Department of Population Medicine and Diagnostic Sciences, Cornell College of Veterinary Medicine, Cornell University, Ithaca, NY, USA.
Department of Veterinary Microbiology and Pathology, Washington State University, Pullman, WA, USA.
Equine Vet J. 2022 Jan;54(1):39-51. doi: 10.1111/evj.13435. Epub 2021 Mar 8.
High-serum γ-Glutamyl Transferase (GGT) activity has been associated with and thought to be a marker of maladaptation to training and possibly poor performance in racehorses, but the cause is unknown.
To investigate possible metabolic and infectious causes for the high GGT syndrome.
Pilot case-control study and nested case-control study.
The case-control study in 2017 included 16 horses (8 cases and 8 controls with median [range] serum GGT 82 [74-148] and 22 [19-28] IU/L, respectively) from the same stable. In 2018, similar testing was performed in a nested case-control study that identified 27 case (serum GGT 50 ≥ IU/L)-control pairs from three stables for further testing. Serum liver chemistries, selenium measurements, viral PCR and metabolomics were performed.
No differences were found in frequency of detection of viral RNA/DNA or copy numbers for equine hepacivirus (EqHV) and parvovirus-hepatitis (EqPV-H) between cases and controls. Mild increases in hepatocellular injury and cholestatic markers in case vs control horses suggested a degree of liver disease in a subset of cases. Metabolomic and individual bile acid testing showed differences in cases compared with controls, including increased abundance of pyroglutamic acid and taurine-conjugated bile acids, and reduced abundance of Vitamin B6. Selenium concentrations, although within or above the reference intervals, were also lower in case horses in both studies.
Observational study design did not allow us to make causal inferences.
We conclude that high GGT syndrome is likely a complex metabolic disorder and that viral hepatitis was not identified as a cause for this syndrome in this cohort of racehorses. Our results support a contribution of oxidative stress and cholestasis in its pathophysiology.
高血清γ-谷氨酰转移酶（GGT）活性与适应不良和表现不佳有关，被认为是赛马的标志物，但原因尚不清楚。
研究高 GGT 综合征的可能代谢和感染原因。
试点病例对照研究和巢式病例对照研究。
2017 年的病例对照研究纳入了来自同一马厩的 16 匹马（8 例病例和 8 例对照，中位数（范围）血清 GGT 分别为 82（74-148）和 22（19-28）IU/L）。2018 年，在嵌套病例对照研究中进行了类似的检测，该研究从三个马厩中确定了 27 例病例（血清 GGT≥50IU/L）-对照配对进行进一步检测。进行了血清肝化学、硒测量、病毒 PCR 和代谢组学检测。
病例和对照组之间未发现检测到的病毒 RNA/DNA 或乙型肝炎病毒（EqHV）和细小病毒-肝炎（EqPV-H）的病毒载量的频率差异。与对照组相比，病例组的肝细胞损伤和胆汁淤积标志物轻度增加，表明一部分病例存在肝脏疾病。与对照组相比，代谢组学和个别胆汁酸检测显示病例组存在差异，包括吡咯烷酮酸和牛磺酸结合胆汁酸的丰度增加，以及维生素 B6 的丰度降低。尽管在参考区间内或之上，在两项研究中病例马的硒浓度也较低。
观察性研究设计不允许我们进行因果推断。
我们得出结论，高 GGT 综合征可能是一种复杂的代谢紊乱，在该赛马队列中未发现病毒性肝炎是该综合征的原因。我们的结果支持氧化应激和胆汁淤积在其病理生理学中的作用。
