Bilirubin-induced Neurologic DysfunctionNCT02691156
Bilirubin Binding Capacity to Assess Bilirubin Load in Preterm Infants
An observational study of Bilirubin-induced Neurologic Dysfunction and Hyperbilirubinemia, run by Stanford University at 1 site in United States.
Trial summary
Most preterm newborns are managed by phototherapy to reverse hyperbilirubinemia with the intent to prevent bilirubin neurotoxicity. A threshold-based relationship between a specific total bilirubin level and need for intervention has been elusive. Read more about this study
- Who is it for?
- Ages 24 to 34 weeksHealthy volunteers can take part
- Conditions the study is for
- Bilirubin-induced Neurologic Dysfunction, Hyperbilirubinemia, Kernicterus
- What is being tested?
- Bilirubin Binding Capacity, End-tidal Carbon Monoxide and Carboxyhemoglobin
- How many people
- 143 participants
- Where
- 1 siteUnited States
- Study dates
- 1 Feb 2016to 31 Aug 2018
- Phase
- Observational
- Are there results?
- None posted in the registry
Key requirements
Who can take part, as listed by the sponsor. Only the study team can confirm whether you are eligible, so take this list to your doctor.
- Ages 24 to 34 weeks
- All sexes
- Healthy volunteers accepted
- Child
Study population: Inpatient premature infants
Who may be able to join
- Patients (GA 24 to ≤34 wks)
Who cannot join
- Major life-threatening anomalies and diagnosed inborn errors of metabolic disorders
- Attending physician or parent refusal
Trial locations and contacts
1 site in 1 country.
United States1 site
Lucile-Packard Children's Hospital at Stanford
Stanford, California, 94305
About this study
Most preterm newborns are managed by phototherapy to reverse hyperbilirubinemia with the intent to prevent bilirubin neurotoxicity. A threshold-based relationship between a specific total bilirubin level and need for intervention has been elusive. This is most likely due to other biomarkers such as hemolysis, developmental maturation, concurrent illnesses, or even interventions, may impede bilirubin/albumin binding. The over-prescription of phototherapy has impacted clinical and family-centered care, and in the extreme preterm infants, it may have augmented their risk of mortality. Thus, the opportunity to individualize phototherapy in in order to reduce its use is unique. The investigators have assembled a transdisciplinary team to examine critical unanswered questions including the role of bilirubin binding capacity (BBC) of an individual during the first week of life in the context of clinical modifiers and antecedents for a domain of bilirubin-induced neurologic disorders, that includes neuro-anatomical, hearing, visual and developmental processing impairments. In this study, the investigator will evaluate two new innovative nanotechniques to quantify bilirubin load for the first time in the context of a clinical decision algorithm to identify those most at risk for any bilirubin-related neurotoxicity. The investigators anticipate that knowledge gained from this study will lead to ethically testable hypotheses to individualize the prescription of phototherapy.
Read the detailed description
The investigator intends to first collect simultaneous and comprehensive "acute phase" measurements of TB, BBC, ETCOc, and COHbc in MPT infants. The investigator will then seek to understand precisely the relationship between GA, TB, BBC, ETCOc, and COHbc levels and the domains of BIND. Third, The investigator will provide a comprehensive database that can be used to improve current neonatal BIND screening practices in the context of lowered and higher BBC. The investigator's working hypothesis is that exposures to modest TB levels in the presence of significantly diminished BBC in the developing neonate result in residual deficits of one or more neuroprocessing function (BIND) at TEA.
