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Journal articles on the topic 'Kernicteru'

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Published: 1 April 2023

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1

Ebbesen, Finn. "Kernicterus." Acta Obstetricia et Gynecologica Scandinavica 89, no. 5 (May 2010): 726. http://dx.doi.org/10.3109/00016340903540653.

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2

Stephenson, John B. P. "Kernicterus." European Journal of Paediatric Neurology 15, no. 2 (March 2011): 181. http://dx.doi.org/10.1016/j.ejpn.2010.12.002.

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3

Watchko, Jon F., and Frank A. Oski. "Kernicterus in Preterm Newborns: Past, Present, and Future." Pediatrics 90, no. 5 (November 1, 1992): 707–15. http://dx.doi.org/10.1542/peds.90.5.707.

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This historical overview of kernicterus in prematurity, from the 1950s to the present, provides a unique perspective on this clinical conundrum. Three separate periods of pediatric history are detailed in relationship to our understanding of kernicterus in the preterm newborn: (1) the pre-intensive care era (1950 to 1965); (2) the low bilirubin kernicterus era (1965 to 1982); and (3) the 1980s. Each period demonstrates selected insights regarding kernicterus in prematurity, and together with recent reports suggest that premature newborns are now at extremely low risk of developing kernicterus when managed using current standards of care. However, the current conservative empiric guidelines for preventing kernicterus are questioned, and it is suggested that additional study is needed to clarify this issue in the 1990s.
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4

Simpson, Kathleen Rice. "Kernicterus Prevention." MCN, The American Journal of Maternal/Child Nursing 32, no. 2 (March 2007): 132. http://dx.doi.org/10.1097/01.nmc.0000264309.07661.c3.

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5

Das, Sumit, and Frank van Landeghem. "Clinicopathological Spectrum of Bilirubin Encephalopathy/Kernicterus." Diagnostics 9, no. 1 (February 28, 2019): 24. http://dx.doi.org/10.3390/diagnostics9010024.

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Bilirubin encephalopathy/kernicterus is relatively rare, but continues to occur despite universal newborn screening. What is more interesting is the spectrum of clinical and even neuropathological findings that have been reported in the literature to be associated with bilirubin encephalopathy and kernicterus. In this review, the authors discuss the array of clinicopathological findings reported in the context of bilirubin encephalopathy and kernicterus, as well as the types of diagnostic testing used in patients suspected of having bilirubin encephalopathy or kernicterus. The authors aim to raise the awareness of these features among both pediatric neurologists and neuropathologists.
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6

Belz, Katie M., Andrew J. Specht, Victoria S. Johnson, and Julia A. Conway. "MRI Findings in a Dog with Kernicterus." Journal of the American Animal Hospital Association 49, no. 4 (July 1, 2013): 286–92. http://dx.doi.org/10.5326/jaaha-ms-5881.

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A severe increase in total bilirubin coincided with a decline in neurologic status to comatose in a 9 yr old spayed female mixed-breed dog being treated for immune-mediated hemolytic anemia. MRI of the brain was performed to investigate potential causes for the neurologic signs. MRI revealed bilaterally symmetrical hyperintensities within the caudate nuclei, globus pallidus, thalamus, deep cerebellar nuclei, and cortical gray matter on T2-weighted and fluid-attenuated inversion recovery (FLAIR) sequences, which coincided with areas of bilirubin deposition and neuronal necrosis (kernicterus) identified on necropsy examination. This is the second case report of an adult dog exhibiting kernicterus, and the first report to document MRI findings associated with that condition. Kernicterus is an uncommonly reported complication of hyperbilirubinemia in dogs, but is potentially underreported due to difficulties in recognizing subtle lesions and distinguishing kernicterus from other potential causes of neurologic abnormalities with readily available antemortem tests. MRI may be helpful in supporting the diagnosis of kernicterus.
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7

Millichap, J. Gordon. "MRI in Kernicterus." Pediatric Neurology Briefs 9, no. 10 (October 1, 1995): 75. http://dx.doi.org/10.15844/pedneurbriefs-9-10-5.

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8

Shah, Zarine, Ashish Chawla, Deepak Patkar, and Sona Pungaonkar. "MRI in kernicterus." Australasian Radiology 47, no. 1 (March 2003): 55–57. http://dx.doi.org/10.1046/j.1440-1673.2003.00973.x.

