Mikkel Malham[1], Christian Jakobsen[1], Ida Vind[2], Marianne K. Vester-Andersen[2,3], Vibeke Wewer[1].

Affiliates

The Paediatric Department, Hvidovre University Hospital [1], The GastroUnit, Hvidovre University Hospital, Denmark[2], Department of Internal medicine, Zealand University Hospital Denmark[3]

Abstract

Background:
The existing population-based comparative studies between adult onset IBD (aIBD) and paediatric onset IBD (pIBD) show that paediatric onset of ulcerative colitis (pUC) present with more extensive disease. In this population-based study, we aim to further characterize the differences in the natural history between pIBD and aIBD.
Methods:
AIBD patients included (>18 years of age) were diagnosed from January 2003 to December 2004. PIBD patients were diagnosed from January 1998 to December 2008 (<15 years of age). All medical records were retrieved manually at time of last follow-up, and clinical data concerning IBD phenotype (Montreal classification) and treatment were registered. Differences regarding medical treatment and surgery was calculated using survival analysis (Kaplan Meier plots and Cox regression analysis).
Results:
446 aIBD (CD/UC 183/263) and 333 pIBD (CD/UC/IBDU 166/145/22) patients were included. Median follow-up time was 6,9 years (aIBD) and 9.2 years (pIBD). In UC, 24% and 65% of aIBD and pIBD, respectively, had extensive disease (E3) (p<0.0001) at diagnosis. In CD, 9% aIBD and 24% pIBD (p<0.0001) had involvement of the upper GI tract (L4a or L4b either alone or in combination with L1-L3). A total of 14% and 42% of aIBD and pIBD patients, respectively, were treated with anti-TNF-alpha (HR: 3.2 (2.4-4.4), p<0.0001) during follow-up time. In UC, 41% and 74% of aUC and pUC, respectively received either azathioprine or 6-mercatopurine (IM) (HR 3.8 (2.8-5.2), p<0.0001). When stratifying for disease extension, the increased risk of treatment with anti-TNF-alpha and IM seen in pUC persisted.
Conclusions:
PIBD is characterised by a more extensive disease than aIBD and is more often treated with immunomodulators and biologic agents. In UC, the increased likelihood of treatment could not be explained by the difference in disease extension. This could indicate that the inflammation in pIBD is more aggressive than in aIBD.