Because disease type was found to be significant, multivariate models were applied for each disease subtype. Older age group, white race, and the second study period remained highly significant for both CD and UC independently.
Several important observations have emerged from the present study. First, the crude incidence rate of IBD in children doubled from 1991 to 2002. Among white children, the incidence rate increased from 1.43/100,000 to 4.15/100,000 during the total study period. These figures are comparable to the incidence rates reported from the Netherlands (24) and Scotland (25), but are half of those reported from north Stockholm (26) and Wisconsin (9). This dissimilarity in the study results could be because of the differences in the characteristics of the study population and differences in the genetic and environmental exposure(s). Studies from the United States and Europe have illustrated a definite increase in the overall mean annual incidence rates of adults and pediatric IBD during the past 4 decades (15–19). The first and largest prospective study of childhood IBD was reported from the British Isles, documenting an incidence of 5.2/100,000 children younger than 16 years of age (16). Another study from Copenhagen reported the mean annual incidences of 8.6/100,000 for CD, 13.4/100,000 for UC, and 1.1/100,000 for IC between the years 2003 and 2005 (27). Factors contributing to such increase could be the greater case ascertainment, the widening case definition, earlier onset in predisposed individuals, greater access to health care, or the real increase in the incidence of IBD in children. Although the rapid rise of the incidence rate in this study cannot be directly related to genetic changes in the populations, genetic and environmental interaction may well be implicated. Additionally, advanced techniques have allowed improving the ability for earlier diagnosis of IBD in children. The sharp increase in the overall incidence of IBD in the present study was more lucid for CD. These findings are consistent with a retrospective study from Scotland that reported a 3-fold increase in the incidence rate of CD among children, whereas the incidence of UC remained unchanged during the same period (25). Additionally, a recent study from the United States reported that the prevalence of CD and UC in children was 43/100,000 and 28/100,000, respectively (28).
Although CD was diagnosed more than UC among the 3 race/ethnic groups in our study, it was more predominant among African American children diagnosed with IBD. A recent study reported that African American and Hispanic patients with CD, but not patients with UC, had lower prevalence of family history of IBD than their white counterparts, concluding that racial difference may reflect underlying genetic variations (35). It is worth pointing out that difference in diet, crowding, and hygiene are changing over time, which could play a role in the etiology of CD and UC independently. The high-fat-intake diet among the African American population could contribute to the etiology of CD, because a study from the United States among urban African Americans found that 77% of their study population had a diet that is high in fat (36). A study from Ireland (37) reported that patients with CD have a higher dietary intake of sucrose, refined carbohydrates, and ω-6 fatty acids and reduced intake of fruits and vegetables. Another study from Japan (38) reported that the intake of total fat, monounsaturated fatty acids, polyunsaturated fatty acids, and ω-6 fatty acids was positively associated with CD risk.
In contrast with other studies, our present study did not find a sex effect on the incidence of IBD. Studies from the United States and the United Kingdom reported a higher proportion of boys than girls diagnosed with CD (9,16). However, other studies reported a higher prevalence of CD among female adults (40,41). The disagreement about the sex-related factor for CD could be related to the age-related factors for the etiologic cause of CD.
The use of data for constructing a retrospective cohort has some shortcomings. First, the studied population presented to a tertiary care from a single center and the possibility of missing some new IBD cases exists because there were 2 to 3 private practices in the same area but opened only in 2000. However, TCH is one of the largest children's hospitals in the nation offering a diverse population at large that closely reflects that of the Texas population. Additionally, missing some cases from other practices would not have influenced the validity of our results because it would have only increased the incidence rate by a small margin (the volume of patients seen in TCH is much higher). The second limitation was that a higher proportion of African American and Hispanic children residing in large cities in general and Houston specifically, may be evaluated more in city or public hospitals than in private hospitals. However, the total number of African American and Hispanic children diagnosed with IBD in these public hospitals is small and would not have affected the overall calculation of the incidence rate in our study. Furthermore, some suspected cases of IBD in children in these hospitals are referred to TCH for further evaluation. The third limitation is the small number of Hispanic children during the first study period, which limited the power to examine whether race/ethnicity is a major risk factor for the IBD etiology. Nevertheless, our total sample size was large enough to allow the examination of age-, sex-, and race-related difference in the 3 subtypes of IBD. A final limitation was that this study was not able to examine the effect of other races because of the small sample size in the IBD registry.
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