Dysfunctional variants of ABCG2 create strong individual and population risks for progression of hyperuricemia: the potential for implementation of genome-personalized nursing
Gout, a common disease, develops after prolonged hyperuricemia with elevated serum uric acid (SUA) levels. Sex, overweight/obesity, heavy drinking, and aging all increase risk. Common dysfunctional variants (polymorphisms) in the ABCG2/BCRP gene are major genetic causes of gout/hyperuricemia. Early management would thus have potential benefits for public health. Several studies report the effectiveness of nurse-led care for gout management. We evaluate here the individual and population genetic effects of ABCG2 in 9244 Japanese study participants, in all of whom ABCG2 variants had a higher population-attributable fraction (PAF; approximately 30%) for progression of hyperuricemia than those for other typical environmental risk factors (overweight/obesity, heavy drinking, and aging). PAFs for aging in males and heavy drinking in females were not significant. All these factors also showed significant individual risk of increased SUA level, and ABCG2 variants had sufficient effect size to allow them to be converted into other environmental factors. To implement genome-personalized nursing, we then mapped onto the process a theoretical framework that is based on a psychological model from behavioral change theory. Because the present results for convertibility will improve the predictability of genetic effects, cognitive interventions by nurses based on individual variants could therefore encourage both inducements of behavioral change: efficacy expectations (self-efficacy) and outcome expectations. We conclude that the framework would function effectively based on cognitive interventions by nurses/paramedics. This theoretical framework has potential as a basis for implementing genome-personalized prevention, medicine and nursing of gout/hyperuricemia, and for optimizing nurse-led care.
Authors
- Takashi Tamura (ORCID: https://orcid.org/0000-0002-1057-744X)
- Itsumi Hashimoto (ORCID: https://orcid.org/0009-0006-1241-8713)
- Yu Toyoda (ORCID: https://orcid.org/0000-0002-7411-0531)
- Yasufumi Kato (ORCID: https://orcid.org/0000-0002-0901-4471)
- Yusuke Kawamura (ORCID: https://orcid.org/0000-0001-5021-1613)
- Risa Tanabe
- Michiru Miura
- Yoko Mitsuda
- Miki Ueno
- Ken Yamamoto (ORCID: https://orcid.org/0000-0002-6512-1773)
- Hirofumi Nakaoka (ORCID: https://orcid.org/0000-0002-8454-1159)
- Kimiko Hayano
- Hiroshi Nakashima (ORCID: https://orcid.org/0000-0002-3551-391X)
- Yuka Miyoshi (ORCID: https://orcid.org/0000-0003-3141-6650)
- Masashi Tsunoda
- Miho Toba
- Tomoko Mizuno
- Nana Takehana
- Akiyoshi Nakayama
- Yoshinobu Hamada
- Nariyoshi Shinomiya
- Seiko Shimizu
- Hirotaka Matsuo
- Rion Kikuchi
Institutions
- Kagoshima University (JP)
- Sasaki Institute (JP)
- National Defense Medical College Hospital (JP)
- Kurume University Medical Center (JP)
- Self-Defense Forces Central Hospital (JP)
- National Defense Medical College (JP)
- Nagoya University (JP)
Publication Details
- Journal
- Human Cell
- Published
- 2025-12-26
- DOI
- https://doi.org/10.1007/s13577-025-01310-y
- Primary Topic
- Gout, Hyperuricemia, Uric Acid
- Type
- article
- Field-Weighted Citation Impact
- 0.00
Funders
- National Defense Medical College