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Haslam, N., Mayberry, J.F., Hawthorne, A.B., Newcombe, R.G., Holmes, G.K. and Probert, C.S. (2000) Measles, Month of Birth, and Crohn’s Disease. Gut, 47, 801-803.
http://dx.doi.org/10.1136/gut.47.6.801

has been cited by the following article:

• TITLE: No Correlation between the Month of Birth and the Likelihood of Developing Inflammatory Bowel Disease Later in Life

  AUTHORS: E. M. De Boer, M. A. Brink, M. H. M. G. Houben, A. H. A. M. van Oijen, W. A. De Boer

  KEYWORDS: Inflammatory Bowel Disease; Season; Seasonality; Month; Birth; Crohn Disease; Colitis Ulcerative

  JOURNAL NAME: Open Journal of Gastroenterology, Vol.4 No.4, April 21, 2014

  ABSTRACT: Background: The etiology of Crohn’s disease (CD) and Ulcerative Colitis (UC) remains unclear. It has been suggested that apart from genetic factors, prenatal or perinatal environmental factors could change the risk of developing inflammatory bowel disease (IBD) later in life. Seasonality in birth distribution over the year has been demonstrated for several immune diseases, but studies on IBD have had inconsistent results. Aim: The aim of this study was to investigate in the Netherlands the effect of the month of birth on the probability to develop IBD later in life. Methods: Birth data from CD patients and UC patients of 4 different Dutch hospitals were compared to a control group of irritable bowel syndrome (IBS) patients from the same hospitals. A chi-square test was used to test whether there was heterogeneity between the monthly and seasonal birth rates of the three groups. Results: The patient cohort consisted of 1183 CD patients and 1293 UC patients. The control group consisted of 2113 IBS patients. Data showed no difference in birth distribution over the year or over the four seasons of IBD patients as compared to the control group. P-values over the year and over the seasons respectively are 0.428 and 0.237 for CD and 0.311 and 0.812 for UC. Conclusions: There is no seasonality in the distribution of births of IBD patients as compared to controls. The hypothesis that environmental factors present at the time of birth play a role in the pathogenesis of IBD is not supported by these data.