- Patients (GA 24 to <34 wks) will be enrolled. Subject exclusion criteria: Major life-threatening anomalies and diagnosed inborn errors of metabolic disorders; attending physician or parent refusal. Clinical data collection: After receiving written informed consent, the research team will complete clinical data forms for infant demographics. The data forms will be consistent with and abstracted from the medical record. No additional information will be collected for this exploratory study. Population: The entire cohort will compromise 60-80 patients. From this cohort, 12 at-risk infants with most impaired BBC and matched with those designated as low-risk will be re-recruited for the follow-up to identify any evidence of BIND in any or all 4 of the outcome variables. Laboratory data: Once inclusion criteria are met, routine neonatal laboratory tests will be as clinically ordered. Each infant will tested for BBC and ETCOc at least 2 intervals (maximum 4 over 12h-7d) during rates-of-rise and -decrease in TB. Subsequent laboratory and clinical data will be paired with research data for statistical analysis. The investigators will compare BIND outcomes at TEA to 3 mos-corrected age (<54 wks PMA) using a re-consented sample size: n=12 for those at high risk with decreased BBC versus a GA-matched controls at low risk (n=12).
- Measurements: 0.1-mL whole blood will be drawn in special heparinized tubes for COHbc determinations and anticoagulated blood set aside for the hematofluorometry.
Plasma for peroxidase UB assays will be stored and labeled without patient identifiers.
Frozen research samples will be transported to the Spectrum Child Health Research (SCHR) Lab for analyses. 1. BBC, TB, and UB will be measured directly: 1a. BBC, TB and UB in 50-μL whole blood using POC hematofluorometry; TB performed by the hospital-based clinical laboratory; and UB in plasma using the peroxidase method (Arrows device).
ETCOc will be determined for those breathing spontaneously.
- Testing and techniques for outcome variables for select at-risk and matched control infants:
- Screening ABR: Two or more simultaneously channels will consist of the electrode pairs of: 1) contralateral to ipsilateral mastoid prominence; 2) vertex to ipsilateral mastoid; and 3) vertex to contralateral mastoid for better identification of waves. Insert tubephone earphone will be used to introduce an acoustic delay to distinguish CM response from artifact. Rarefaction clicks at 90, (75), 60, (45), and 30 dBnHL will be delivered monaurally to the right and left ears. RE and LE, ≥2 repetitions, ≥2,000 sweeps/repetition. Separate recording to rarefaction and condensation clicks will be obtained at 90 dB. The surface electrical activity will be amplified x10,000 and filtered from 30-3,000 Hz. Latencies and peak-to-trough amplitudes of waves and CM from the outer hair cells in the inner ear of the ABRs will be scored independently by "masked" interpreters (Drs. Oghalia and Popelka).
- Screening Visual Brainstem Responses after TEA (at 50-54 wks PMA): All infants in this subcohort will be evaluated using the sVEP technique described above.68 Electrodes are placed across the back of the visual cortex, midline and 2 cm to the left and right, with a reference lead at the occipital vertex. Thresholds and suprathreshold measurements will be compared with controls. Further, the infants in the bilirubin cohort can serve a case series with a dose response plot determined, comparing thresholds with TB levels. Bin averages for each type of vision can also be compared to the same for control infants to determine whether suprathreshold measures vary to any significant degree from controls (Fig. 3). Evidence from other studies of CNS damage suggests that lower signal amplitudes and thresholds correlate with CNS damage. Support for this sample size is based on practical considerations an ad hoc sample size calculation.
- Neuroimaging of the brain will be performed by conventional MRI at TEA; this is the routine near-term neuroimaging for preterm infants in our institution. MRI is performed in unsedated infants, using a 3-Tesla platform with sequences that include Sagittal T1 FLAIR, Axial DWI, T2 FRFSE, FLAIR, GRE, and SSFSE, and Coronal SSFSE and 3D SPGR over 30 min. Drs. Barnes and Hintz, who will be masked to the acute phase biomarkers data, will interpret imaging utilizing a central reader form that includes white matter scoring according to a widely used classification system, and data regarding location, number, size, and imaging characteristics of lesions. Dr. Bhutani will correlate these data to the acute biomarkers.
- Conditions
- Bilirubin-induced Neurologic Dysfunction, Hyperbilirubinemia, Kernicterus, Infant, Premature, Infant, Low Birth Weight
- Being tested
- Bilirubin Binding Capacity, End-tidal Carbon Monoxide, Carboxyhemoglobin
- Keywords
- Hematofluorometer
- Medical subject headings
- Hyperbilirubinemia, Kernicterus, Premature Birth
What participants receive
What participants receive. In a randomised study each person is assigned to one group by chance.
