Background <p>Abnormal circulating lipid levels have been suggested in relation to lymphoid malignancy (LM) risk.</p> Methods <p>We studied UK Biobank participants (<i>n</i> = 403,625) with serum data for cholesterol (total [TC], high-density lipoprotein [HDL], direct low-density lipoprotein [LDL]), triglycerides (TG), and apolipoproteins A1 and B (ApoA1, ApoB). We conducted principal component (PC) analysis and multivariate Cox regression models to estimate hazard ratio (HR) overall, by lipid-lowering drug use and follow-up interval.</p> Results <p>During an average of 10.5 years of follow-up, 3006 incident LMs occurred (including 667 multiple myelomas [MM], 2193 non-Hodgkin lymphomas [NHL]). Among medication non-users, most lipid levels were inversely associated with risk of most endpoints (HR<sub>Q4vsQ1</sub>range: 0.37 to 0.79), especially closer to diagnosis. In contrast LDL/HDL ratio and PC1 (highly loaded in LDL and ApoB) were consistently positively associated with chronic/small lymphocytic leukaemia risk in each follow-up period and with NHL and B-cell NHL risk within 5 years. Further, LD, ApoB and TG levels were positively associated with MM risk after 10+ years (HR<sub>1-SD</sub>range = 1.26 to 1.60).</p> Conclusion <p>Lipid depletion closer to LM diagnosis might reflect cancer cell metabolism and warrants further work examining individuals with precursor conditions. The MM-specific long-term risk might reflect the known MM-obesity association.</p>

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Serum lipid levels and risk of lymphoid malignancies in the UK Biobank study

  • Sara Hermosa,
  • Yolanda Benavente,
  • Elena Cabezudo,
  • Juan Sainz,
  • Marta Farràs,
  • Laia Alemany,
  • Brenda M. Birmann,
  • Delphine Casabonne

摘要

Background

Abnormal circulating lipid levels have been suggested in relation to lymphoid malignancy (LM) risk.

Methods

We studied UK Biobank participants (n = 403,625) with serum data for cholesterol (total [TC], high-density lipoprotein [HDL], direct low-density lipoprotein [LDL]), triglycerides (TG), and apolipoproteins A1 and B (ApoA1, ApoB). We conducted principal component (PC) analysis and multivariate Cox regression models to estimate hazard ratio (HR) overall, by lipid-lowering drug use and follow-up interval.

Results

During an average of 10.5 years of follow-up, 3006 incident LMs occurred (including 667 multiple myelomas [MM], 2193 non-Hodgkin lymphomas [NHL]). Among medication non-users, most lipid levels were inversely associated with risk of most endpoints (HRQ4vsQ1range: 0.37 to 0.79), especially closer to diagnosis. In contrast LDL/HDL ratio and PC1 (highly loaded in LDL and ApoB) were consistently positively associated with chronic/small lymphocytic leukaemia risk in each follow-up period and with NHL and B-cell NHL risk within 5 years. Further, LD, ApoB and TG levels were positively associated with MM risk after 10+ years (HR1-SDrange = 1.26 to 1.60).

Conclusion

Lipid depletion closer to LM diagnosis might reflect cancer cell metabolism and warrants further work examining individuals with precursor conditions. The MM-specific long-term risk might reflect the known MM-obesity association.