急性肠胃炎中的高尿酸血症是由通过ABCG2的尿酸排泄减少所致。

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

作者信息

Matsuo Hirotaka, Tsunoda Tomoyuki, Ooyama Keiko, Sakiyama Masayuki, Sogo Tsuyoshi, Takada Tappei, Nakashima Akio, Nakayama Akiyoshi, Kawaguchi Makoto, Higashino Toshihide, Wakai Kenji, Ooyama Hiroshi, Hokari Ryota, Suzuki Hiroshi, Ichida Kimiyoshi, Inui Ayano, Fujimori Shin, Shinomiya Nariyoshi

机构信息

Department of Integrative Physiology and Bio-Nano Medicine, National Defense Medical College, Tokorozawa, Saitama 359-8513, Japan.

Department of Pediatric Hepatology and Gastroenterology, Saiseikai Yokohamashi Tobu Hospital, Yokohama, Kanagawa 230-0012, Japan.

出版信息

Sci Rep. 2016 Aug 30;6:31003. doi: 10.1038/srep31003.

DOI:10.1038/srep31003

PMID:27571712

原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5004129/

Abstract

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 × 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 × 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.

摘要

为了阐明人类中通过ABCG2进行肠道尿酸排泄的生理和病理生理作用，我们分别对终末期肾病（血液透析）患者和急性肠胃炎患者的ABCG2功能失调常见变体Q126X（rs72552713）和Q141K（rs2231142）进行了基因分型。ABCG2功能障碍使106名血液透析患者的血清尿酸（SUA）水平显著升高（P = 1.1×10⁻⁴），这证明了ABCG2在肠道尿酸排泄中的生理作用，因为他们的尿酸排泄几乎依赖于通过ABCG2的肠道排泄。此外，无论脱水程度如何，ABCG2功能障碍均使67名急性肠胃炎患者的SUA显著升高（P = 6.3×10⁻³），这证明了ABCG2在急性肠胃炎中的病理生理作用。这些发现首次表明了人类中ABCG2介导的肠道尿酸排泄，并表明肠道上皮作为除吸收途径外的排泄途径在生理和病理生理方面的重要性。此外，SUA升高不仅可能是脱水的有用标志物，还可能是肠道上皮损伤的标志物。