Bilirubin Binding CapacityDiagnostic test
Also called BBC
Research laboratory assay of bilirubin binding capacity
End-tidal Carbon MonoxideDiagnostic test
Also called ETCOc
Noninvasive bedside test to measure exhaled end-tidal carbon monoxide levels for the detection of hemolysis
CarboxyhemoglobinDiagnostic test
Also called COHbc
Laboratory assay of carboxyhemoglobin levels for the detection of hemolysis
| Study group | Role | What they receive |
|---|---|---|
| Premature Infants | Premature infants GA 24 to ≤34 wks at risk for hyperbilirubinemia will have BBC, ETCOc, and COHbc measured during 0-7 days of life. Receives: Diagnostic Test: Bilirubin Binding Capacity; Diagnostic Test: End-tidal Carbon Monoxide; Diagnostic Test: Carboxyhemoglobin |
What is being measured
The primary outcome is the main question the study is designed to answer.
Age-specific gradations of BBC values for each week of GA and in order to characterize degree of disordered BBC.
This aim addresses the hypothesis that there are functional degrees and extents of BBC that can be objectively graded to quantify insufficient BBC. These data will define BBC ranges to guide objective, accurate thresholds that identify what levels of TB compared to the BBC is "safe". Infants with insufficient (>45% saturation) and near-normal (<25% saturation) BBC will be identified as select cohorts and then further tested for BIND at term-equivalent age.
Measured: postnatal age 0-7 days
Secondary outcomes (1)
Determinants of bilirubin load (using rates of bilirubin production) on BBC
This aim addresses the hypothesis that biochemical markers of bilirubin load, individually or collectively, related to excessive bilirubin production and insufficient BBC, define the mechanisms of bilirubin load for maturational age (both term PMA and GA). The studies are directed toward translating diverse components of bilirubin loads: serum albumin, BBC, and TB rate-of-rise and decrease. These data will integrate measurements of bilirubin load using established indices of bilirubin production that accurately characterize early signs of BIND at term equivalent age that may be associated with neuroanatomical changes, and NDI.
Measured: postnatal age 0-7 days
Timeline
From the start of the study to its completion; the mark is today. Estimated dates are the sponsor’s plan.
- First posted25 Feb 2016 (estimated)
- Study start1 Feb 2016
- Primary completion31 Aug 2018
- Study completion31 Aug 2018
Resources
- Official record on ClinicalTrials.govThe registry entry this page is built from, with its full change history.
- Publications (26)Papers the sponsor has linked to this study.
- Other trials for Bilirubin-induced Neurologic DysfunctionStudies of the same condition, open and under way.
- More trials run by Stanford UniversityThe sponsor's other registered studies.
- What the trial phases meanHow a treatment moves from first tests in people to approval.
More details
For doctors and researchers: how the study is designed, who runs it, and its registry IDs.
Study design
- Study type
- Observational
- Observational model
- Cohort
- Time perspective
- Prospective
- Enrolment
- 143 participants (actual)
Sponsor and investigators
- Lead sponsor
- Stanford University
- Sponsor type
- University, hospital or other
- Collaborators
- Smith-Kettlewell Eye Research Institute
- Responsible party
- Sponsor
- Investigators
- Vinod K Bhutani, MD, Principal investigator, Stanford University
IDs, dates and publications
- ClinicalTrials.gov ID
- NCT02691156
- Sponsor's protocol ID
- IRB-31187
- Status last verified
- Sep 2021
- First submitted
- 16 Feb 2016
- Last updated
- 1 Oct 2021
- Results posted
- No
- Data monitoring committee
- Yes
- Individual data sharing
- No
Publications
Lamola AA, Bhutani VK, Du L, Castillo Cuadrado M, Chen L, Shen Z, Wong RJ, Stevenson DK. Neonatal bilirubin binding capacity discerns risk of neurological dysfunction. Pediatr Res. 2015 Feb;77(2):334-9. doi: 10.1038/pr.2014.191. Epub 2014 Nov 24.
