Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Hyperbilirubinemia, Neonatal”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 19 recordsLinked to original sources
PubMedDate not supplied

[Evoked auditory potentials in neonatal hyperbilirubinemia].

Neonatal hyperbilirubinemia (greater than 20 mg%) is an audiological risk factor. In order to check early detection of bilirubin-induced neurological damage in the brainstem, 19 newborns were enrolled in the present study. The criteria was a bilirubin level ranging from 12 to 20 mg%. A likely mechanism for bilirubin intoxication may be the slowing and desynchronization of acoustic stimuli in the brainstem. Auditory brainstem responses were performed using non filtered clicks at 100 dB SPL (peak equivalent). Absolute and interpeak latencies of waves I and V were measured and correlated to bilirubinemia upon acoustic stimulation and maximal bilirubinemia observed during neonatal observation. Significant correlations were noted between bilirubinemia and V or V-I latencies. No significant correlation was observed between bilirubinemia and wave I latencies. Similar results were obtained in a restricted group of term neonates with hyperbilirubinemia. It is, thus, concluded that hyperbilirubinemia affects the upper auditory pathways.

Auditory Pathways↗
PubMed1983

Effect of segmental epidural analgesia on neonatal serum bilirubin concentration and incidence of neonatal hyperbilirubinemia.

Neonatal serum bilirubin levels were determined at the ages of 12 hrs, 2 days, 3 days, 4 days and 5 days in 80 infants. Forty-three mothers had received segmental epidural analgesia at the height of Th 10-12 for pain relief during the first stage of labor. The analgesic agent used was 0.5% bupivacaine. The individual doses were of 4 ml. Thirty-seven mothers served as a control group. The groups were further divided into smaller groups according to whether oxytocin was used for induction or acceleration of labor--or not. The results showed no statistically significant differences in the neonatal serum bilirubin levels at different times between the epidural and the control groups, whether oxytocin was used or not. Nor did the incidence of neonatal hyperbilirubinemia cases differ between the groups.

Anesthesia, Epidural↗
PubMed2003

Neonatal hyperbilirubinemia in Japanese neonates: analysis of the heme oxygenase-1 gene and fetal hemoglobin composition in cord blood.

Neonatal hyperbilirubinemia is frequent and severe in Japanese infants. Although the G71R mutation of the bilirubin uridine diphosphate-glucuronosyltransferase gene is associated with severe neonatal hyperbilirubinemia in this population, it accounts for only half of the neonates with severe hyperbilirubinemia. It was suggested that increased bilirubin production would also be associated with severe neonatal hyperbilirubinemia in Japanese infants. To elucidate the genetic factors causing severe hyperbilirubinemia in these patients, we studied two notable factors associated with bilirubin production: heme oxygenase-1, a key enzyme of heme metabolism, and fetal Hb composition, a factor possibly associated with heme load in neonates. We first determined the sequences of promoter and all coding regions of the heme oxygenase-1 gene in Japanese neonates who had undergone phototherapy, but found no mutation except for the polymorphic (GT)n repeats in the promoter region. These repeats modulate the transcription of the heme oxygenase-1 gene, and the longer repeat sequences are known to reduce the transcription. We detected a significant difference in the allele frequencies of each number of (GT)n repeats between Japanese and German populations. However, we could not find a relation between those polymorphisms and neonatal hyperbilirubinemia. We next analyzed the state of Hb switching of the gamma- to beta-globin chain and the phenotype of gamma-globin chain isoforms in cord blood. We found no relation between fetal Hb composition and neonatal hyperbilirubinemia. Further studies are required to elucidate genetic or environmental factors in neonatal hyperbilirubinemia in Japanese infants.

Chromatography, High Pressure Liquid↗
PubMed1993

[The influence of neonatal hyperbilirubinemia on neonatal behavior].

