Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0029713 (immaturity)
 4,335 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The content and distribution of phospholipids (PL) in red blood cells (RBC) of PK and of G6PD deficiency were found to differ in both disorders. RBC immaturity could not be excluded as reason for PL alterations in PK deficiency. The relative diminution of phosphatidylethanolamine in G6PD deficiency may be connected with the enzyme depletion in this disorder and its influence on the PL of RBC membranes. Moist or all fatty acid deviations seem to be conditioned by RBC immaturity. Nearly all PL fatty acid aberrations in G6PD deficiency RBC were observed also in PK deficiency RBC. Additional deviations of PL fatty acids in PK deficiency RBC may be caused by the stronger immaturity of the cells in this disorder.
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PMID:Phospholipid content and phospholipid fatty acid composition of red blood cells in enzyme defect hemolytic anemias. 734 Mar 36

Late preterm gestation is an important risk factor for the development of severe neonatal hyperbilirubinemia and kernicterus. An exaggerated hepatic immaturity contributes to the greater prevalence, severity, and duration of neonatal jaundice in late preterm infants. Breast milk feeding is almost uniformly present and large for gestational age status, male sex, and G6PD deficiency are over-represented among that cohort of late preterm infants with kernicterus. Attention to screening measures for jaundice in the newborn nursery, the provision of lactation support, parental education, timely postdischarge follow-up, and appropriate treatment when clinically indicated should help to reduce the risk of late preterm neonates developing severe neonatal jaundice or kernicterus.
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PMID:Hyperbilirubinemia and bilirubin toxicity in the late preterm infant. 1714 8

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.
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PMID:The Preterm Infant: A High-Risk Situation for Neonatal Hyperbilirubinemia Due to Glucose-6-Phosphate Dehydrogenase Deficiency. 2723 11