An 8 mo old spayed female mixed-breed dog was presented for pale mucous membranes. The dog was diagnosed with intravascular immune-mediated hemolytic anemia (IMHA) and was started on medical management including corticosteroids, thromboprophylaxis, a packed red blood cell transfusion, and IV immunoglobulin. The dog developed severe hyperbilirubinemia (total bilirubin 48.1 mg/dL) and was referred for centrifugal plasmapheresis. Before treatment, the dog was stuporous to comatose, had intermittent opisthotonos, forelimb extension, and an absent menace consistent with acute bilirubin encephalopathy (ABE). The dog underwent a previously reported protocol of three therapeutic plasma exchange (TPE) treatments 24 hr apart. Moderate improvement was noted in her neurological status, although autoagglutination and hemolysis persisted, and the protocol was deemed inadequate. A fourth TPE treatment was performed on day 6. The following morning, the dog was autoagglutination negative. Her neurological status gradually improved, and she was discharged from the hospital on day 12. The dog remains neurologically normal and continues to do well at home on monotherapy with mycophenolate. Continued plasmapheresis treatments should be offered as a treatment option for severe cases of IMHA in the face of persistent disease, because TPE is able to provide ongoing support and stabilization, particularly in the face of ABE.

Prevention of neonatal bilirubin injury exemplifies success of systems approach to avert adverse neonatal and childhood outcomes that rely on strategies including prenatal identification of Rhesus sensitization, universal maternal blood typing, risk assessment for neonatal extreme hyperbilirubinemia (EHB), unfettered access to safe, effective phototherapy, and application of patient safety principles. India\'s diverse landscape suggests varied real-time experiences of neonatal hyperbilirubinemia and consequent infant mortality rates (IMR). Utilizing Global Burden of Disease (GBD) database, the authors examined national and subnational trends, infant mortality timing, and the disease burden from hemolytic and perinatal jaundice over 30 y (1999 to 2019). They also assessed the correlation of EHB-IMR with socio-demographic index and health expenditure per capita, estimating economic losses from EHB-related infant mortality to guide policy decisions at national and state domains. From 1990 to 2019, India delivered 811,078,415 livebirths of which, 1,189,856 infant deaths were due to EHB. EHB-related deaths decreased from 57,773 in 1990 to 19,664 in 2019, a 60% reduction vs. 40% in overall IMR. Early (0-6 d), late (7-27 d), and post-neonatal (28-364 d) deaths accounted for 61%, 34%, and 5% of mortality, respectively. Uttar Pradesh and Bihar contributed to 38% of all EHB deaths. Economic analysis estimate losses between US $7.2 and 11.7 billion for the year 2019 secondary to EHB-related mortality. The present analysis reveals consistent declines across all states to reach current EHB-IMR of 0.8 per 1,000 live-births in India by 2019. Significant economic impact of lost human productivity highlight ongoing need for targeted life-saving public health strategies.

UNASSIGNED: Exchange transfusion (ET) is an effective treatment for acute bilirubin encephalopathy and extreme neonatal hyperbilirubinemia (ENH). It can reduce mortality and morbidity. This study aimed to investigate the trends and risk factors of ENH requiring ET in hospitalized neonates in Iran.
UNASSIGNED: A retrospective analysis of medical records of neonates who underwent ET due to ENH was conducted from 2011 to 2021, in Shiraz, Iran. Clinical records were used to gather demographic and laboratory data. The quantitative data were expressed as mean±SD, and qualitative data was presented as frequency and percentage. P<0.05 was considered statistically significant.
UNASSIGNED: During the study, 377 ETs were performed for 329 patients. The annual rate of ET decreased by 71.2% during the study period. The most common risk factor of ENH was glucose-6-phosphate dehydrogenase (G6PD) deficiency (35%), followed by prematurity (13.06%), ABO hemolytic disease (7.6%), sepsis (6.4%), Rh hemolytic disease (6.08%), and minor blood group incompatibility (3.34%). In 28.52% of the cases, the cause of ENH was not identified. 17 (5.1%) neonates had acute bilirubin encephalopathy, of whom 6 (35.29%) had G6PD deficiency, 6 (35.29%) had ABO incompatibility, and 2 (11.76%) had Rh incompatibility.
UNASSIGNED: Although the rate of ET occurrence has decreased, it seems necessary to consider different risk factors and appropriate guidelines for early identification and management of neonates at risk of ENH should be developed. The findings of the study highlighted the important risk factors of ENH in southern Iran, allowing for the development of appropriate prevention strategies.

Neonatal hyperbilirubinemia is one of the most common conditions managed by pediatricians. Although many infants are affected, most will experience complete resolution without complication. Acute bilirubin encephalopathy and kernicterus are rare yet debilitating sequelae of severe hyperbilirubinemia that can be avoided through careful monitoring and treatment with phototherapy. Appropriate management of neonatal hyperbilirubinemia must balance the risks of these severe conditions with the effects of overtreatment. Released in 2022, the American Academy of Pediatrics revised the clinical practice guideline for the management of hyperbilirubinemia, which aims to provide that balance through updates to the previous guideline. This article will provide the reader with (1) an evidence-based harm and benefit analysis of the guideline, (2) an overview of key changes and clarifications made in the new guideline, and (3) a practical summary of guideline updates. [Pediatr Ann. 2024;53(6):e208-e216.].

