https://www.ncbi.nlm.nih.gov/pubmed/28005582

Ocete-Hita E, Salmerón-Fernández M, Urrutia-Maldonado E, Muñoz-de-Rueda P, Salmerón-Ruiz M, Martinez-Padilla M, Ruiz-Extremera A.J Pediatr Gastroenterol Nutr. 2017 May;64(5):742-747. doi: 10.1097/MPG.0000000000001502.

Abstract

OBJECTIVES:
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.

PATIENTS AND METHODS:
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.

RESULTS:
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.

CONCLUSIONS:
Polymorphisms that are low producers of interleukin-10 occur more frequently in children who have experienced hepatotoxicity.