A new theory of biliary atresia

Klippel, Charles H.

doi:10.1016/0022-3468(72)90274-6

Cited by 25 publications

(9 citation statements)

References 12 publications

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“…A associação entre a AVBEH e as anomalias da veia porta e artéria hepática sugere que uma lesão isquêmica intraútero pode influenciar o desenvolvimento das vias biliares, podendo ter algum papel na patogênese da atresia 58,59 .…”

Section: Diminuição Do Suprimento Arterial Hepáticounclassified

Extrahepatic biliary atresia: current concepts and future directions

Carvalho¹,

Ivantes²,

Bezerra³

2007

J Pediatr (Rio J)

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ResumoObjetivos: Apresentar uma revisão atualizada sobre atresia das vias biliares extra-hepáticas, com ênfase em etiopatogenia, abordagens diagnósticas e terapêuticas e prognóstico. Conclusão:A atresia das vias biliares extra-hepáticas continua sendo a principal indicação de transplante hepático em crianças, e a mudança deste panorama depende de um melhor entendimento da etiopatogenia da obstrução biliar nos diferentes fenótipos da doença.Investigações futuras a respeito do papel do interferon gama e de outras citocinas são necessárias para avaliar se esses aspectos seriam potenciais alvos de intervenção terapêutica.J Pediatr (Rio J). 2007;83(2):105-120: Atresia das vias biliares extra-hepáticas, etiopatogenia, diagnóstico, tratamento e prognóstico. AbstractObjective: To provide an updated review on extrahepatic biliary atresia, focusing mainly on its etiopathogenesis, diagnosis, treatment and prognosis.Sources: MEDLINE and PubMed databases were searched using the following keywords: biliary atresia, etiopathogenesis, diagnosis, treatment, prognosis, children. Summary of the findings:Extrahepatic biliary atresia is the main indication for liver transplantation among pediatric patients. As to its

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Section: Diminuição Do Suprimento Arterial Hepáticounclassified

Extrahepatic biliary atresia: current concepts and future directions

Carvalho¹,

Ivantes²,

Bezerra³

2007

J Pediatr (Rio J)

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“…We administered PGE 1 to rats just after birth because PGE 1 has a dilatory effect on the ductus venosus and ductus arteriosus [19][20][21] and because the blood flow to the BD would be decreased due to the decreased patency of these vessels [22]. Of note, the PG-induced BDPF was not remarkable, as described before.…”

Section: Discussionmentioning

confidence: 89%

“…In addition, the administration of prostaglandin (PG) E, a vasodilator, leads to the development of a persistent ductus venosus and ductus arteriosus in neonatal animals [19][20][21]. Theoretically, the persistence of the ductus arteriosus induces a decrease in the blood flow in the hepatic artery [22]. Therefore, it is hypothesized that cholestasis in neonatal small animals would be induced by hypoxia/ischemia in the BDs and/or liver tissue, which could be achieved by PG treatment and/or ligation of the hepatic artery.…”

Section: Introductionmentioning

confidence: 99%

Development of an experimental model of cholestasis induced by hypoxic/ischemic damage to the bile duct and liver tissues in infantile rats

et al. 2011

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“…There are many predisposing factors to the development of inspissated bile, sludge, or cholelithiasis in neonates 31,32 Ceftriaxone pseudolithiasis, composed of precipitated ceftriaxone, is reported to occur in 29.5% to 45.7% of children treated with ceftriaxone 33 . The pseudolithiasis occurs after 4 to 22 days (mean, 9 days) of ceftriaxone therapy and resolves after 2 to 63 days (mean, 15 days) from the end of treatment 34 .Cefotaxime, was previously reported to be associated with pseudolithiasis in 2 of 34 infants (6%) who had cholelithiasis 31 .…”

Section: Inspissated Bile Syndromementioning

confidence: 97%

Revival of Landing's Concept of Infantile Obstructive Cholangiopathy A Plea to Hand Over the 2 Week Old Jaundiced Full Term Neonate to the Surgeon!