PubMed 25420178Practice parameter: management of hyperbilirubinemia in the healthy term newborn. American Academy of Pediatrics. Provisional Committee for Quality Improvement and Subcommittee on Hyperbilirubinemia. Pediatrics. 1994 Oct;94(4 Pt 1):558-65. No abstract available.
PubMed 7755691American Academy of Pediatrics Subcommittee on Hyperbilirubinemia. Management of hyperbilirubinemia in the newborn infant 35 or more weeks of gestation. Pediatrics. 2004 Jul;114(1):297-316. doi: 10.1542/peds.114.1.297.
PubMed 15231951Bhutani VK, Johnson LH, Shapiro SM. Kernicterus in sick and preterm infants (1999-2002): a need for an effective preventive approach. Semin Perinatol. 2004 Oct;28(5):319-25. doi: 10.1053/j.semperi.2004.09.006.
PubMed 15686262Bhutani VK, Vilms RJ, Hamerman-Johnson L. Universal bilirubin screening for severe neonatal hyperbilirubinemia. J Perinatol. 2010 Oct;30 Suppl:S6-15. doi: 10.1038/jp.2010.98.
PubMed 20877410Dennery PA, Seidman DS, Stevenson DK. Neonatal hyperbilirubinemia. N Engl J Med. 2001 Feb 22;344(8):581-90. doi: 10.1056/NEJM200102223440807. No abstract available.
PubMed 11207355Johnson L, Bhutani VK, Karp K, Sivieri EM, Shapiro SM. Clinical report from the pilot USA Kernicterus Registry (1992 to 2004). J Perinatol. 2009 Feb;29 Suppl 1:S25-45. doi: 10.1038/jp.2008.211.
PubMed 19177057Maisels MJ. What's in a name? Physiologic and pathologic jaundice: the conundrum of defining normal bilirubin levels in the newborn. Pediatrics. 2006 Aug;118(2):805-7. doi: 10.1542/peds.2006-0675. No abstract available.
PubMed 16882840Watchko JF, Maisels MJ. Jaundice in low birthweight infants: pathobiology and outcome. Arch Dis Child Fetal Neonatal Ed. 2003 Nov;88(6):F455-8. doi: 10.1136/fn.88.6.f455.
PubMed 14602689Watchko JF, Oski FA. Kernicterus in preterm newborns: past, present, and future. Pediatrics. 1992 Nov;90(5):707-15.
PubMed 1408544Morris BH, Oh W, Tyson JE, Stevenson DK, Phelps DL, O'Shea TM, McDavid GE, Perritt RL, Van Meurs KP, Vohr BR, Grisby C, Yao Q, Pedroza C, Das A, Poole WK, Carlo WA, Duara S, Laptook AR, Salhab WA, Shankaran S, Poindexter BB, Fanaroff AA, Walsh MC, Rasmussen MR, Stoll BJ, Cotten CM, Donovan EF, Ehrenkranz RA, Guillet R, Higgins RD; NICHD Neonatal Research Network. Aggressive vs. conservative phototherapy for infants with extremely low birth weight. N Engl J Med. 2008 Oct 30;359(18):1885-96. doi: 10.1056/NEJMoa0803024.
PubMed 18971491O'Shea TM, Dillard RG, Klinepeter KL, Goldstein DJ. Serum bilirubin levels, intracranial hemorrhage, and the risk of developmental problems in very low birth weight neonates. Pediatrics. 1992 Dec;90(6):888-92.
PubMed 1279513Oh W, Tyson JE, Fanaroff AA, Vohr BR, Perritt R, Stoll BJ, Ehrenkranz RA, Carlo WA, Shankaran S, Poole K, Wright LL; National Institute of Child Health and Human Development Neonatal Research Network. Association between peak serum bilirubin and neurodevelopmental outcomes in extremely low birth weight infants. Pediatrics. 2003 Oct;112(4):773-9. doi: 10.1542/peds.112.4.773.
