(SDAS) Prenatal and Early Life Predictors of Pediatric Onset Inflammatory Bowel Disease
Grantee: Kaiser Foundation Hospitals
Principal Investigator: Lisa J. Herrinton
Project Number: R40MC11266
Project Date: 2/1/2009
Final Report
Age group(s)
- Women/Maternal
- Prenatal
- Perinatal/Infancy (0-12 months)
- Toddlerhood (13-35 months)
- Early Childhood (3-5 years)
- Middle Childhood (6-11 years)
- Adolescence (12-18 years)
Abstract
Background: Pediatric inflammatory bowel disease (IBD) is a chronic illness that affects as many as 100,000 children in the U.S. The disease can be devastating to children and their families because it is chronic and disabling, and because of the embarrassment and shame associated with impaired bowel function, which often has psychological effects on the developing child. IBD is putatively caused by a combination of genetic and environmental factors that affect the development and response of the immune system. Infections, breastfeeding and cigarette smoking have been hypothesized to affect risk in adult onset disease, but knowledge is limited, and pediatric onset disease is especially under-studied. Studying risk factors in pediatric onset disease is important because the etiology likely differs between adults and children, as children have more severe disease. Previous studies of prenatal and early life risk factors of IBD have been limited by following a small number of primarily adult onset cases from referral centers, use of exposure information based on post-diagnostic self-reported questionnaires with long periods of recall, and the inability to identify biologically relevant time points of exposure. Objective: To identify prenatal and early life risk factors in the development of pediatric onset IBD. Our long-term goal is to elucidate etiologic pathways combining both environmental and genetic determinants. Specific Aims: #1: Assess the relationship of infections with risk of pediatric onset IBD. Both pre- and post-natal infections are of interest. We will explore the type of infection and the specific time period of infection prior to disease onset. #2: Assess the relationship of breastfeeding with risk of pediatric onset IBD. Any breastfeeding and duration of breastfeeding will be examined. #3: Assess the relationship of cigarette smoke exposure with risk of pediatric onset IBD. Both pre- and post-natal exposure to cigarette smoke will be assessed, with examination of specific time periods during development and relative to age at IBD diagnosis. Study Design: We propose to study three potential environmental risk factors for IBD-- infections, breastfeeding and exposure to cigarette smoke--in addition to family history of disease. The proposed case-control study will include 665 children diagnosed with IBD between 1996 and 2006 while they were members of our well characterized, comprehensive, integrated health-care delivery system. Controls will be matched to cases on age, sex and length of enrollment. Information will be collected retrospectively from prospectively recorded computerized clinical information. Data will be analyzed using conditional logistic regression analysis. Impact: The findings from the proposed study will provide valuable information for researchers and clinicians and have significant clinical and public health implications including identification of potential interventions for children at identified high risk of disease. This project addresses Healthy People 2010 Goal 1: Increase Quality and Years of Healthy Life by identifying interventions that could increase the years of healthy life for children at high risk for IBD. The Maternal, Infant and Child Health goal of improving the health and well-being of women, infants, children, and families is addressed by identifying breastfeeding and cigarette smoke as potential modifiable factors for pediatric onset IBD.Publications
Listed is descending order by year published.
Hutfless S, Li DK, Heyman MB, Bayless TM, Abramson O, Herrinton LJ. Prenatal and perinatal characteristics associated with pediatric-onset inflammatory bowel disease. Dig Dis Sci. 2012 Aug;57(8):2149-2156.
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