Key Points Question What is the incidence of hazardous neonatal hyperbilirubinemia, and does an association exist between the quality of neonatal care and kernicterus? Findings In this population-based cohort study of 992 378 live-born children in Sweden from 2008 to 2016, 67 newborns were exposed to serum bilirubin levels of 30 mg/dL (510 μmol/L) or higher, of whom 13 developed kernicterus. Root cause analysis indicated that 11 of these 13 kernicterus cases (85%) were potentially avoidable because they were associated with suboptimal screening, diagnosis, or treatment. Meaning Kernicterus observed in a high-resource setting was associated with nonadherence to best practice guidelines and thus might have been prevented in a majority of infants.

Background and Objectives: Among otherwise healthy adults, there is a subgroup of individuals who develop symptoms of hypoglycemia during episodes of food restriction. The aim of the present study was to investigate whether such individuals develop hypoglycemia or react abnormally in other metabolic aspects during a 24-hour fast. Subjects and Methods: Ninety medical students were asked if they wanted to participate. Sixteen were selected; none dropped out. A 24-hour fast was performed at a hospital ward. Blood samples and questionnaires were taken at eight specific times. Result: During the fast, the sensitive group reported significantly higher scores on 'irritation' and 'shakiness'. However, no hypoglycemia occurred and the lowest detected blood glucose concentration was 3.7 mmol/l. There were no differences between the groups in plasma glucose, cortisol, growth hormone (GH), insulin, b-hydroxybutyrate (b-OH) and lactate levels. The blood pressures and heart rates were also similar. Conclusions: Adults, despite subjective signs of hypoglycemia, can fast without any metabolic or endocrine derangement.

In the affected boy, KH seems to be the result of a reduced capacity to use ketone bodies, leading to increased peripheral metabolism of glucose that cannot be met by hepatic glucose production. Because the boys are homozygotic twins and only one of them is affected, the ketotic hypoglycemia is most likely caused by an altered imprinting of gene(s) involved in regulating metabolic pathways.

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