Two groups of neonates, 30 cases with hyperbilirubinemia (307.8 +/- 99.86 mumol/L) and 30 normal newborns (control group with bilirubin 80.37 +/- 35.74 mumol/L), were evaluated with Neonatal Behavioral Assessment Scale (NBAS) and followed up at the age of 2 months and 5 months. All cases in the two groups were evaluated with NBAS at ages of 2-3 days, 12-14 days and 26-28 days. The results showed that there were statistically significant differences between the two groups in the aspects of attention and social responsiveness, the ability to modulate state of consciousness, the motor integrity and the reflexes. We also found that while the level of bilirubin was below 205.2 mumol/L, there was no correlation between the level of bilirubin and NBAS (r = -0.095, P > 0.02), but when bilirubin was at or above the level of 205.2 mumol/L, there was significant negative correlation (r = -0.53, P < 0.001) between the two. The follow-up revealed that 9 of 23 jaundiced infants had abnormal auditory reactions or abnormal muscle tonus at the age of 2 months; 8 of the 9 infants recovered, but 1 still had abnormal muscle tonus by the age of 5 months. The study suggests that hyperbilirubinemia above the level of 205.2 mumol/L would affect neonatal behavior and the greater the severity of jaundice, the more significant the influence on neonatal behavior. The effects on some jaundiced infants may last 5 months or more. NBAS is a valuable scale for early detection of mild brain dysfunctions which are less obvious on clinical examination.

Brain↗
PubMed1995

Hospital readmission due to neonatal hyperbilirubinemia.

Severe neonatal hyperbilirubinemia can occur without apparent reason in term healthy breast-fed infants and some develop kernicterus. The aim of our study was to assess the incidence of severe hyperbilirubinemia in term healthy newborns discharged from the hospital. From January 1 through December 31, 1994, 6705 infants were delivered at Bikur-Cholim and Misgav-Ladach Community Hospitals. All 1448 newborns discharged with a serum bilirubin level > 10.0 mg/dL were instructed to return to the hospital within 3 days for follow-up, as well as bilirubin determination. Twenty-one newborns with a bilirubin level > 18.0 mg/dL were identified and readmitted at mean +/- standard deviation (SD) 5.5 +/- 1.8 (range, 5 to 10 days of life). This represents 1.7% of the 1220 infants who returned for follow-up examination. Mean +/- SD serum bilirubin levels at readmission were 19.6 +/- 2.5 mg/dL. All but one of the infants were breast-fed. No cases of ABO incompatibility were found and two newborns were glucose-6-phosphate dehydrogenase (G6PD)-deficient. Sepsis work-up and direct Coomb's tests were negative in all cases. None had hemolysis or were found to have any cause for hyperbilirubinemia other than breast-feeding. Phototherapy was provided in all but two cases, and an exchange transfusion was performed in one case. Three additional infants, with bilirubin levels < 10 mg/dL at discharge, were readmitted due to hyperbilirubinemia. One was diagnosed with neonatal hepatitis. We conclude that, based on our study population, 0.36% of term infants may subsequently develop severe neonatal hyperbilirubinemia in the first postnatal week.(ABSTRACT TRUNCATED AT 250 WORDS)

Breast Feeding↗
PubMed2005

Neonatal hyperbilirubinemia and the bilirubin uridine diphosphate-glucuronosyltransferase gene: the common -3263T > G mutation of phenobarbital response enhancer module is not associated with the neonatal hyperbilirubinemia in Japanese.

BACKGROUND: Neonatal hyperbilirubinemia is frequent and severe in Japanese newborns. Previously, it has been reported that half of the Japanese neonates with severe hyperbilirubinemia carried the 211G > A (p.G71R) mutation of the bilirubin uridine diphosphate-glucuronosyltransferase (UGT1A1) gene causing Gilbert syndrome. Recently, it was reported that the -3263T > G mutation in the phenobarbital response enhancer module in UGT1A1 was associated with the majority of cases of Gilbert syndrome. The gene frequency of the -3263T > G mutation was determined and the relation with neonatal hyperbilirubinemia in Japanese was studied. METHODS: UGT1A1 in 119 neonates born at Yamagata University Hospital, Yamagata, Japan, and 26 subjects who had undergone phototherapy due to severe hyperbilirubinemia at four other hospitals were studied. The gene frequency of -3263T > G mutation in Japanese, Korean, Chinese and German healthy adult controls was also determined. Hyperbilirubinemia was assessed with a Jaundice Meter and UGT1A1 was analyzed by sequence determination or restriction enzyme method. RESULTS: The gene frequency of the -3263T > G mutation was 0.26 in Japanese subjects and was similar to the prevalence in Korean, Chinese and German populations. However, there was no significant increase in the gene frequency of the mutation in the neonates who required phototherapy for hyperbilirubinemia compared to that in the neonates without severe hyperbilirubinemia. In addition, neonates with or without the mutation did not show a significant change in the level of bilirubin and the mutation also did not show a synergic effect with the 211G > A mutation on the level of bilirubin. CONCLUSION: The -3263T > G mutation is not likely to be associated with the neonatal hyperbilirubinemia in Japanese.