PubMed 14523165Yeo KL, Perlman M, Hao Y, Mullaney P. Outcomes of extremely premature infants related to their peak serum bilirubin concentrations and exposure to phototherapy. Pediatrics. 1998 Dec;102(6):1426-31. doi: 10.1542/peds.102.6.1426.
PubMed 9832580Johnson L, Bhutani VK. The clinical syndrome of bilirubin-induced neurologic dysfunction. Semin Perinatol. 2011 Jun;35(3):101-13. doi: 10.1053/j.semperi.2011.02.003.
PubMed 21641482
Study at a glance
From the registry record, last updated by the sponsor on 1 Oct 2021. Recruitment status is as the sponsor reported it: confirm with the study team.
- Official title
- Bilirubin Binding Capacity to Assess Bilirubin Load in Preterm Infants
- ClinicalTrials.gov ID
- NCT02691156
- Acronym / sponsor ID
- IRB-31187
- Conditions
- Bilirubin-induced Neurologic Dysfunction, Hyperbilirubinemia, Kernicterus, Infant, Premature, Infant, Low Birth Weight
- Keywords
- Hematofluorometer
- Study type
- Observational
- Recruitment status
- Completed
- Enrolment
- 143 participants (actual)
- Lead sponsor
- Stanford UniversityUniversity, hospital or other
- Collaborators
- Smith-Kettlewell Eye Research Institute
- Study start
- 1 Feb 2016 (actual)
- Primary completion
- 31 Aug 2018 (actual)
- Study completion
- 31 Aug 2018 (actual)
- First posted
- 25 Feb 2016 (estimated)
- Results
- Not posted in the source record
Clinical summary
The research question as the sponsor registered it. This describes what the study plans to test, not what it found.
Most preterm newborns are managed by phototherapy to reverse hyperbilirubinemia with the intent to prevent bilirubin neurotoxicity. A threshold-based relationship between a specific total bilirubin level and need for intervention has been elusive. This is most likely due to other biomarkers such as hemolysis, developmental maturation, concurrent illnesses, or even interventions, may impede bilirubin/albumin binding. The over-prescription of phototherapy has impacted clinical and family-centered care, and in the extreme preterm infants, it may have augmented their risk of mortality. Thus, the opportunity to individualize phototherapy in in order to reduce its use is unique. The investigators have assembled a transdisciplinary team to examine critical unanswered questions including the role of bilirubin binding capacity (BBC) of an individual during the first week of life in the context of clinical modifiers and antecedents for a domain of bilirubin-induced neurologic disorders, that includes neuro-anatomical, hearing, visual and developmental processing impairments. In this study, the investigator will evaluate two new innovative nanotechniques to quantify bilirubin load for the first time in the context of a clinical decision algorithm to identify those most at risk for any bilirubin-related neurotoxicity. The investigators anticipate that knowledge gained from this study will lead to ethically testable hypotheses to individualize the prescription of phototherapy.
Detailed description
The investigator intends to first collect simultaneous and comprehensive "acute phase" measurements of TB, BBC, ETCOc, and COHbc in MPT infants. The investigator will then seek to understand precisely the relationship between GA, TB, BBC, ETCOc, and COHbc levels and the domains of BIND. Third, The investigator will provide a comprehensive database that can be used to improve current neonatal BIND screening practices in the context of lowered and higher BBC. The investigator's working hypothesis is that exposures to modest TB levels in the presence of significantly diminished BBC in the developing neonate result in residual deficits of one or more neuroprocessing function (BIND) at TEA.
- Patients (GA 24 to <34 wks) will be enrolled. Subject exclusion criteria: Major life-threatening anomalies and diagnosed inborn errors of metabolic disorders; attending physician or parent refusal. Clinical data collection: After receiving written informed consent, the research team will complete clinical data forms for infant demographics. The data forms will be consistent with and abstracted from the medical record. No additional information will be collected for this exploratory study. Population: The entire cohort will compromise 60-80 patients. From this cohort, 12 at-risk infants with most impaired BBC and matched with those designated as low-risk will be re-recruited for the follow-up to identify any evidence of BIND in any or all 4 of the outcome variables. Laboratory data: Once inclusion criteria are met, routine neonatal laboratory tests will be as clinically ordered. Each infant will tested for BBC and ETCOc at least 2 intervals (maximum 4 over 12h-7d) during rates-of-rise and -decrease in TB. Subsequent laboratory and clinical data will be paired with research data for statistical analysis. The investigators will compare BIND outcomes at TEA to 3 mos-corrected age (<54 wks PMA) using a re-consented sample size: n=12 for those at high risk with decreased BBC versus a GA-matched controls at low risk (n=12).