Hyperbilirubinemia in newborns may progress to acute bilirubin encephalopathy (ABE), posing short- and long-term health risks. Despite extensive research identifying numerous mRNAs, lncRNAs, circRNAs, and miRNAs associated with brain injury, their roles in neonatal bilirubin-induced brain injury remain elusive. This study employed whole-transcriptome sequencing to ascertain the differentially expressed (DE) RNA profiles in a newborn ABE rat model, followed by bioinformatic analysis. A time-series competing endogenous RNA (ceRNA) regulatory network was established, and the expression trends of 9 arbitrarily chosen RNAs were verified through quantitative real-time polymerase chain reaction(qRT-PCR). In comparison with the control group, we identified 595, 888, and 1448 DE mRNAs; 22, 37, and 37 DE miRNAs; 1945, 1869, and 1997 DE lncRNAs; and 31, 28, and 36 DE circRNAs at 6 h, 12 h, and 24 h, respectively. Predominantly, these DERNAs contribute to biological functions and pathways associated with inflammation, immunity, metabolism, cell death, and neurodevelopmental regulation. Moreover, we constructed ceRNA networks of DE lncRNA/circRNA-DE miRNA-DE mRNA based on time series. The qRT-PCR expression trends for the selected 9 RNAs were generally similar to the RNA-seq outcomes. This investigation uniquely delineated the temporal expression patterns of mRNA and non-coding RNA in ABE, establishing ceRNA networks and identifying potential molecular mechanisms underlying bilirubin-induced hippocampal damage. Nonetheless, further studies are warranted to corroborate these findings in humans.

Hyperbilirubinemia is one of the most common occurrence in newborns and is toxic to the brain, resulting in neurological sequelae such as auditory impairment, with potential to evolve to chronic bilirubin encephalopathy and long-term cognitive impairment in adults. In the early postnatal period, neurogenesis is rigorous and neuroinflammation is detrimental to the brain. What are the alterations in neurogenesis and the underlying mechanisms of bilirubin encephalopathy during the early postnatal period? This study found that, there were a reduction in the number of neuronal stem/progenitor cells, an increase in microglia in the dentate gyrus (DG) and an inflammatory state in the hippocampus, characterized by increased levels of IL-6, TNF-α, and IL-1β, as well as a decreased level of IL-10 in a rat model of bilirubin encephalopathy (BE). Furthermore, there was a significant decrease in the number of newborn neurons and the expression of neuronal differentiation-associated genes (NeuroD and Ascl1) in the BE group. Additionally, cognitive impairment was observed in this group. The administration of minocycline, an inhibitor of microglial activation, resulted in a reduction of inflammation in the hippocampus, an enhancement of neurogenesis, an increase in the expression of neuron-related genes (NeuroD and Ascl1), and an improvement in cognitive function in the BE group. These results demonstrate that microglia play a critical role in reduced neurogenesis and impaired brain function resulting from bilirubin encephalopathy model, which could inspire the development of novel pharmaceutical and therapeutic strategies.

UNASSIGNED: Hypernatremia may facilitate the diffusion of bilirubin through the blood-brain barrier and increase the risk of bilirubin encephalopathy. This study was conducted to compare the prognosis of jaundice infants with those with jaundice and hypernatremia.
UNASSIGNED: A total of 615 term infants with idiopathic jaundice with or without hypernatremia were enrolled in this cohort study with 24-months follow-up at Ghaem Hospital, Mashhad, Iran, between 2010 and 2022. An in-house questionnaire including the laboratory evaluation and neonatal characteristics was used as the data collection tool. The follow-up of neonatal development status was performed using the Denver test II at 6, 12, 18, and 24 months after discharging from hospital.
UNASSIGNED: Normal outcomes were seen in 555 (90.2%) out of 615 studied infants, while 60 cases (9.8%) showed abnormal outcomes. Serum levels of sodium (P = 0.017), bilirubin (P = 0.001), urea (P = 0.024), and creatinine (P = 0.011) as well as hyperthermia (P = 0.046) and unconsciousness (P = 0.005) showed significant differences between the two groups. Approximately 16% of the newborns with both jaundice and hypernatremia, and 9% of those with only jaundice had unfavorable prognoses. Also, bilirubin level had the most predictive power (91.3%).
UNASSIGNED: Our results suggest that hypernatremia or jaundice alone, may affect the prognosis of infants aged 2 years; but jaundice and hypernatremia together, will intensify the developmental problems in jaundice infants. However, the role of hyperbilirubinemia in the incidence of complications is more than hypernatremia.

OBJECTIVE: Identifying factors that can better predict the prognosis of neonates with hyperbilirubinemia is important. In this study, we aimed to evaluate the relationship between electroencephalography (EEG) findings and two-year prognosis in neonates with severe hyperbilirubinemia.
METHODS: In a cohort prospective study, we studied neonates with a total serum bilirubin level of higher than 18 mg/dL, who were admitted to the neonatal intensive care unit (NICU) of Ghaem hospital, Mashhad, Iran. EEG was recorded upon admission, for all neonates. Patients\' data, including demographic characteristics, admission information, and pregnancy and birth data were gathered by obtaining history from parents and studying case files. Also, the relationship between initial EEG findings and final developmental status was assessed.
RESULTS: Mean and standard deviation age of patients were 5.46 ± 3.13 days and average serum total bilirubin level was 23.97 ± 4.34 mg/dL at admission. Our findings revealed a significant correlation between the presence of trace alternant on EEG and developmental delay (P = .001). Presence of trace alternant waves on initial EEG at admission was significantly associated with developmental delay in the two year (P = .005).
CONCLUSIONS: These results indicate a relationship between developmental prognosis and the severity of hyper bilirubinemia in neonates. Also, our findings show that the presence of trace alternate waves on the initial EEG is significantly associated with developmental delay of the neonate in the future.

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