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9

Shapiro, Steven M., Vinod K. Bhutani, and Lois Johnson. "Hyperbilirubinemia and Kernicterus." Clinics in Perinatology 33, no. 2 (June 2006): 387–410. http://dx.doi.org/10.1016/j.clp.2006.03.010.

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10

Leite, Emanuelly Falcão de Sousa, and Gidelson Gabriel Gomes. "Diagnósticos e tratamentos de kernicterus / diagnostic and treatment of kernicterus." Brazilian Journal of Health Review 4, no. 2 (April 20, 2021): 9046–55. http://dx.doi.org/10.34119/bjhrv4n2-411.

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11

Juretschke, Linda. "Kernicterus: Still a Concern." Neonatal Network 24, no. 2 (March 2005): 7–19. http://dx.doi.org/10.1891/0730-0832.24.2.7.

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The presence of yellow staining and damage to the brain caused by unconjugated bilirubin was first described by Hervieux in 1847. Kernicterus, the technical term used to describe the intense yellow staining in the basal ganglia of the brain, was first used by Schmorl in 1903. Perhaps as many as 60 percent of all babies born each year in the U.S. are diagnosed with clinical jaundice. Kernicterus is a preventable brain injury caused by severe jaundice, yet it remains a threat today. Because of this, anyone caring for newborns must be aware of the risks and treatment for hyperbilirubinemia and the sequelae of this seemingly benign entity.
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12

Muralt, G. "The Prophylaxis of Kernicterus." Developmental Medicine & Child Neurology 4, no. 2 (November 12, 2008): 133–46. http://dx.doi.org/10.1111/j.1469-8749.1962.tb03122.x.

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13

YEUNG, C. Y. "Kernicterus in term infants." Journal of Paediatrics and Child Health 21, no. 4 (November 1985): 273–74. http://dx.doi.org/10.1111/j.1440-1754.1985.tb00163.x.

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14

Poland, Ronald L. "Preventing kernicterus: Almost there." Journal of Pediatrics 140, no. 4 (April 2002): 385–86. http://dx.doi.org/10.1067/mpd.2002.124310.

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15

Newman, Thomas B., and M. Jeffrey Maisels. "How to avoid kernicterus." Journal of Pediatrics 142, no. 2 (February 2003): 212–13. http://dx.doi.org/10.1067/mpd.2003.70.

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16

Cashore, William. "Kernicterus and Bilirubin Encephalopathy." Seminars in Liver Disease 8, no. 02 (May 1988): 163–67. http://dx.doi.org/10.1055/s-2008-1040536.

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17

Roth, Philip, and Richard A. Polin. "Controversial Topics in Kernicterus." Clinics in Perinatology 15, no. 4 (December 1988): 965–90. http://dx.doi.org/10.1016/s0095-5108(18)30687-0.

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18

Hansen, Thor Willy Ruud. "Kernicterus: an international perspective." Seminars in Neonatology 7, no. 2 (April 2002): 103–9. http://dx.doi.org/10.1053/siny.2002.0118.

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19

AlOtaibi, Suad F., Susan Blaser, and Daune L. MacGregor. "Neurological Complications of Kernicterus." Canadian Journal of Neurological Sciences / Journal Canadien des Sciences Neurologiques 32, no. 3 (August 2005): 311–15. http://dx.doi.org/10.1017/s0317167100004182.

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ABSTRACT:Objective and Background:Prevention of bilirubin encephalopathy relies on the detection of newborns who are at risk of developing serious hyperbilirubinemia. The objective of this study was to reassess the clinical syndrome of kernicterus as neurodiagnostic studies have become more readily available and can be used to evaluate these infants.Methods:The study population was neonates born at term or near term admitted to The Hospital for Sick Children in Toronto, Ontario, Canada, between January 1990 and May 2000. During the study period, there were 9776 admissions (average number of admissions per year – 888 infants). The inclusion criteria were that patients had total serum bilirubin levels of > 400μmol/L at the time of diagnosis and no evidence of hypoxic ischemic encephalopathy. Records were reviewed to establish neurodevelopment outcomes.Results:Twelve neonates (nine males) were identified. Bilirubin levels at the time of diagnosis ranged from 405 to 825μmol/L. Causes of these elevated levels included glucose-6-phosphate dehydrogenase deficiency (seven patients), dehydration (three patients), sepsis (one patient), and was undetermined in one patient. Abnormal visual evoked potentials were found in three of nine patients and abnormal brainstem auditory evoked potentials in seven of ten patients. Abnormal electroencephalograms were documented in five patients studied. Brain magnetic resonance imaging results were abnormal in three of four patients.Conclusions:Magnetic resonance imaging typically showed an increased signal in the posteromedial aspect of the globus pallidus and was, therefore, useful in the assessment of the structural changes of chronic bilirubin encephalopathy after kernicterus.
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20