- Measurements: 0.1-mL whole blood will be drawn in special heparinized tubes for COHbc determinations and anticoagulated blood set aside for the hematofluorometry.
Plasma for peroxidase UB assays will be stored and labeled without patient identifiers.
Frozen research samples will be transported to the Spectrum Child Health Research (SCHR) Lab for analyses. 1. BBC, TB, and UB will be measured directly: 1a. BBC, TB and UB in 50-μL whole blood using POC hematofluorometry; TB performed by the hospital-based clinical laboratory; and UB in plasma using the peroxidase method (Arrows device).
ETCOc will be determined for those breathing spontaneously.
- Testing and techniques for outcome variables for select at-risk and matched control infants:
- Screening ABR: Two or more simultaneously channels will consist of the electrode pairs of: 1) contralateral to ipsilateral mastoid prominence; 2) vertex to ipsilateral mastoid; and 3) vertex to contralateral mastoid for better identification of waves. Insert tubephone earphone will be used to introduce an acoustic delay to distinguish CM response from artifact. Rarefaction clicks at 90, (75), 60, (45), and 30 dBnHL will be delivered monaurally to the right and left ears. RE and LE, ≥2 repetitions, ≥2,000 sweeps/repetition. Separate recording to rarefaction and condensation clicks will be obtained at 90 dB. The surface electrical activity will be amplified x10,000 and filtered from 30-3,000 Hz. Latencies and peak-to-trough amplitudes of waves and CM from the outer hair cells in the inner ear of the ABRs will be scored independently by "masked" interpreters (Drs. Oghalia and Popelka).
- Screening Visual Brainstem Responses after TEA (at 50-54 wks PMA): All infants in this subcohort will be evaluated using the sVEP technique described above.68 Electrodes are placed across the back of the visual cortex, midline and 2 cm to the left and right, with a reference lead at the occipital vertex. Thresholds and suprathreshold measurements will be compared with controls. Further, the infants in the bilirubin cohort can serve a case series with a dose response plot determined, comparing thresholds with TB levels. Bin averages for each type of vision can also be compared to the same for control infants to determine whether suprathreshold measures vary to any significant degree from controls (Fig. 3). Evidence from other studies of CNS damage suggests that lower signal amplitudes and thresholds correlate with CNS damage. Support for this sample size is based on practical considerations an ad hoc sample size calculation.
- Neuroimaging of the brain will be performed by conventional MRI at TEA; this is the routine near-term neuroimaging for preterm infants in our institution. MRI is performed in unsedated infants, using a 3-Tesla platform with sequences that include Sagittal T1 FLAIR, Axial DWI, T2 FRFSE, FLAIR, GRE, and SSFSE, and Coronal SSFSE and 3D SPGR over 30 min. Drs. Barnes and Hintz, who will be masked to the acute phase biomarkers data, will interpret imaging utilizing a central reader form that includes white matter scoring according to a widely used classification system, and data regarding location, number, size, and imaging characteristics of lesions. Dr. Bhutani will correlate these data to the acute biomarkers.
