ◽  
Vol 3 ◽  
pp. 3-3
Author(s):  
Frank van Bel ◽  
Floris Groenendaal
Keyword(s):  
Brain Damage ◽  
Birth Asphyxia ◽  
Optimal Reduction

scholarly journals Antenatal allopurinol for reduction of birth asphyxia induced brain damage (ALLO-Trial); a randomized double blind placebo controlled multicenter study

2010 ◽  
Vol 10 (1) ◽  
Author(s):  
Joepe J Kaandorp ◽  
Manon JNL Benders ◽  
Carin MA Rademaker ◽  
Helen L Torrance ◽  
Martijn A Oudijk ◽  
...  
Keyword(s):  
Brain Damage ◽  
Multicenter Study ◽  
Birth Asphyxia ◽  
Double Blind ◽  
Double Blind Placebo

Hypobaric Hypoxia Postconditioning Reduces Brain Damage and Improves Antioxidative Defense in the Model of Birth Asphyxia in 7-Day-Old Rats

2013 ◽  
Vol 39 (1) ◽  
pp. 68-75 ◽  
Author(s):  
Marcin Gamdzyk ◽  
Dorota Makarewicz ◽  
Marta Słomka ◽  
Apolonia Ziembowicz ◽  
Elzbieta Salinska
Keyword(s):  
Brain Damage ◽  
Hypobaric Hypoxia ◽  
Birth Asphyxia ◽  
Antioxidative Defense ◽  
Old Rats

scholarly journals Antenatal Allopurinol Reduces Hippocampal Brain Damage After Acute Birth Asphyxia in Late Gestation Fetal Sheep

2013 ◽  
Vol 21 (2) ◽  
pp. 251-259 ◽  
Author(s):  
Joepe J. Kaandorp ◽  
Jan B. Derks ◽  
Martijn A. Oudijk ◽  
Helen L. Torrance ◽  
Marline G. Harmsen ◽  
...  
Keyword(s):  
Brain Damage ◽  
Birth Asphyxia ◽  
Late Gestation ◽  
Fetal Sheep

scholarly journals Hyperinsulinism in Infancy and Childhood: When an Insulin Level Is Not Always Enough

2008 ◽  
Vol 54 (2) ◽  
pp. 256-263 ◽  
Author(s):  
Andrew A Palladino ◽  
Michael J Bennett ◽  
Charles A Stanley
Keyword(s):  
Brain Damage ◽  
Ectopic Expression ◽  
Insulin Response ◽  
Birth Asphyxia ◽  
Severe Hypoglycemia ◽  
Insulin Level ◽  
Phenotypic Characterization ◽  
Congenital Hyperinsulinism ◽  
Drug Induced ◽  
Glucose Levels

Abstract Background: Hypoglycemia in infants and children can lead to seizures, developmental delay, and permanent brain damage. Hyperinsulinism (HI) is the most common cause of both transient and permanent disorders of hypoglycemia. HI is characterized by dysregulated insulin secretion, which results in persistent mild to severe hypoglycemia. The various forms of HI represent a group of clinically, genetically, and morphologically heterogeneous disorders. Content: Congenital hyperinsulinism is associated with mutations of SUR-1 and Kir6.2, glucokinase, glutamate dehydrogenase, short-chain 3-hydroxyacyl-CoA dehydrogenase, and ectopic expression on β-cell plasma membrane of SLC16A1. Hyperinsulinism can be associated with perinatal stress such as birth asphyxia, maternal toxemia, prematurity, or intrauterine growth retardation, resulting in prolonged neonatal hypoglycemia. Mimickers of hyperinsulinism include neonatal panhypopituitarism, drug-induced hypoglycemia, insulinoma, antiinsulin and insulin-receptor stimulating antibodies, Beckwith-Wiedemann Syndrome, and congenital disorders of glycosylation. Laboratory testing for hyperinsulinism may include quantification of blood glucose, plasma insulin, plasma β-hydroxybutyrate, plasma fatty acids, plasma ammonia, plasma acylcarnitine profile, and urine organic acids. Genetic testing is available through commercial laboratories for genes known to be associated with hyperinsulinism. Acute insulin response (AIR) tests are useful in phenotypic characterization. Imaging and histologic tools are also available for diagnosing and classifying hyperinsulinism. The goal of treatment in infants with hyperinsulinism is to prevent brain damage from hypoglycemia by maintaining plasma glucose levels above 700 mg/L (70 mg/dL) through pharmacologic or surgical therapy. Summary: The management of hyperinsulinism requires a multidisciplinary approach that includes pediatric endocrinologists, radiologists, surgeons, and pathologists who are trained in diagnosing, identifying, and treating hyperinsulinism.

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