Asian People↗
PubMed1989

Immunological profile in neonatal hyperbilirubinemia.

Thirty cases of neonatal hyperbilirubinemia of varying etiology, severity and duration; and twenty six normal healthy newborns were subjected to various tests of cellular and humoral immunity. The results revealed a significant depression of all the parameters of cellular immunity in neonatal hyperbilirubinemia of greater than or equal to 10 mg/dl as compared to the control values. The depression of immunological profile in these newborns was seen to be more pronounced with increasing duration and severity of jaundice. A limited assessment of the humoral immunity by the B cell count and serum immunoglobulin IgG levels, however, showed no significant difference from the control.

B-Lymphocytes↗
PubMed2006

Visual evoked potentials in neonatal hyperbilirubinemia.

The management of neonatal hyperbilirubinemia is very standardized. However, there is a lack of an objective method to evaluate the cerebral effects of bilirubin apart from brainstem auditory evoked potentials. There were few studies evaluating the effects of hyperbilirubinemia or phototherapy on the visual pathway in infants with hyperbilirubinemia. Serial visual evoked potentials of two groups of term neonates (N = 24)--group 1 with moderate hyperbilirubinemia (n = 16) and group 2 with severe hyperbilirubinemia (n = 8)--were evaluated prospectively. All infants had regular physical, neurologic, visual, and auditory evaluations until 3 years. Four (16%) had abnormal visual evoked potentials before 1 year, and the abnormalities returned to normal thereafter. There was no significant difference in visual evoked potentials between the two groups. All had normal neurodevelopmental status by 3 years, with the exception of one child from the severe group with ABO incompatibility with transient mild motor delay, hypotonia, and abnormal visual evoked potential. There were no abnormal effects of phototherapy on visual evoked potentials in infants with neonatal hyperbilirubinemia after 1 year of age. Although our sample size was small, the results suggest that the effects of hyperbilirubinemia on visual evoked potentials might be transient. (J Child Neurol 2006;21:58-62).

Child Development↗
PubMed2006

Incidence and causes of severe neonatal hyperbilirubinemia in Canada.

BACKGROUND: Severe hyperbilirubinemia is the most common cause of neonatal readmission to hospital in Canada even though, in the majority of cases, risk factors can be identified before discharge. Severe neonatal hyperbilirubinemia and kernicterus continue to be reported worldwide in otherwise healthy term infants. We conducted this study to estimate the incidence of severe neonatal hyperbilirubinemia in Canada and to determine underlying causes, improved knowledge of which would be valuable to help identify strategies for risk reduction. METHODS: Data on term infants 60 days of age and younger with unconjugated hyperbilirubinemia were collected prospectively through the Canadian Paediatric Surveillance Program from 2002 to 2004. Infants were included if they had a peak serum total bilirubin level of more than 425 micromol/L or underwent an exchange transfusion. Infants with rhesus iso-immunization or who were born at less than 36 weeks' gestation were excluded. RESULTS: Of 367 cases reported, 258 were confirmed to be severe neonatal hyperbilirubinemia, for an estimated incidence of 1 in 2480 live births. Causes were identified in 93 cases and included ABO incompatibility (n = 48), glucose-6-phosphate dehydrogenase deficiency (n = 20), other antibody incompatibility (n = 12) and hereditary spherocytosis (n = 7). The mean peak bilirubin level reported was 471 micromol/L (standard deviation [SD] 76 micromol/L, range 156-841 micromol/L). Fifty-seven infants (22.1%) underwent an exchange transfusion. A total of 185 infants (71.7%) were readmitted to hospital, 121 (65.4%) of them within 5 days of age. INTERPRETATION: Severe neonatal hyperbilirubinemia continues to occur frequently in Canada. In the majority of cases, the underlying cause was not identified. The high readmission rate within days after initial discharge indicates a need for a more thorough assessment of newborn infants and consideration of strategies to identify at-risk newborns, such as predischarge measurement of serum bilirubin levels.

Adult↗
PubMed1988

Recurrence risk of neonatal hyperbilirubinemia in siblings.