Study design
- Observational model
- Cohort
- Time perspective
- Prospective
- Number of arms
- 1
| Arm | Type | Receives |
|---|---|---|
| Premature Infants | – | Diagnostic Test: Bilirubin Binding Capacity, Diagnostic Test: End-tidal Carbon Monoxide, Diagnostic Test: CarboxyhemoglobinPremature infants GA 24 to ≤34 wks at risk for hyperbilirubinemia will have BBC, ETCOc, and COHbc measured during 0-7 days of life. |
Who may qualify
- Ages
- 24 to 34 weeks
- Sex
- All
- Healthy volunteers
- Accepted
- Age groups
- Child
- Study population
- Inpatient premature infants
Key inclusion criteria (1 listed)
- Patients (GA 24 to ≤34 wks)
Key exclusion criteria (2 listed)
- Major life-threatening anomalies and diagnosed inborn errors of metabolic disorders
- Attending physician or parent refusal
Eligibility is decided by the study team after screening; this overview does not establish that a patient qualifies. Full inclusion and exclusion criteria.
Interventions
| Intervention | Type | Arms |
|---|---|---|
| Bilirubin Binding CapacityAlso: BBCResearch laboratory assay of bilirubin binding capacity | Diagnostic test | Premature Infants |
| End-tidal Carbon MonoxideAlso: ETCOcNoninvasive bedside test to measure exhaled end-tidal carbon monoxide levels for the detection of hemolysis | Diagnostic test | Premature Infants |
| CarboxyhemoglobinAlso: COHbcLaboratory assay of carboxyhemoglobin levels for the detection of hemolysis | Diagnostic test | Premature Infants |
Primary outcome
Age-specific gradations of BBC values for each week of GA and in order to characterize degree of disordered BBC.
Time frame: postnatal age 0-7 days
This aim addresses the hypothesis that there are functional degrees and extents of BBC that can be objectively graded to quantify insufficient BBC. These data will define BBC ranges to guide objective, accurate thresholds that identify what levels of TB compared to the BBC is "safe". Infants with insufficient (>45% saturation) and near-normal (<25% saturation) BBC will be identified as select cohorts and then further tested for BIND at term-equivalent age.
1 secondary outcome
Determinants of bilirubin load (using rates of bilirubin production) on BBC
Time frame: postnatal age 0-7 days
Results and safety
The study is completed, but results are not available in the source record. That does not mean the treatment did or did not work.
Research links
- Official record on ClinicalTrials.govLast updated by the sponsor 1 Oct 2021.
- Background: PubMed 25420178Lamola AA, Bhutani VK, Du L, Castillo Cuadrado M, Chen L, Shen Z, Wong RJ, Stevenson DK. Neonatal bilirubin binding capacity discerns risk of neurological dysfunction. Pediatr Res. 2015 Feb;77(2):334-9. doi: 10.1038/pr.2014.191. Epub 2014 Nov 24.
- Background: PubMed 7755691Practice parameter: management of hyperbilirubinemia in the healthy term newborn. American Academy of Pediatrics. Provisional Committee for Quality Improvement and Subcommittee on Hyperbilirubinemia. Pediatrics. 1994 Oct;94(4 Pt 1):558-65. No abstract available.
- Background: PubMed 15231951American Academy of Pediatrics Subcommittee on Hyperbilirubinemia. Management of hyperbilirubinemia in the newborn infant 35 or more weeks of gestation. Pediatrics. 2004 Jul;114(1):297-316. doi: 10.1542/peds.114.1.297.
- Background: PubMed 15686262Bhutani VK, Johnson LH, Shapiro SM. Kernicterus in sick and preterm infants (1999-2002): a need for an effective preventive approach. Semin Perinatol. 2004 Oct;28(5):319-25. doi: 10.1053/j.semperi.2004.09.006.
- Background: PubMed 20877410Bhutani VK, Vilms RJ, Hamerman-Johnson L. Universal bilirubin screening for severe neonatal hyperbilirubinemia. J Perinatol. 2010 Oct;30 Suppl:S6-15. doi: 10.1038/jp.2010.98.
- Background: PubMed 11207355Dennery PA, Seidman DS, Stevenson DK. Neonatal hyperbilirubinemia. N Engl J Med. 2001 Feb 22;344(8):581-90. doi: 10.1056/NEJM200102223440807. No abstract available.