Okumura, A., H. Kidokoro, H. Shoji, T. Nakazawa, M. Mimaki, K. Fujii, H. Oba, and T. Shimizu. "Kernicterus in Preterm Infants." PEDIATRICS 123, no. 6 (May 11, 2009): e1052-e1058. http://dx.doi.org/10.1542/peds.2008-2791.

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21

Waser, Marco, Paul Kleihues, and Paul Frick. "Kernicterus in an adult." Annals of Neurology 19, no. 6 (June 1986): 595–98. http://dx.doi.org/10.1002/ana.410190614.

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22

Manchanda, Smita, Akhila Prasad, and Barindra Prasad Baruah. "MRI Findings in Kernicterus." Indian Journal of Pediatrics 80, no. 2 (September 19, 2012): 181–82. http://dx.doi.org/10.1007/s12098-012-0878-6.

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23

IVES, N. KEVIN. "Kernicterus in Preterm Infants; Lest We Forget (To Turn on the Lights)." Pediatrics 90, no. 5 (November 1, 1992): 757–59. http://dx.doi.org/10.1542/peds.90.5.757.

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Watchko and Oski have a reputation for stimulating debate on the topic of neonatal jaundice. As scriptwriters of "Vigintiphobia: a one-act play,"1 they questioned the `standard practice' applied to the management of jaundice in otherwise healthy term infants. In the current issue of Pediatrics2 they again court controversy by turning their attention to treatment thresholds and the risk of kernicterus in jaundiced preterm infants. We are provided with a thoroughly researched historical review of the risk of kernicterus in the preterm infant from 1950 to the 1990s. The story is presented as a journey of experience from the pre-intensive care era, through the so-called `low bilirubin kernicterus era' (1965 through 1982), to the present.
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24

Soeetomenggolo, Taslim S. "Blood Bilirubin Content in Neonatal Tetanus Patient with Hyperbilirubinemia during Treatment with Intravenous Diazepam." Paediatrica Indonesiana 32, no. 3-4 (January 28, 2019): 59–64. http://dx.doi.org/10.14238/pi32.3-4.1992.59-64.

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An evaluation on 128 neonatal tetanus patients with hyperbilirubinemia was done at the Department of Child Health, Dr. Cipto Mangunkusumo General Hospital, Jakarta. The patients were treated with high dosages of diazepam intravenously. This drug is potential to cause the increase of blood bilirubin, and in turn this latter condition is potential to cause kernicterus. Of the 128 patients there were 70 males and 58 females. The age of the patients were mostly (79.6 %) 4- 7 days. Fourteen of the 128 patients showed the increase of their blood bilirubin content during the second day of treatment, but after that it declined gradually during the next 3 days. The mortality of the 14 patients was 8 (57.1 %), so far no kernicterus was recorded among them. Among the 128 patients, 114 patients showed the decrease of their blood bilirubin content during the treatment. During 3 days the blood bilirubin content became less than 10 mg/dL. No kernicterus was recorded among those patients. It was concluded that intravenous diazepam is not dangerous in patients with mild and moderate hyperbilirubinemia, and no kernicterus was recorded during evaluation.
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25

STERN, LEO, and ROLF BRODERSEN. "Kernicterus Research and the Basic Sciences: A Prospect for Future Development." Pediatrics 79, no. 1 (January 1, 1987): 154–56. http://dx.doi.org/10.1542/peds.79.1.154.

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Kernicterus was a major problem of pediatrics in the first half of this century. Important progress has taken place since pediatricians have mastered rhesus disease, introduced exchange transfusion, avoided giving sulfonamides, and have placed at risk infants under blue light. These measures, and above all the general improvements in intensive care in modern neonatology units, have reduced the problem so that kernicterus is now mainly seen as secondary to prematurity, respiratory distress, and severe infections.1 There, it remains a challenge to both clinical and basic science. The mechanism (or mechanisms?) of bilirubin transfer from plasma to brain has not been settled; agreement has not been reached on laboratory methods for predicting kernicterus; and satisfactory guidance about which drugs to avoid, other than the bilirubin-displacing sulfonamides, remains to be given.
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26

Brown, A. K. "Kernicterus: Past, Present, and Future." NeoReviews 4, no. 2 (February 1, 2003): 33e—40. http://dx.doi.org/10.1542/neo.4-2-e33.

