Adenovirus infection: A potential risk for developing intussusception in pediatric patients

• Main Authors: Ukarapol N., Khamrin P., Khorana J., Singhavejsakul J., Damrongmanee A., Maneekarn N.
• Format: Journal
• Published: 2017
• Online Access: https://www.scopus.com/inward/record.uri?partnerID=HzOxMe3b&scp=84984850860&origin=inward; http://cmuir.cmu.ac.th/jspui/handle/6653943832/41360
• Institution: Chiang Mai University

© 2016 Wiley Periodicals, Inc. The pathogenesis of intussusception without obvious anatomical leading points remains unclear. The objective of this study was to determine a feasibility of association between certain gastroenteritis viruses and intussusception. This was a prospective cohort study. Forty intussusception cases and 136 acute gastroenteritis controls with comparable age and gender were separately consecutively enrolled and relevant clinical data of both groups were recorded. The clinical specimens collected from all patients were screened for adenovirus, rotavirus, norovirus, and astrovirus by PCR and RT-PCR using specific primers. The genomes of detected viruses were characterized further to identify their genotypes by nucleotide sequencing. In 40 intussusception cases, adenovirus, rotavirus, and norovirus were detected in 12 (30.0%), 2 (5.0%), and 2 (5.0%), respectively while astrovirus was undetectable. In contrast, 136 acute gastroenteritis patients, adenovirus, rotavirus, and norovirus were detected in 11 (8.1%), 24 (17.7%), and 24 (17.7%) patients, respectively and again astrovirus was undetectable. The detection of adenovirus in intussusception patients was significantly higher than those in the control group (P < 0.001) with an odd ratio of 4.87 (95%CI: 1.95, 12.16). Interestingly, molecular analysis of adenovirus genome demonstrated that all of adenovirus detected in intussusception patients belonged to adenovirus C. This could be a potential risk factor or pathogenesis for developing intussusception in the cases of those without apparent anatomical leading points. J. Med. Virol. 88:1930–1935, 2016. © 2016 Wiley Periodicals, Inc.