Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0728731 (prematurity)
 7,134 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A study was made of 3718 newborn infants with jaundice in excess of physiological levels. Prematurity, haemolytic disease, haematomas or infections were present in 1278 patients. Of the remaining 2440 neonates, 137 were deficient in glucose-6-phosphate dehydrogenase (G-6-PD) and 2303 had idiopathic hyperbilirubinaemia. Exchange transfusion was necessary in 59 (42,7%) of the patients with G-6-PD deficiency and in 426 (18,5%) of those with idiopathic hyperbilirubinaemia. Kernicterus occurred in 3 infants (2,2%) with G-6-PD deficiency and in 3 (0,13%) with idiopathic hyperbilirubinaemia. These findings indicate that G-6-PD deficiency contributes significantly to the severity of neonatal jaundice in the population group studied and should be regarded as a potentially dangerous condition.
 ...
PMID:The effect of glucose-6-phosphate dehydrogenase deficiency on the severity of neonatal jaundice in Cape Town. 707 90

Prematurity-mediated cerebral damage has been associated with oxidative stress. The aim of the present work was to study the possible role played by free oxygen radicals generated by mitochondrial respiratory function in cerebral injury in preterm neonates. Our results show that whereas total glutathione concentrations are similar in term and preterm neonates, the GSH/GSSG ratio decreases sharply in preterm neonates immediately after birth. This effect is not due to a lack of enzymes involved in GSH regeneration, such as glutathione reductase and glucose-6-phosphate dehydrogenase, but to a significant increase in free-radical generation in preterm rat brain as shown by the increase in lipoperoxidation. Because the mitochondrion is the main source of free radicals in the cell, mitochondrial respiratory function was studied in the brain of preterm neonates. Our results show that prematurity prevented the postnatal increases in complex II-III activity and ATP concentrations that occur in term neonates at 5 min after delivery. All these effects were counteracted by the oxygen supply, suggesting that the inhibition of mitochondrial function is caused by restricted oxygen availability. Consequently, cerebral damage associated with prematurity may be mediated by mitochondrial free-radical generation as a consequence of hypoxia undergone by preterm neonates at birth.
 ...
PMID:Oxidative stress in preterm rat brain is due to mitochondrial dysfunction. 1175 37

Prematurity and glucose-6-phosphate dehydrogenase (G6PD) deficiency are risk factors for neonatal hyperbilirubinemia. The 2 conditions may interact additively or synergistically, contributing to extreme hyperbilirubinemia, with the potential for bilirubin neurotoxicity. This hyperbilirubinemia is the result of sudden, unpredictable, and acute episodes of hemolysis in combination with immaturity of bilirubin elimination, primarily of conjugation. Avoidance of contact with known triggers of hemolysis in G6PD-deficient individuals will prevent some, but not all, episodes of hemolysis. All preterm infants with G6PD deficiency should be vigilantly observed for the development of jaundice both in hospital and after discharge home.
...
PMID:The Preterm Infant: A High-Risk Situation for Neonatal Hyperbilirubinemia Due to Glucose-6-Phosphate Dehydrogenase Deficiency. 2723 11

A 33-week gestation boy with Mediterranean glucose-6-phosphate dehydrogenase (G6PD) and a glutathione S-transferase Mu 1 null mutations (GSTM1*0/*0) developed prolonged indirect hyperbilirubinemia (PIH). He had no laboratory evidence of haemolysis or infection, and no exposure to oxidising agents. He has two full-term older brothers who have no history of neonatal hyperbilirubinemia. One brother, who was exclusively breast fed, has only Mediterranean G6PD and the other has only GSTM1*0/*0. The three boys have no mutation in the uridine diphosphate glucuronosyltransferase 1A1 gene. This suggests that a combination of all or any two of prematurity, G6PD deficiency and GSTM1*0/*0 is a possible risk factor for PIH. However, this remains to be confirmed.
 ...
PMID:Prolonged indirect hyperbilirubinemia in a moderately preterm boy with Mediterranean glucose-6-phosphate dehydrogenase and glutathione S-transferase Mu 1 null mutations. 2806 91

Fovea plana (FP) describes the abnormal absence of the foveal pit in the retina. It is a sign that is associated with prematurity, albinism, and other ophthalmic disorders. The authors present the optical coherence tomography angiographic findings in a case of a 19-year-old male with FP and glucose-6-phosphate dehydrogenase (G6PD) deficiency. G6PD deficiency is a very common condition that typically presents with hemolytic anemia and jaundice. G6PD deficiency is also known to affect vision, but these pathologies have been less well-characterized. To the authors' knowledge, this is the first report of G6PD deficiency in FP. [Ophthalmic Surg Lasers Imaging Retina. 2017;48:664-667.].
 ...
PMID:OCT Angiographic Findings in Glucose-6-Phosphate Dehydrogenase Deficiency. 2881 42