Outcomes among Newborns with Total Serum Bilirubin Levels of 25 mg per Deciliter or More

Abstract

When treated with phototherapy or exchange transfusion, total serum bilirubin levels in the range included in this study were not associated with adverse neurodevelopmental outcomes in infants born at or near term.

Transient neonatal hyperthyrotropinemia is a risk factor for developing persistent hyperthyrotropinemia in childhood with repercussion on developmental status

“…Our study also confirms the finding that mean TSH levels are higher in children with antecedents of TNH, indicating that thyroid function is not completely normal, but compensates with a normal T 4 secretion (21), and the fact that linear growth was similar in both cohorts, possibly due to a compensatory effect on growing large bone tissue for this reason (13,14).…”

“…There is considerable controversy regarding the long-term effects of TNH in the neonatal period on the development of persistent hyperthyrotropinemia (PH) during later childhood (age, 6 years), defined as a serum TSH level above the upper limit of the statistically defined reference range while the serum T 4 level is within the reference range, without clinical manifestations (8). Miki et al (9) and Tyfield et al (10) claim that TNH has no long-term adverse consequences, whereas Calaciura et al (11) and Leonardi et al (12) state that, in newborns with hyperthyrotropinemia (normal T 4 levels and elevated TSH levels on confirmatory test), this condition requires a considerable time frame to distinguish between permanent and transient cases, compared with normal controls having significantly higher TSH values in childhood; but unfortunately, these studies do not consider the question in appropriate epidemiological terms of the risk of developing PH in later childhood, and its potential impact on growth and development (13). In practice, our study addresses a question about the health of children who are diagnosed during neonatal screening programs with a mild transient form of thyroid dysfunction and for whom no clear evidence for treatment indications exists today.…”

Neurodevelopment after moderate hyperbilirubinemia at term

“…At 18 mo, the children with moderate hyperbilirubinemia were more active than the infants without moderate hyperbilirubinemia. The latter finding is at variance with previous studies (2,(7)(8)(9). However, Jangaard et al (8) found a relationship between a bilirubin level of ≥325 µmol/l and attention-deficit disorder and an association of bilirubin level ≥230 µmol/l with autism.…”

Commentary on the bilirubin supplement

“…6 Nonetheless, a blood bilirubin level, in and of itself, is rarely sufficient to predict toxicity in the individual case or even in a population. 7 Thus, scientists remain focused on trying to predict which infants are most likely to develop excessive bilirubin accumulation in tissues outside the circulation, a phenomenon dependent upon more than the absolute level per se, but also upon albumin-binding capacity and affinity, the unbound or 'free' bilirubin (B f ) as well as the transporters that can facilitate bilirubin's movement out of the brain. 8,9 Excessive bilirubin production, as in the case of hemolysis (from any cause), is the main driver of load on the system and can often overload it.…”

“…10 It is not surprising that hemolysis has been associated empirically with an increased risk of bilirubin-induced injury. 7 However, impaired conjugation such as that associated with Gilbert's disease can further exacerbate the load, contributing to more B f , capable of entering the brain tissue. 10 The genetic polymorphisms 11,12 contributing to overload situations (that is, HO-1 overexpression 13 or uridine diphosphoglucuronate glucuronosyltransferase deficiency) only exacerbate natural exigencies, such as prematurity, infection or acquired causes of heme degradation.…”