title: P-Selectin (CD62P) Expression in Liver Tissue of Biliary Atresia: A New Perspective in Etiopathogenesis.
abstract: OBJECTIVE
  The etiology of biliary atresia (BA) is still elusive. Inflammation plays a key role in bile duct and liver injury. The recruitment and accumulation of inflammatory cells is largely dependent on adhesion molecules. We aimed to investigate P-selectin (CD62P) expression in liver tissue in patients with BA compared with other neonatal cholestatic disorders.
  
  
  METHODS
  The study included 63 infants with neonatal cholestasis in 2 groups: BA group (n = 32) and non-BA group (n = 31) with non-BA cholestatic disorders as controls. Demographic, clinical, laboratory, ultrasonographic, and histopathological parameters were collected. P-selectin immunostaining was performed. Immunostaining in bile duct epithelium, cellular infiltrate, and vascular endothelial cells were scored as positive or negative.
  
  
  RESULTS
  The frequency of P-selectin-positive endothelium, platelets, and bile duct epithelium was significantly higher in the BA group (72%, 72%, and 63%, respectively) than in the non-BA group (32%, 16%, and 13%, respectively) with P of 0.002, <0.0001, and <0.0001, respectively. Few mononuclear cellular infiltrates in portal tract expressed P-selectin and were comparable in both groups (P = 0.932). Of interest, the platelet count was significantly higher in the BA group (532 ± 172) than in the non-BA group (406 ± 158), and 68.8% of the BA group had thrombocytosis versus 25% in the controls (P = 0.001 for both).
  
  
  CONCLUSIONS
  The significant expression of P-selectin in endothelium, platelets, and bile duct epithelium in patients with BA suggests a potential role for this adhesion molecule in the pathogenesis of this devastating neonatal hepatic disorder. It further suggests that platelets in BA are activated and may have a role in the inflammatory process in BA.
authors.affiliation: *Department of Pediatric Hepatology †Department of Pathology, National Liver Institute, Menofiya University, Shebin El-koom, Menofiya, Egypt.
authors.forename: Mostafa M
authors.initials: MM
authors.lastname: Sira
authors.forename: Ahmad M
authors.initials: AM
authors.lastname: Sira
authors.forename: Nermine A
authors.initials: NA
authors.lastname: Ehsan
authors.forename: Asmaa
authors.initials: A
authors.lastname: Mosbeh
mesh_terms: D001652:Bile Ducts / Q000378:metabolism* / Q000473:pathology; D001656:Biliary Atresia / Q000378:metabolism*; D001792:Blood Platelets / Q000378:metabolism; D015815:Cell Adhesion Molecules / Q000378:metabolism; D002779:Cholestasis / Q000378:metabolism*; D004730:Endothelium, Vascular / Q000378:metabolism; D005260:Female; D006801:Humans; D007223:Infant; D007231:Infant, Newborn; D007249:Inflammation / Q000378:metabolism*; D008099:Liver / Q000378:metabolism* / Q000473:pathology; D008297:Male; D019007:P-Selectin / Q000378:metabolism*; D013922:Thrombocytosis / Q000150:complications
chemical_list: D015815:Cell Adhesion Molecules; D019007:P-Selectin; C546937:SELP protein, human