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27

Millichap, J. Gordon. "Kernicterus Re-Emergence and Prevention." Pediatric Neurology Briefs 14, no. 11 (November 1, 2000): 84. http://dx.doi.org/10.15844/pedneurbriefs-14-11-6.

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28

Newman, T. B., M. J. Maisels, R. A. Zimmerman, and M. C. Harris. "Magnetic Resonance Imaging and Kernicterus." PEDIATRICS 109, no. 3 (March 1, 2002): 555. http://dx.doi.org/10.1542/peds.109.3.555-a.

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29

Newman, Thomas B., and M. Jeffrey Maisels. "Magnetic Resonance Imaging and Kernicterus." Pediatrics 109, no. 3 (March 1, 2002): 555. http://dx.doi.org/10.1542/peds.109.3.555b.

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30

HERNÁNDEZ CH, MARTA, M. IGNACIA SCHMIDT C, and ISIDRO HUETE L. "Encefalopatía por Kernicterus: Serie clínica." Revista chilena de pediatría 84, no. 6 (December 2013): 659–66. http://dx.doi.org/10.4067/s0370-41062013000600009.

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31

Sangster, C. R., C. K. Stevenson, B. A. Kidney, D. L. Montgomery, and A. L. Allen. "Kernicterus in an Adult Dog." Veterinary Pathology 44, no. 3 (May 2007): 383–85. http://dx.doi.org/10.1354/vp.44-3-383.

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32

Martin, Gilbert I. "Editor's Perspective: Jaundice, Bilirubin, Kernicterus." Journal of Perinatology 21, S1 (December 2001): S2. http://dx.doi.org/10.1038/sj.jp.7210623.

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33

Garone, Giacomo, Federica Graziola, Federico Vigevano, and Alessandro Capuano. "Vertical Gaze Palsy in Kernicterus." Neuropediatrics 50, no. 04 (May 7, 2019): 262–63. http://dx.doi.org/10.1055/s-0039-1685527.

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34

Schyve, Paul M. "Editorial: Microsystems, Macrosystems, and Kernicterus." Joint Commission Journal on Quality and Safety 30, no. 11 (November 2004): 591–92. http://dx.doi.org/10.1016/s1549-3741(04)30069-9.

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35

Loynachan, Alan T., N. M. Williams, and J. F. Freestone. "Kernicterus in a Neonatal Foal." Journal of Veterinary Diagnostic Investigation 19, no. 2 (March 2007): 209–12. http://dx.doi.org/10.1177/104063870701900215.

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36

Nakamura, Hajime. "Assessing the risk of kernicterus." Indian Journal of Pediatrics 54, no. 5 (September 1987): 625–31. http://dx.doi.org/10.1007/bf02751269.

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37

Sonne, Luciana, Djeison Lutier Raymundo, Bianca Santana De Cecco, Adriana Da Silva Santos, Caroline Argenta Pescador, Eduardo Conceição De Oliveira, and David Driemeier. "Kernicterus in an Adult Dog." Acta Scientiae Veterinariae 46 (January 9, 2018): 3. http://dx.doi.org/10.22456/1679-9216.85116.