Sharma

Gupta

2014

J. paediatr. surg. Bangladesh

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:The concept of infantile obstructive cholangiopathy started in 1974 by Landing and remained till early 1980s. However, the concept has not been used much since then as nothing new has developed over the last 40 years sufficient enough to change the course of the disease or identify its etiology. This review article is an attempt to consolidate evidence on review of literature pointing towards a common etiopathological process leading to the spectrum of anomalies constituting neonatal cholestasis. The importance of early referral of any case with neonatal jaundice in a full term neonate, preferably at 2 weeks age is highlighted. This will help to identify and treat more cases within the correctable range and prevent the disease from progressing to a life threatening situation especially in developing countries where the resources for liver transplantation are meagre. Introduction:Newborn babies are at increased propensity for developing hyperbilirubinemia due to increased bilirubin production or its decreased excretion. The increased production is attributed to a greater red cell mass per kg as compared to adults and a shorter life span of red blood cells. The decreased excretion is attributed to defective uptake of bilirubin due to hepatic immaturity and decreased ligandin, defective conjugation due to decreased uridine diphospho glucuronyl transferase (UDPG-T) activity, decreased hepatic excretion of bilirubin and increased enterohepatic circulation due to higher levels of glucuronidase Review Article REVIVAL OF LANDING'S CONCEPT OF INFANTILE Physiological Jaundice:The physiologic jaundice seen in newborn babies appears on the third day of life and usually lasts till the tenth day in full term babies. It appears slightly earlier in preterm babies and may last upto two weeks. However, the serum bilirubin levels do not exceed 12 mg % in full term babies and 15 mg % in preterm babies. The normal range of total and conjugated bilirubin are <1 mg/dl and <0.25 mg/dl respectively, although jaundice can only be appreciated in newborn babies only when the total bilirubin is greater than 5 mg/dL Physiological jaundice may be accentuated by immaturity, birth asphyxia, acidosis, hypothermia, hypoglycemia, septicemia, blood group incompatibilities, drugs like salicylates, gentamycin, sulpha drugs, cephalhematoma, polycythemia, hypothyroidism intrauterine infections and breast milk jaundice. At high levels, unconjugated bilirubin can cross the blood-brain barrier and cause brain injury (kernicterus). The usual therapy for unconjugated jaundice is phototherapy and occasionally exchange transfusion. Neonatal Cholestasis :Infants with the persistence of jaundice beyond the physiologic limits, in the absence of an apparent medical cause, need to be investigated without much delay. The causes for Conjugated Hyperbilirubinemia (neonatal cholestasis) include obstructive and nonobstructive disorders. These are broadly called extrahepatic biliary obstruction and neonatal hepatitis. Cholestasis thus results from either to s...

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A new theory of biliary atresia

Cited by 25 publications

References 12 publications

Extrahepatic biliary atresia: current concepts and future directions

Extrahepatic biliary atresia: current concepts and future directions

Development of an experimental model of cholestasis induced by hypoxic/ischemic damage to the bile duct and liver tissues in infantile rats

Revival of Landing's Concept of Infantile Obstructive Cholangiopathy A Plea to Hand Over the 2 Week Old Jaundiced Full Term Neonate to the Surgeon!

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A new theory of biliary atresia

Cited by 25 publications

References 12 publications

Extrahepatic biliary atresia: current concepts and future directions

Extrahepatic biliary atresia: current concepts and future directions

Development of an experimental model of cholestasis induced by hypoxic/ischemic damage to the bile duct and liver tissues in infantile rats

Revival of Landing's Concept of Infantile Obstructive Cholangiopathy  A Plea to Hand Over the 2 Week Old Jaundiced Full Term Neonate to the Surgeon!

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Revival of Landing's Concept of Infantile Obstructive Cholangiopathy A Plea to Hand Over the 2 Week Old Jaundiced Full Term Neonate to the Surgeon!