Journal
RHEUMATOLOGY
Volume 57, Issue 10, Pages 1769-1776Publisher
OXFORD UNIV PRESS
DOI: 10.1093/rheumatology/key171
Keywords
urate; hyperuricemia; vitamin C; Mendelian randomization
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Funding
- Michaelsen Foundation, Copenhagen, Denmark
- Danish Council for Independent Research, Medical Sciences, Copenhagen, Denmark
- Chief Physician Johan Boserup and Lise Boserup Foundation, Haslev, Denmark
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Objective. Gout is the most common form of inflammatory arthritis and is caused by hyperuricaemia. Some studies have found a reduction in plasma urate with vitamin C supplementation. We tested the hypothesis that high plasma vitamin C is causally associated with low plasma urate and low risk of hyperuricaemia, using a Mendelian randomization approach. Methods. We measured plasma urate and genotyped for the SLC23A1 rs33972313 vitamin C variant in 106 147 individuals from the Copenhagen General Population Study, of which 24 099 had hyperuricaemia. We measured plasma vitamin C in 9234 individuals and genotyped for the SLC2A9 rs7442295 urate variant in 102 345 individuals. Results. Each 10 mu mol/l higher plasma vitamin C was associated with a -2.3(95%CI: -0.69 to -3.9) mu mol/l lower plasma urate after multivariable adjustments. The SLC23A1 rs33972313 GG genotype was associated with a 9% (5.6%, 11.9%) higher plasma vitamin C compared with M and AG combined but was not associated with plasma urate (P= 0.31). Likewise, for each 10 mu mol/l higher plasma vitamin C the odds ratios for hyperuricaemia were 0.92 (0.86, 0.98) observationally after multivariable adjustments, but 1.01 (0.84, 1.23) genetically. Conclusion. High plasma vitamin C was associated with low plasma urate and with low risk of hyperuricaemia. However, the SLC23A1 genetic variant causing lifelong high plasma vitamin C was not associated with plasma urate levels or with risk of hyperuricaemia. Thus, our data do not support a causal relationship between high plasma vitamin C and low plasma urate.
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