title: Analysis of Immunogenetic Factors in Idiosyncratic Drug-induced Liver Injury in the Pediatric Population.
abstract: Idiosyncratic drug-induced liver injury is a multifactorial complex disease, in which the toxic potential of the drug, together with genetic and acquired factors and deficiencies in adaptive processes, which limit the extent of damage, can determine susceptibility, and make individuals unique in their development of hepatotoxicity. The aim of the present study is to analyse the genetic factors (human leukocyte antigen [HLA], cytokine polymorphisms, and killer cell immunoglobulin-like receptor [KIR] genotype) of children who experience an episode of drug-induced liver injury.
  
  
  
  Prospective multicentre case-control study. The subjects included in the study were 30 paediatric patients-infants and children ages between 0 and 15 years and who presented possible liver disease associated with the intake of medicines, herbal products, drugs, or toxins. As a control group, 62 subjects were selected.
  
  
  
  Although HLAC0401 and HLADQB0603 may provide a hepatoprotective mechanism in the paediatric population, HLADQA0102 and HLA-DR12 are more commonly found in sick children and their presence may be related to liver damage. The KIR inhibitor KIR3DL1 was not present in any child in the control group.
  
  
  
  Polymorphisms that are low producers of interleukin-10 occur more frequently in children who have experienced hepatotoxicity.
authors.affiliation: *Complejo Hospitalario Universitario de Granada, UGC Médico Quirúrgica de la Infancia, Cuidados Intensivos Pediátricos, Universidad de Granada, CIBERehd †Complejo Hospitalario Universitario de Granada, UGC Médico Quirúrgica de la Infancia ‡Laboratorios Investigación, ibs, Complejo Hospitalario Universitario de Granada, Granada §Hospital Universitario La Paz, Madrid ||Complejo Hospitalario de Jaén, Jaén ¶Complejo Hospitalario Universitario de Granada, Universidad de Granada, CIBERehd, Granada, Spain.
authors.forename: Esther
authors.initials: E
authors.lastname: Ocete-Hita
authors.forename: MaJ
authors.initials: M
authors.lastname: Salmerón-Fernández
authors.forename: Emilia
authors.initials: E
authors.lastname: Urrutia-Maldonado
authors.forename: Paloma
authors.initials: P
authors.lastname: Muñoz-de-Rueda
authors.forename: María
authors.initials: M
authors.lastname: Salmerón-Ruiz
authors.forename: MaC
authors.initials: M
authors.lastname: Martinez-Padilla
authors.forename: Angela
authors.initials: A
authors.lastname: Ruiz-Extremera
mesh_terms: D000293:Adolescent; D016022:Case-Control Studies; D056486:Chemical and Drug Induced Liver Injury / Q000235:genetics* / Q000276:immunology*; D002648:Child; D002675:Child, Preschool; D016207:Cytokines / Q000235:genetics; D005260:Female; D005819:Genetic Markers; D005838:Genotype; D006680:HLA Antigens / Q000235:genetics; D006801:Humans; D055261:Immunogenetic Phenomena; D007223:Infant; D007231:Infant, Newborn; D008297:Male; D011110:Polymorphism, Genetic; D011446:Prospective Studies; D054340:Receptors, KIR / Q000235:genetics; D054341:Receptors, KIR3DL1 / Q000235:genetics; D012307:Risk Factors
chemical_list: D016207:Cytokines; D005819:Genetic Markers; D006680:HLA Antigens; C515083:KIR3DL1 protein, human; D054340:Receptors, KIR; D054341:Receptors, KIR3DL1