The recurrence of neonatal hyperbilirubinemia (NHB) in full siblings was studied in 3301 live infants born between 1966 and 1986 to 1669 male US Army veterans who were part of a nationwide health study. The study population included 580 sibships with one infant, 679 with two, and 410 with three or more. Hospital of birth medical records were abstracted on these children. Neonatal hyperbilirubinemia was defined as present if the recorded peak bilirubin level was greater than 205 mumol/L in the absence of hemolytic disease of the newborn. The risk of NHB in newborns who have one or more prior sibs with NHB was 3.1 times higher than that of newborns who have prior sibs without NHB (10.3% vs 3.6%). Simultaneous adjustment for risk factors for NHB, such as feeding patterns, year of birth, maternal obstetric events, and infant health variables, did not explain the excess risk of NHB in sibs. Moreover, the risk of severe NHB (peak bilirubin level, greater than 257 mumol/L) in newborns who have one or more prior sibs with severe NHB was 12.5 times higher than that of newborns who have prior sibs without severe NHB (10.5% vs 0.9%). Separate analyses in sibships where all sibs were breast-fed and in sibships where all sibs were bottle-fed gave similar results. These data clearly suggest the familial nature of NHB. The higher risk of recurrence of NHB in sibs does not seem to be due to known environmental risk factors for NHB.

Bilirubin↗
PubMed2006

Management of neonatal hyperbilirubinemia: pediatricians' practices and educational needs.

BACKGROUND: Early detection and treatment of neonatal hyperbilirubinemia is important in the prevention of bilirubin-induced encephalopathy. In this study, we evaluated the New Jersey pediatricians' practices and beliefs regarding the management of neonatal hyperbilirubinemia and their compliance with the recommendations made by the American Academy of Pediatrics (AAP) in 1994. METHODS: A survey questionnaire was mailed to a random sample of 800 pediatricians selected from a list of 1623 New Jersey Fellows of the AAP initially in October 2003 and then in February 2004 for the non-respondents. In addition to the physicians' demographic characteristics, the questionnaire addressed various aspects of neonatal hyperbilirubinemia management including the diagnosis, treatment, and follow up as well as the pediatricians' beliefs regarding the significance of risk factors in the development of severe hyperbilirubinemia. RESULTS: The adjusted response rate of 49.1% (n = 356) was calculated from the 725 eligible respondents. Overall, the practicing pediatricians reported high utilization (77.9%) of the cephalocaudal progression of jaundice and low utilization (16.1%) of transcutaneous bilirubinometry for the quantification of the severity of jaundice. Most of the respondents (87.4%) identified jaundice as an indicator for serum bilirubin (TSB) testing prior to the neonate's discharge from hospital, whereas post-discharge, only 57.7% felt that a TSB was indicated (P < 0.01). If the neonate's age was under 72 hours, less than one-third of the respondents reported initiation of phototherapy at TSB levels lower than the treatment parameters recommended by the AAP in 1994, whereas if the infant was more than 72 hours old, almost 60% were initiating phototherapy at TSB lower than the 1994 AAP guidelines. Most respondents did not regard neonatal jaundice noted after discharge and gestational ages 37-38 weeks as being significant in the development of severe hyperbilirubinemia. However, the majority did recognize the importance of jaundice presenting within the first 24 hours and Rh/ABO incompatibility. CONCLUSION: The pediatricians' practices regarding the low utilization of laboratory diagnosis for the quantification of jaundice after discharge and underestimation of risk factors that contribute to the development of severe hyperbilirubinemia are associated with initiation of phototherapy at lower than AAP recommended treatment parameters and recognition of neonatal hyperbilirubinemia as an important public health concern.

Adult↗
PubMedDate not supplied

Cochlear and brain stem responses in hearing loss following neonatal hyperbilirubinemia.

The site of lesion in hearing loss following neonatal hyperbilirubinemia is unclear. Histopathological studies have implicated the brain stem auditory nuclei while other investigations have hinted at a lesion in the cochlea. In order to clarify this issue, attempts were made to record responses from the auditory pathway in 13 patients with hearing loss following neonatal hyperbilirubinemia. The neural response from the auditory nerve was absent in 11 of the 13 patients and present only in response to high intensity stimuli in 2 patients. However, the response of the cochlear hair cells (cochlear microphonic potential) was present in 9 of the 13 patients. In most other cases of sensorineural hearing loss, with no history of hyperbilirubinemia, the hair cell response was absent. This is functional evidence for auditory nerve damage in cases of hearing loss following neonatal hyperbilirubinemia while the hair cells are spared.

Adult↗