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Transcutaneous bilirubin level to predict hyperbilirubinemia in preterm neonates.

ABSTRACT: Background: Hyperbilirubinemia is common in neonates, with higher prevalence among preterm neonates, which can lead to severe hyperbilirubinemia. Assessment of total serum bilirubin (TSB) and use of a transcutaneous bilirubinometer (TcB) are existing methods to identify and predict hyperbilirubinemia. This study aimed to determine TcB cut-off values during the first day for preterm neonates to predict hyperbilirubinemia at 48 and 72 hours. Methods: A total of 90 neonates born ?35 weeks were included in the study. They were divided into two groups (Group I: 1000-1500 grams; Group II: 1501-2000 grams). The bilirubin level was measured on the sternum using TcB at the ages of 12, 24, and 72 h. TSB measurements were taken on the third day or if TcB level reached ± 1.24 mg/dL phototherapy threshold and if TcB showed abnormal results (Group I: 5.76-8.24 mg/dL; Group II: 8.76-11.24 mg/dL). Hyperbilirubinemia was defined as TSB ?7 mg/dL for group I and >10 mg/dL for group II. Results: In total, 38 group I neonates and 48 group II neonates were observed. Almost half of neonates in group I (44.7%) were suffering from hyperbilirubinemia at the age of 48 hours, with 45.8% of group II at the age of 72 hours. To predict hyperbilirubinemia at the age of 48 hours, the best 24-hour-age TcB cut-off values were calculated to be 4.5 mg/dL for group I and 5.8 mg/dL for group II. To predict hyperbilirubinemia at the age of 72 hours, we determined 24-hour-age TcB value of 5.15 mg/dL for group II. Conclusion: TcB values in the early days of life can be used as hyperbilirubinemia predictors on the following days for preterm neonates. Close monitoring should be managed for those with TcB values higher than the calculated cut-off values.

SUBMITTER: Rahmawati D

PROVIDER: S-EPMC7499403 | biostudies-literature | 2020

REPOSITORIES: biostudies-literature

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Transcutaneous bilirubin level to predict hyperbilirubinemia in preterm neonates.

Rahmawati Dewi D Sampurna Mahendra Tri Arif MTA Etika Risa R Utomo Martono Tri MT Bos Arend F AF

F1000Research 20200428

<b>Background:</b> Hyperbilirubinemia is common in neonates, with higher prevalence among preterm neonates, which can lead to severe hyperbilirubinemia. Assessment of total serum bilirubin (TSB) and the use of a transcutaneous bilirubinometry (TcB) are existing methods that identify and predict hyperbilirubinemia. This study aimed to determine TcB cut-off values during the first day for preterm neonates to predict hyperbilirubinemia at 48 and 72 hours. <b>Methods:</b> This cohort study was condu ...[more]

PMID: 33014346

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Project description:BackgroundHyperbilirubinemia is a devastating complication in patients admitted to an intensive care unit (ICU). The sequential organ failure assessment (SOFA) score classifies hyperbilirubinemia without further detailed analyses for bilirubin increase above 12 mg/dL. We evaluated whether the level of bilirubin increase in patients with extreme hyperbilirubinemia (total bilirubin ≥ 12 mg/dL) affects and also helps estimate mortality or recovery.MethodsA retrospective cohort analysis comprising 427 patients with extreme hyperbilirubinemia admitted to the ICU of Samsung Medical Center, Seoul, Korea between 2011 and 2015 was conducted. Extreme hyperbilirubinemia was classified into four grades: grade 1 (12-14.9 mg/dL), grade 2 (15-19.9 mg/dL), grade 3 (20-29.9 mg/dL), and grade 4 (≥ 30 mg/dL). These grades were then assessed for their association with hospital mortality and recovery from hyperbilirubinemia to SOFA grade (point) 2 or below (total bilirubin < 6 mg/dL). The influences of various factors, some of which caused extreme hyperbilirubinemia, while others induced bilirubin recovery, were assessed.ResultsA total of 427 patients (mean age: 59.8 years, male: 67.0%) were evaluated, and the hospital mortality for these patients was very high (76.1%). Extreme hyperbilirubinemia was observed in 111 (grade 1, 26.0%), 99 (grade 2, 23.2%), 131 (grade3, 30.7%), and 86 (grade 4, 20.1%) patients with mortality rates of 62.2%, 71.7%, 81.7%, and 90.7%, respectively (p < 0.001). The peak bilirubin value correlated with the mortality (odds ratio [OR], 1.09; 95% confidence interval [CI], 1.04-1.15, p < 0.001). Compared to those with grade 1 extreme hyperbilirubinemia, the mortality rate gradually increased as the grade increased (OR [95% CI]: 1.92 [0.70-5.28], 3.55 [1.33-9.48], and 12.47 [3.07-50.59] for grades 2, 3 and 4, respectively). The main causes of extreme hyperbilirubinemia were infection including sepsis and hypoxic hepatitis. The recovery from hyperbilirubinemia was observed in 110 (25.8%) patients. Mortality was lower for those who recovered from hyperbilirubinemia than for those who did not (29.1% vs. 92.4%, p < 0.001). The favorable factors of bilirubin recovery were albumin and ursodeoxycholic acid (UDCA).ConclusionsThis study determined that the level of extreme hyperbilirubinemia is an important prognostic factor in critically ill patients. We expect the results of this study to help predict the clinical course of and determine the optimal treatment for extreme hyperbilirubinemia.

Project description:Background: Unconjugated bilirubin (UCB) is more than the final product of heme catabolism. Mildly elevated systemic bilirubin concentrations, such as in Gilbert syndrome (GS), protect against various oxidative stress-mediated and metabolic diseases, including cardiovascular disease, type 2 diabetes mellitus, metabolic syndrome, cancer, and age-related disease. The Gunn rat is an animal model of hereditary hyperbilirubinemia widely used in assessing the effect of high serum bilirubin concentration in various organs. The present work aims to understand if life-long hyperbilirubinemia and bilirubin-priming might contribute to protection against atherosclerosis and diabetic nephropathy (DN) at the cellular level. Methods: Primary aortic endothelial cells and podocytes obtained from hyperbilirubinemic homozygous jj and normobilirubinemic heterozygous Nj Gunn rats were exposed to Palmitic Acid (PA) and Angiotensin II (Ang II), respectively, and the effects on cell viability and the activation of damage-related metabolic pathways evaluated. Results were validated on immortalized H5V and HK2 cells exposed to damage after UCB pretreatment. Results: In both primary cell models, cells obtained from jj Gunn rats showed as significantly higher than Nj Gunn rats at any dose of the toxic agent. Reduction in CHOP expression and IL-6 release was observed in jj primary aortic endothelial cells exposed to PA compared to Nj cells. The same occurred on H5V pretreated with Unconjugated bilirubin. Upon Ang II treatment, primary podocytes from jj Gunn rats showed lower DNA fragmentation, cleaved caspase-3, and cleaved PARP induction than primary podocytes from Nj Gunn rats. In HK2 cells, the induction by Ang II of HIF-1α and LOXl2 was significantly reduced by UCB pretreatment. Conclusion: Our data suggest that in models of atherosclerosis and DN life-long hyperbilirubinemia exposure or bilirubin-priming significantly contribute to decrease the injury by enhancing thecellular defensive response.

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Transcutaneous bilirubin level to predict hyperbilirubinemia in preterm neonates.

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Transcutaneous bilirubin level to predict hyperbilirubinemia in preterm neonates.

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