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Background: Kernicterus or bilirubin encephalopathy is a condition rarely observed in animal characterized by a yellowish discoloration of the central nervous system. It is a potentially fatal condition due to bilirubin neurotoxic effects caused by the increase of non-conjugated bilirubin pigment, which passes blood brain barrier and has been attributed to an imbalance between albumin and bilirubin levels. Intracellular bilirubin is toxic for cells and can cause decrease in protein synthesis, specially albumin, depression of cell respiration and cellular death. This paper describes kernicterus in a 2-year-old Great Dane female dog.Case: Clinically, the animal showed apathy, lethargy, weight loss and jaundice, which progressed to vomiting and neurological signs characterized by loss of consciousness and eventually coma. Blood parameters were within normal range, except for high levels of alanine aminotransferase (523 U/L), suggesting a liver lesion. The animal was submitted to euthanasia due to the poor prognosis, and at post-mortem examination it showed dehydration and severe jaundice, especially oral, vaginal and ocular mucosas, subcutaneous tissue and blood vessels intima surface. The liver had an accentuated lobular pattern, and the stomach mucosa was reddened. Multiple petechiae were observed in the epicardium, as well as icterus in the blood vessels of the heart. Furthermore, the brain and cerebellum cortex, thalamic region and nuclei region of brainstemshowed extensive icteric areas. Microscopically, the liver presented a mononuclear portal hepatitis, centrilobular necrosis and presence of yellowish pigments. The brain had neuronal necrosis, mild vacuolization of the white matter, perineuronal edema and Alzheimer type II astrocytes, while cerebellum showed Purkinje cells necrosis. Hepatic cooper measurement was within range values, and direct imunofluorescence for the detection of Leptospira sp. was negative.Discussion: Kernicterus pathogenesis has been extensively studied, as the condition is commonly seen in neonatal humans. Diagnosis is based on gross and microscopic lesions in brain, which are consistent with bilirubin encephalopathy caused by the necrosis and degeneration of neurons. This condition is related to cases of intense hyperbilirubinemia, which exceedsthe albumin binding capacity and, therefore, the excess of unconjugated bilirubin that can pass through the blood brain barrier. Liver disease causes deficient production of protein, especially albumin, decreasing the potential binding capacity to bilirubin, and consequently causing hyperbilirubinemia. In this case, the previously detected hepatic lesion suggested by liver enzymes increased, probably led to protein production dysfunction, causing hypoalbuminemia and hyperbilirubinemia. Unfortunately, albumin and bilirubin seric levels could not be measured. Decrease in albumin production along with the excess of unconjugated bilirubin caused the jaundice, and in cases like this one described, the blood brain barrieris compromised and the kernicterus occurs. Unconjugated bilirubin has negative effect in the glutamate uptake causing extracellular accumulation of it, which is consequently neurotoxic, causing necrosis and degeneration leading to a characteristic encephalopathy in animals with kernicterus. In this report, it was not possible to determine the primary hepatic disease, however this caused clinical neurotoxic disease, known as bilirubin encephalopathy.Keywords: kernicterus, icterus, dog.
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38

Campos, Francielle Santana, and Izailza Matos Dantas Lopes. "Kernicterus: relato de caso clínico." Brazilian Journal of Health Review 6, no. 2 (March 14, 2023): 5396–406. http://dx.doi.org/10.34119/bjhrv6n2-073.

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Introdução: Kernicterus é uma enfermidade crônica, irreversível resultante da toxicidade ocasionada pelo acúmulo de elevada quantidade de bilirrubina indireta no sistema nervoso central, em especial, nos núcleos da base e do tronco cerebral. As principais complicações são atetose, paralisia cerebral distônica, surdez e disfunção intelectual. O presente relato de caso teve como objetivo descrever um caso de Kernicterus em maternidade filantrópica no nordeste do Brasil que teve seguimento no ambulatório de especialidades da referida maternidade. Nasceu a termo, sexo masculino, com boa vitalidade, apresentou nas primeiras 24 horas icterícia neonatal que não melhorou com uso de fototerapia necessitando realizar exsanguinotransfusão no quarto dia de vida com redução satisfatória dos níveis de bilirrubina indireta. No seguimento ele apresentou retardo do neurodesenvolvimento com diagnóstico de paralisia cerebral distônica, aos 2 anos de idade. Conclusão: No caso apresentado, a abordagem multiprofissional foi fundamental para o melhor prognóstico deste paciente.
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39

Watchko, Jon F., and Diana Claassen. "Kernicterus in Premature Infants: Current Prevalence and Relationship to NICHD Phototherapy Study Exchange Criteria." Pediatrics 93, no. 6 (June 1, 1994): 996–99. http://dx.doi.org/10.1542/peds.93.6.996.

