Risk factors for Burkitt lymphoma: a nested case-control study in the UK Clinical Practice Research Datalink

Parisa Karimi, Brenda M. Birmann, Lesley A. Anderson, Charlene M. McShane, Shahinaz M. Gadalla, Joshua N. Sampson, Sam M. Mbulaiteye*

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

10 Citations (Scopus)


Burkitt lymphoma (BL) occurs as three subtypes: endemic BL, immunosuppression-related BL and sporadic BL. Descriptive studies of BL age-specific incidence patterns have suggested multimodal peaks near 10, 40 and 70 years of age, but the risk factors for BL at different ages are unknown. We investigated risk factors for BL in the United Kingdom among 156 BL cases and 608 matched BL-free controls identified in the Clinical Practice Research Datalink (CPRD) between 1992 and 2016. Associations with pre-diagnostic body mass index, cigarette smoking, alcohol consumption, hepatitis, Epstein–Barr virus (EBV), human immunodeficiency virus infection and acquired immune deficiency syndrome (HIV/AIDS), malaria, allergic and autoimmune conditions, and prednisone use were evaluated. Overall, we identified inverse associations between smoking and BL risk, and positive associations between prior EBV infection, HIV/AIDS and prescription or use of prednisone with BL risk. In age-group stratified analyses, BL was associated with malaria exposure (vs. no exposure, odds ratio [OR] 8·00, 95% confidence interval [CI] 1·46–43·7) among those aged 20–59 years old and with hepatitis infection (vs. no infection, OR 3·41, 95% CI 1·01–11·5) among those aged 60+ years old. The effects of EBV, malaria, HIV/AIDS, prednisone and hepatitis on BL remained significant in mutually-adjusted age-group-specific analyses. No risk factors were associated with childhood BL. We report novel associations for BL in non-endemic settings.

Original languageEnglish
Pages (from-to)505-514
Number of pages10
JournalBritish Journal of Haematology
Issue number4
Early online date20 Apr 2018
Publication statusPublished - May 2018

Bibliographical note

We thank Ms. Emily Carver, Ruth Parsons, and David Ruggieri at Information Management Services Inc. (Calverton, MD, USA) for coordinating data and preparing data analysis files. This work supported by contracts from the Intramural Research Program of the Division of Cancer Epidemiology and Genetics, National Cancer Institute (NCI) (contract number: HHSN261201500328P) National Institutes of Health, Department of Health and Human Services. The study is based in part on data from the Clinical Practice Research Datalink GOLD database obtained from the UK Medicines and Healthcare Products Regulatory Agency. The content of this publication, the interpretation, and the conclusions contained in this study are those of the author/s alone and do not reflect the views of the UK Medicines and Healthcare Products Regulatory Agency or the Department of Health and Human Services, nor does mention of trade names, commercial products, or organizations imply endorsement by the US Government. The funders did not influence on the study design, the analysis, the interpretation of data, the writing of the report or the decision to submit the article for publication.


  • Burkitt lymphoma
  • Epstein–Barr virus
  • Falciparum malaria
  • prednisone
  • smoking


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