The phenotype and course of inflammatory bowel disease in UK patients of Bangladeshi descent

Authors

  • J. R. Goodhand,

    1. Centre for Digestive Diseases, Blizard Institute of Cell and Molecular Science, Barts and the London School of Medicine and Dentistry, London, UK
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    • Denotes co first authors.

  • N. Kamperidis,

    1. Centre for Digestive Diseases, Blizard Institute of Cell and Molecular Science, Barts and the London School of Medicine and Dentistry, London, UK
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    • Denotes co first authors.

  • N. M. Joshi,

    1. Centre for Digestive Diseases, Blizard Institute of Cell and Molecular Science, Barts and the London School of Medicine and Dentistry, London, UK
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  • M. Wahed,

    1. Centre for Digestive Diseases, Blizard Institute of Cell and Molecular Science, Barts and the London School of Medicine and Dentistry, London, UK
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  • Y. Koodun,

    1. Centre for Digestive Diseases, Blizard Institute of Cell and Molecular Science, Barts and the London School of Medicine and Dentistry, London, UK
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  • E. J. Cantor,

    1. Centre for Digestive Diseases, Blizard Institute of Cell and Molecular Science, Barts and the London School of Medicine and Dentistry, London, UK
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  • N. M. Croft,

    1. Centre for Digestive Diseases, Blizard Institute of Cell and Molecular Science, Barts and the London School of Medicine and Dentistry, London, UK
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  • F. L. Langmead,

    1. Centre for Digestive Diseases, Blizard Institute of Cell and Molecular Science, Barts and the London School of Medicine and Dentistry, London, UK
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  • J. O. Lindsay,

    1. Centre for Digestive Diseases, Blizard Institute of Cell and Molecular Science, Barts and the London School of Medicine and Dentistry, London, UK
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  • D. S. Rampton

    Corresponding author
    • Centre for Digestive Diseases, Blizard Institute of Cell and Molecular Science, Barts and the London School of Medicine and Dentistry, London, UK
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Correspondence to:

Prof. D. S. Rampton, Endoscopy Unit, The Royal London Hospital, London E1 1BB, UK.

E-mail: d.rampton@qmul.ac.uk

Summary

Background

We have tested the hypotheses that compared with local white Caucasians, UK-resident patients of Bangladeshi descent develop inflammatory bowel disease (IBD) at a younger age; more often have Crohn's disease than ulcerative colitis (UC); and have a more aggressive disease course.

Aim

To test the hypotheses that compared to white Caucasian patients of English, Scottish or Welsh descent, patients of Bangladeshi descent develop IBD at a younger age; more often have Crohn's disease; and have a more aggressive disease course by screening case-records of these patients.

Methods

We screened the case-records of 132 Bangladeshi and 623 white Caucasian consecutive out-patients. We then matched each Bangladeshi to a patient of white Caucasian descent for age at diagnosis and disease duration. Data on migration status, phenotype, disease course, treatments and extra-intestinal manifestations and complications were obtained.

Results

No differences were seen in the adjusted age at diagnosis of IBD between Bangladeshi and white Caucasian patients. More Bangladeshis than white Caucasian patients (P < 0.01) were diagnosed with Crohn's disease than UC. Crohn's phenotype at diagnosis was similar in both groups. However, multivariate Cox logistic regression analyses showed that Bangladeshis developed perianal complications (HR [95% confidence interval CI] 8.6 [1.4, 53.1], P = 0.02), and received anti-TNFs (HR [95% CI] 3.0 [1.2, 7.7], P = 0.02) earlier and underwent surgery later (HR [95% CI] 0.4 [0.2, 0.9], P = 0.03) than white Caucasians. More Bangladeshis with UC had extensive disease (24/40 [60%]) than white Caucasians (16/49 [33%], P = 0.02). Overall, more Bangladeshis were anaemic and vitamin D deficient.

Conclusions

Bangladeshi patients with IBD more frequently have Crohn's than UC. Bangladeshis with Crohn's more frequently develop perianal disease, have earlier medication escalation and undergo surgery later than white Caucasians. Bangladeshis have more extensive UC than white Caucasians. The relative contributions of genotype and environmental factors, including vitamin D, to these phenotypic differences require additional study.

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