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Objective. This study was undertaken to determine the current prevalence of kernicterus in premature neonates and to relate the occurrence of kernicterus to 1) the categorization of the infant as "at risk" by National Institute of Child Health and Human Development (NICHD) Phototherapy Study exchange transfusion criteria, and 2) the clinical management of the infant's hyperbilirubinemia. Design. Retrospective review of postmortem and clinical records. Setting. Magee-Womens Hospital, a University of Pittsburgh Medical Center affiliated hospital with approximately 10 000 deliveries per year and a Level III Neonatal Intensive Care Unit with about 1400 admissions annually. Subjects. All neonates autopsied between January 1, 1984 and June 30, 1993 who were <34 weeks gestation and who lived at least 48 hours; a total of 81 infants. Results. Three infants had kernicterus resulting in a prevalence rate of 4%. These cases included: 1) a 33-week newborn with nonimmune hydrops and a peak bilirubin of 26 mg/dl; 2) a 25-week newborn with asphyxia, hyaline membrane disease, grade IV intraventricular hemorrhage, necrotizing enterocolitis, meconium peritonitis, sepsis, prolonged acidosis, and a peak bilirubin of 11.3 mg/dl; and 3) a 24-week newborn with asphyxia, hyaline membrane disease, grade III intraventricular hemorrhage, and a peak serum bilirubin of 18.5 mg/dl. Of the remaining 78 infants who did not have kernicterus, peak bilirubin ranged from 3.6 to 22.5 mg/dl and 56% had bilirubin levels greater than that suggested as a criterion for exchange transfusion by NICHD Phototherapy Study guidelines; yet all but three were managed with phototherapy alone. Conclusions. We conclude that kernicterus is currently an uncommon event in preterm infants, even when bilirubin levels are allowed to rise above those previously thought to place the premature infant at risk.
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40

Yang, Fu-Chen, Jay L. Vivian, Catherine Traxler, Steven M. Shapiro, and John A. Stanford. "MGE-Like Neural Progenitor Cell Survival and Expression of Parvalbumin and Proenkephalin in a Jaundiced Rat Model of Kernicterus." Cell Transplantation 31 (January 2022): 096368972211011. http://dx.doi.org/10.1177/09636897221101116.

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Kernicterus is a permanent condition caused by brain damage from bilirubin toxicity. Dystonia is one of the most debilitating symptoms of kernicterus and results from damage to the globus pallidus (GP). One potential therapeutic strategy to treat dystonia in kernicterus is to replace lost GP neurons and restore basal ganglia circuits through stem cell transplantation. Toward this end, we differentiated human embryonic stem cells (hESCs) into medial ganglion eminence (MGE; the embryological origin of most of the GP neurons)-like neural precursor cells (NPCs). We determined neurochemical phenotype in cell culture and after transplanting into the GP of jaundiced Gunn rats. We also determined grafted cell survival as well as migration, distribution, and morphology after transplantation. As in the GP, most cultured MGE-like NPCs expressed γ-aminobutyric acid (GABA), with some co-expressing markers for parvalbumin (PV) and others expressing markers for pro-enkephalin (PENK). MGE-like NPCs survived in brains at least 7 weeks after transplantation, with most aggregating near the injection site. Grafted cells expressed GABA and PV or PENK as in the normal GP. Although survival was low and the maturity of grafted cells varied, many cells produced neurite outgrowth. While promising, our results suggest the need to further optimize the differentiation protocol for MGE-like NPC for potential use in treating dystonia in kernicterus.
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41

Tsao, Pei-Chen, Hsin-Ling Yeh, Yen-Chen Chang, Po-Huang Chiang, Yu-Shih Shiau, Szu-Hui Chiang, Wen-Jue Soong, Mei-Jy Jeng, and Kwang-Jen Hsiao. "Outcomes of neonatal jaundice in Taiwan." Archives of Disease in Childhood 103, no. 10 (February 22, 2018): 927–29. http://dx.doi.org/10.1136/archdischild-2017-314063.

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ObjectiveTo investigate the burden of clinically significant neonatal jaundice (SNJ) in Taiwan, 2000–2010.Study designThe nationwide, population-based health insurance database in Taiwan was used to investigate the incidence, kernicterus rate and mortality rates of SNJ cohort born between 2000 and 2010.ResultsFrom 2000 to 2010, up to 242 546 patients admitted with neonatal jaundice (NJ) were identified. The incidence of SNJ was 5.9% in 2000 and increased to 13.7% in 2010 (P<0.001). The mortality rate significantly decreased from 0.51% in 2000 to 0.26% in 2010 (P<0.001) and the average incidence of kernicterus was 0.86 per 100 000 live births, indicating dramatically decreased rates compared with earlier rates in Taiwan.ConclusionsIn spite of the increased incidence rates, the rates of mortality and kernicterus in patients with NJ significantly declined in Taiwan. The public health prevention programme, clinicians’ awareness and effective management might contribute to the reduction of these acute severe sequelae.
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42

Ip, S. "Hyperbilirubinemia and Kernicterus: 50 Years Later." PEDIATRICS 114, no. 1 (July 1, 2004): 263–64. http://dx.doi.org/10.1542/peds.114.1.263.