- Background: PubMed 19177057Johnson L, Bhutani VK, Karp K, Sivieri EM, Shapiro SM. Clinical report from the pilot USA Kernicterus Registry (1992 to 2004). J Perinatol. 2009 Feb;29 Suppl 1:S25-45. doi: 10.1038/jp.2008.211.
- Background: PubMed 16882840Maisels MJ. What's in a name? Physiologic and pathologic jaundice: the conundrum of defining normal bilirubin levels in the newborn. Pediatrics. 2006 Aug;118(2):805-7. doi: 10.1542/peds.2006-0675. No abstract available.
- Background: PubMed 14602689Watchko JF, Maisels MJ. Jaundice in low birthweight infants: pathobiology and outcome. Arch Dis Child Fetal Neonatal Ed. 2003 Nov;88(6):F455-8. doi: 10.1136/fn.88.6.f455.
- Background: PubMed 1408544Watchko JF, Oski FA. Kernicterus in preterm newborns: past, present, and future. Pediatrics. 1992 Nov;90(5):707-15.
- Background: PubMed 18971491Morris BH, Oh W, Tyson JE, Stevenson DK, Phelps DL, O'Shea TM, McDavid GE, Perritt RL, Van Meurs KP, Vohr BR, Grisby C, Yao Q, Pedroza C, Das A, Poole WK, Carlo WA, Duara S, Laptook AR, Salhab WA, Shankaran S, Poindexter BB, Fanaroff AA, Walsh MC, Rasmussen MR, Stoll BJ, Cotten CM, Donovan EF, Ehrenkranz RA, Guillet R, Higgins RD; NICHD Neonatal Research Network. Aggressive vs. conservative phototherapy for infants with extremely low birth weight. N Engl J Med. 2008 Oct 30;359(18):1885-96. doi: 10.1056/NEJMoa0803024.
- Background: PubMed 1279513O'Shea TM, Dillard RG, Klinepeter KL, Goldstein DJ. Serum bilirubin levels, intracranial hemorrhage, and the risk of developmental problems in very low birth weight neonates. Pediatrics. 1992 Dec;90(6):888-92.
- Individual participant dataSharing planned: No
Referral and contact
AzTrials does not enrol participants or take referrals. Contact the study team or a site listed below; they decide who can take part. This study is not recruiting at the moment.
Vinod K Bhutani, MD principal investigator
Stanford University
1 site in 1 country: see every site and its status.
Questions about this trial
What is this clinical trial studying?
An observational study of Bilirubin-induced Neurologic Dysfunction and Hyperbilirubinemia, run by Stanford University at 1 site in United States.
The full registered description is in the About this study section and the official record.
Who may be eligible to take part?
The sponsor lists 1 inclusion and 2 exclusion criteria. Eligibility is decided by the study team after screening, so read the full criteria and contact a listed site.
Is this clinical trial currently recruiting?
The record says: finished, as of the sponsor's last update on 1 Oct 2021. Status can change between updates, so confirm with the study contact before making plans.
Where is the study taking place?
The record lists 1 site in United States. Whether a site is taking part right now should be confirmed with that site. See every site.
What are the possible benefits and risks?
They depend on the study and the treatment, and no study can promise a benefit. The study team explains the known risks during informed consent, before anyone joins; the record itself does not list them.
Are results available for this study?
The study is completed, but results are not available in the source record. That does not mean the treatment did or did not work.
How can a doctor refer a patient or contact the research team?
The record lists no contact. The official record names the sponsor, who can be asked directly. AzTrials does not enrol participants or take referrals.
What does the primary outcome measure?
Age-specific gradations of BBC values for each week of GA and in order to characterize degree of disordered BBC. (time frame: postnatal age 0-7 days). It is what the study was designed to measure, not a finding.
Where can I read the original study information?
On the ClinicalTrials.gov record for NCT02691156, which also lists 26 linked publications.
Does a listing mean the treatment is approved or proven to work?
No. A listing means the study is registered. It does not show that the treatment is safe, works, or is approved by a regulator.
How often is this information updated?
AzTrials copies changed records from ClinicalTrials.gov every night and reloads the whole registry every week. The sponsor last updated this record on 1 Oct 2021.