Author Affiliations: Program in Medical Sciences, Department of Biochemistry, Faculty of Medicine, Chulalongkorn University, Bangkok 10330, Thailand (Udomsinprasert W, Honsawek S, Anomasiri W); Center for Excellence in Omics-Nano Medical Technology Development Project, Department of Clinical Chemistry, Faculty of Allied Health Sciences, Chulalongkorn University, Bangkok 10330, Thailand (Tencomnao T); Department of Surgery, Faculty of Medicine, Chulalongkorn University, Bangkok 10330, Thailand (Vejchapipat P); Center of Excellence in Clinical Virology, Department of Pediatrics, Faculty of Medicine, Chulalongkorn University, Bangkok 10330, Thailand (Chongsrisawat V, Poovorawan Y)

Corresponding Author: Yong Poovorawan, MD, Center of Excellence in Clinical Virology, Department of Pediatrics, Faculty of Medicine, Chulalongkorn University and King Chulalongkorn Memorial Hospital, Rama IV road, Patumwan, Bangkok 10330, Thailand (Tel: +662-256-4929; Fax: +662-256-4909; Email: Yong.P@chula.ac.th)

doi: 10.1007/s12519-012-0377-x

Background: Biliary atresia (BA) is an intractable neonatal inflammatory and obliterative cholangiopathy, leading to progressive fibrosis and cirrhosis. Adiponectin, an anti-inflammatory adipokine, is known to play a possible role in liver diseases. The objective of our study was to determine the relationship between adiponectin gene polymorphisms and BA susceptibility.

Methods: A total of 106 BA patients and 107 healthy controls were included in this study. Two single nucleotide polymorphisms (SNPs) of the adiponectin gene, +45T/G (rs2241766) and +276G/T (rs1501299), were genotyped by polymerase chain reaction-restriction fragment length polymorphism analysis.

Results: Genotype distributions of +45 T/G and +276 G/T SNPs were seen in the Hardy-Weinberg equilibrium for both BA patients and controls. The frequency of the G/G genotype at +276G/T was significantly higher in BA patients than in the controls (P=0.009). Regarding +45T/G in BA patients, the frequency of the T/T genotype tended to be lower than in the controls, but the difference was not significant. Moreover, the G allele at +276G/T in BA patients was more common than in the controls (P=0.0043). In contrast, the frequency of the T allele at +45T/G was not significantly different between BA patients and the controls. None of the haplotypes studied was found to significantly influence the risk of BA.

Conclusions: +276G/T SNP is strongly associated with BA, particularly with the G allele. We postulate that the +276G/T adiponectin gene polymorphism confers increased susceptibility to BA.

Key words: adiponectin; biliary atresia; polymerase chain reaction-restrictionfragment length polymorphism; single nucleotide polymorphism

World J Pediatr 2012;8(4):328-334