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43

Penn, Anna A., Dieter R. Enzmann, Jin S. Hahn, and David K. Stevenson. "Kernicterus in a Full Term Infant." Pediatrics 93, no. 6 (June 1, 1994): 1003–6. http://dx.doi.org/10.1542/peds.93.6.1003.

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Neonatal jaundice can represent a benign physiologic process or be the harbinger of serious illness with associated severe neurotoxicity. The neurological manifestations of kernicterus, a condition resulting from the deposition of unconjugated bilirubin in the central nervous system, are rarely seen in modern neonatal care, but jaundice, which reflects elevated serum bilirubin levels, is one of the most common findings in the neonatal period.1 More than half of all term infants will develop some neonatal jaundice and at least 6% will have a serum bilirubin concentration above 12.9 mg/dL.2 The appropriate treatment of hyperbilirubinemia is currently a topic of much debate in pediatrics, particularly treatment of full term infants without risk factors for hemolytic disease.3,4
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Amini, Naser, Babak Bakhshayesh Eghbali, Sara Ramezani, Vahid Hosseinpour Sarmadi, Peiman Brouki Milan, Seyedeh Sara Ashraf, Ghazaleh Larijani, et al. "Animal Kernicterus Models: Progress and Challenges." Brain Research 1770 (November 2021): 147624. http://dx.doi.org/10.1016/j.brainres.2021.147624.

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45

Rennie, Janet M., Jeanette Beer, and Michele Upton. "Learning from claims: hyperbilirubinaemia and kernicterus." Archives of Disease in Childhood - Fetal and Neonatal Edition 104, no. 2 (May 25, 2018): F202—F204. http://dx.doi.org/10.1136/archdischild-2017-314622.

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We examined claims made against the National Health Service (NHS) involving neonatal jaundice in order to determine whether there were lessons that could be learnt from common themes.This was a retrospective anonymised study using information from the NHS Resolution database for 2001–2011.Twenty cases (16 males) had sufficient information for analysis. Fifteen had confirmed cerebral palsy and two young children had damage to the globus pallidus without confirmed CP. In three cases, the outcome was uncertain. Two were extremely preterm, five were born at 34–36 weeks’ gestation. Jaundice was typically present very early in life; in four cases, it was noted at less than 24hours of age, and in 14 cases, it was first noted on the second to third day. There was a lag between recognition and readmission, with a range of 26–102 hours. The peak serum bilirubin level was over 600 µmol/L in all the babies born at term. An underlying diagnosis was found in all but two; six had glucose-6-phosphatase deficiency (one also had Gilbert’s syndrome); five were diagnosed with ABO incompatibility; three with Rh haemolytic disease; one with spherocytosis and three preterm. The total cost of these claims by August 2017 was almost £150.5 million. This figure is likely to rise.These data show that, in the group who litigate, babies who develop kernicterus generally have an underlying diagnosis. We recommend adherence to theNational Institute for Health and Care Excellence guideline that recommends measuring the bilirubin level within 6 hours in all babies who are visibly jaundiced.
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Thyagarajan, Baskaran, and Sharad S. Deshpande. "Cotrimoxazole and neonatal kernicterus: a review." Drug and Chemical Toxicology 37, no. 2 (October 7, 2013): 121–29. http://dx.doi.org/10.3109/01480545.2013.834349.

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Walker, C. H. "Neonatology--then and now. Kernicterus (1957)." Archives of Disease in Childhood 64, no. 5 (May 1, 1989): 770. http://dx.doi.org/10.1136/adc.64.5.770.

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48

Ahlfors, Charles E. "Benzyl alcohol, kernicterus, and unbound bilirubin." Journal of Pediatrics 139, no. 2 (August 2001): 317–19. http://dx.doi.org/10.1067/mpd.2001.116281.

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Paksoy, Yahya, Hasan Koç, and Bülent Oğuz Genç. "Bilateral Mesial Temporal Sclerosis and Kernicterus." Journal of Computer Assisted Tomography 28, no. 2 (March 2004): 269–72. http://dx.doi.org/10.1097/00004728-200403000-00018.

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50

Gourley, Glenn R. "Breast-feeding, neonatal jaundice and kernicterus." Seminars in Neonatology 7, no. 2 (April 2002): 135–41. http://dx.doi.org/10.1053/siny.2002.0101.

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