Hyperuricemia in acute gastroenteritis is caused by decreased urate excretion via ABCG2

被引：54

作者：

Matsuo, Hirotaka ^{[1
]}

Tsunoda, Tomoyuki ^{[2
]}

Ooyama, Keiko ^{[3
]}

Sakiyama, Masayuki ^{[1
,4
]}

Sogo, Tsuyoshi ^{[2
]}

Takada, Tappei ^{[5
]}

Nakashima, Akio ^{[6
]}

Nakayama, Akiyoshi ^{[1
]}

Kawaguchi, Makoto ^{[1
,7
]}

Higashino, Toshihide ^{[1
]}

Wakai, Kenji ^{[8
]}

Ooyama, Hiroshi ^{[3
]}

Hokari, Ryota ^{[9
]}

Suzuki, Hiroshi ^{[5
]}

Ichida, Kimiyoshi ^{[6
,10
]}

Inui, Ayano ^{[2
]}

Fujimori, Shin ^{[11
]}

Shinomiya, Nariyoshi ^{[1
]}

机构：

[1] Natl Def Med Coll, Dept Integrat Physiol & Bionano Med, Tokorozawa, Saitama 3598513, Japan

[2] Saiseikai Yokohamashi Tobu Hosp, Dept Pediat Hepatol & Gastroenterol, Yokohama, Kanagawa 2300012, Japan

[3] Ryougoku East Gate Clin, Sumida Ku, Tokyo 1300026, Japan

[4] Natl Def Med Coll, Dept Dermatol, Tokorozawa, Saitama 3598513, Japan

[5] Tokyo Univ Hosp, Dept Pharm, Bunkyo Ku, Tokyo 1138655, Japan

[6] Jikei Univ, Sch Med, Dept Internal Med, Div Kidney & Hypertens,Minato Ku, Tokyo 1058471, Japan

[7] Natl Def Med Coll, Dept Urol, Tokorozawa, Saitama 3598513, Japan

[8] Nagoya Univ, Grad Sch Med, Dept Prevent Med, Nagoya, Aichi 4618673, Japan

[9] Natl Def Med Coll, Dept Internal Med, Tokorozawa, Saitama 3598513, Japan

[10] Tokyo Univ Pharm & Life Sci, Dept Pathophysiol, Hachioji, Tokyo 1920392, Japan

[11] Teikyo Univ, Sch Med, Dept Internal Med, Itabashi Ku, Tokyo 1738605, Japan

来源：

SCIENTIFIC REPORTS | 2016年 / 6卷

关键词：

MULTIINSTITUTIONAL COLLABORATIVE COHORT; RESISTANCE PROTEIN TRANSPORTER; COMMON DYSFUNCTIONAL VARIANTS; PATHOGENESIS; DISEASE; RISK; GENE; GOUT;

D O I：

10.1038/srep31003

中图分类号：

O [数理科学和化学]; P [天文学、地球科学]; Q [生物科学]; N [自然科学总论];

学科分类号：

07 ; 0710 ; 09 ;

摘要：

To clarify the physiological and pathophysiological roles of intestinal urate excretion via ABCG2 in humans, we genotyped ABCG2 dysfunctional common variants, Q126X (rs72552713) and Q141K (rs2231142), in end-stage renal disease (hemodialysis) and acute gastroenteritis patients, respectively. ABCG2 dysfunction markedly increased serum uric acid (SUA) levels in 106 hemodialysis patients (P = 1.1 x 10(-4)), which demonstrated the physiological role of ABCG2 for intestinal urate excretion because their urate excretion almost depends on intestinal excretion via ABCG2. Also, ABCG2 dysfunction significantly elevated SUA in 67 acute gastroenteritis patients (P = 6.3 x 10(-3)) regardless of the degree of dehydration, which demonstrated the pathophysiological role of ABCG2 in acute gastroenteritis. These findings for the first time show ABCG2-mediated intestinal urate excretion in humans, and indicates the physiological and pathophysiological importance of intestinal epithelium as an excretion pathway besides an absorption pathway. Furthermore, increased SUA could be a useful marker not only for dehydration but also epithelial impairment of intestine.

引用

页数：6

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