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Query: UMLS:C0728731 (prematurity)
 7,134 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Glucose-6-phosphate dehydrogenase (G6PD) deficiency was detected in 16 (69.6%) of a group of 23 neonates who had unexplained moderate or severe jaundice. This proportion is significantly more than the 9.4% observed or the 22.2% expected in Jamaican neonates who are not moderately or severely jaundiced (P less than 0.003), and significantly more than the 12.6% observed or the 21.0% expected in older Jamaican children and adults (P less than 0.003). Phenobarbitone therapy and phototherapy reduced the need for exchange transfusion but this was necessary in eight patients. Two babies developed kernicterus and one died. On the other hand, only two of 21 neonates who were identified as G6PD deficient at birth subsequently became moderately or severely jaundiced, and this could be attributed to other causes in both cases. These findings indicate that apparently spontaneous neonatal jaundice is important in infants who have the G6PD A--enzyme. However, the jaundice is probably precipitated by unknown factors to which the G6PD deficient neonate is more susceptible than the infant who is not G6PD deficient. THere is also a slightly increased incidence of G6PD deficiency in neonates who develop jaundice because of ABO or Rh(D) iso-immune disease, infection or prematurity.
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PMID:Glucose-6-phosphate dehydrogenase deficiency and neonatal jaundice in Jamaica. 50 36

Jaundice among Nigerian preterm infants under special care was studied to determine the incidence of clinical jaundice, the predisposing factors and outcome among those with significant hyperbilirubinaemia (SBR greater than or equal to 10mg/dl). The incidence of jaundice among 292 preterm infants over an 18-month period was 71.2%. The male: female ratio was 1:1.04. Of the 74 infants with serum bilirubin 10mg/dl or more, prematurity alone was the identified cause in 44 (59.5%), Glucose-6-phosphate dehydrogenase (G-6-PD) deficiency and septicaemia were the only additional factors in 13 (17.6%) and 7 (9.5%) respectively, while multiple aetiological factors (prematurity, septicaemia and G-6-PD deficiency) were identified in six (8.1%) of the babies. Septicaemia was associated with higher mean bilirubin levels and the highest mortality. The two kernicteric infants in the study had septicaemia. Thus, the single most important cause of jaundice was prematurity. G-6-PD deficiency alone did not appear to increase the incidence and severity of hyperbilirubinaemia in this study. Septicaemia should be suspected and promptly treated in order to reduce mortality and risk of kernicterus among preterm infants with hyperbilirubinaemia.
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PMID:Neonatal jaundice among Nigerian preterm infants. 208 1

Neonatal jaundice is a leading cause of hospitalization in the first week of life worldwide. If inappropriately managed, it may result in significant bilirubin-induced mortality and disability. We set out to describe the epidemiology of neonatal hyperbilirubinemia as well as the practices and challenges in the care of infants with significant neonatal hyperbilirubinemia (SNH) in Nigeria, as basis for policy intervention and research priorities. We systematically searched PubMed, Scopus, EMBASE, Cumulative Index to Nursing and Allied Health Literature, WHO Library Database, African Index Medicus, African Journals Online, and local journals for studies published between January 1960 and December 2014. We included studies, without restriction on methodological design that provided evidence on the incidence/prevalence, etiological /risk factors and adverse outcomes of hyperbilirubinemia, care-seeking practices, diagnosis and treatment, as well as follow-up evaluation of infants with SNH in Nigeria. A total of 558 studies were identified from all sources out of which 198 (35.5%) were finally selected. SNH accounted for about one in five neonatal admissions and has been associated consistently with substantial case fatality and neuro-developmental sequelae such as cerebral palsy and auditory impairments, especially among out-born babies. Glucose-6-phosphate dehydrogenase (G6PD) deficiency, prematurity/low birth weight, infection, and ABO incompatibility were most frequently, and Rhesus disease rarely, associated with SNH. Late presentation at appropriate health facilities was common and resulted in high rates of acute bilirubin encephalopathy (ABE), kernicterus and avoidable exchange transfusions. Uniform practice guidelines, including developmental assessment and surveillance of infants with SNH, were rare at all levels of healthcare delivery. In summary, since 1960, SHN persists as a major contributor to neonatal mortality and developmental disabilities in Nigeria. The underpinning maternal, perinatal and neonatal factors as well as systems-based constraints are not insurmountable. Systematic and sustained interventions are warranted to curtail the disproportionate and perennial burden of this condition in this population.
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PMID:The burden and management of neonatal jaundice in Nigeria: A scoping review of the literature. 2675 12