Department of Molecular and Human Genetics, Baylor College of Medicine, Houston, TX, USA.
Department of Molecular and Human Genetics, Baylor College of Medicine, Houston, TX, USA; Baylor Genetics, Houston, TX, USA.
Mol Genet Metab. 2020 Sep-Oct;131(1-2):147-154. doi: 10.1016/j.ymgme.2020.07.013. Epub 2020 Aug 5.
Inborn errors of metabolism (IEM) involving the non-oxidative pentose phosphate pathway (PPP) include the two relatively rare conditions, transketolase deficiency and transaldolase deficiency, both of which can be difficult to diagnosis given their non-specific clinical presentations. Current biochemical testing approaches require an index of suspicion to consider targeted urine polyol testing. To determine whether a broad-spectrum biochemical test could accurately identify a specific metabolic pattern defining IEMs of the non-oxidative PPP, we employed the use of clinical metabolomic profiling as an unbiased novel approach to diagnosis. Subjects with molecularly confirmed IEMs of the PPP were included in this study. Targeted quantitative analysis of polyols in urine and plasma samples was accomplished with chromatography and mass spectrometry. Semi-quantitative unbiased metabolomic analysis of urine and plasma samples was achieved by assessing small molecules via liquid chromatography and high-resolution mass spectrometry. Results from untargeted and targeted analyses were then compared and analyzed for diagnostic acuity. Two siblings with transketolase (TKT) deficiency and three unrelated individuals with transaldolase (TALDO) deficiency were identified for inclusion in the study. For both IEMs, targeted polyol testing and untargeted metabolomic testing on urine and/or plasma samples identified typical perturbations of the respective disorder. Additionally, untargeted metabolomic testing revealed elevations in other PPP metabolites not typically measured with targeted polyol testing, including ribonate, ribose, and erythronate for TKT deficiency and ribonate, erythronate, and sedoheptulose 7-phosphate in TALDO deficiency. Non-PPP alternations were also noted involving tryptophan, purine, and pyrimidine metabolism for both TKT and TALDO deficient patients. Targeted polyol testing and untargeted metabolomic testing methods were both able to identify specific biochemical patterns indicative of TKT and TALDO deficiency in both plasma and urine samples. In addition, untargeted metabolomics was able to identify novel biomarkers, thereby expanding the current knowledge of both conditions and providing further insight into potential underlying pathophysiological mechanisms. Furthermore, untargeted metabolomic testing offers the advantage of having a single effective biochemical screening test for identification of rare IEMs, like TKT and TALDO deficiencies, that may otherwise go undiagnosed due to their generally non-specific clinical presentations.
涉及非氧化戊糖磷酸途径 (PPP) 的先天性代谢错误 (IEM) 包括两种相对罕见的情况,即转酮醇酶缺乏症和 transaldolase 缺乏症,由于其非特异性临床表现,这两种疾病都难以诊断。目前的生化检测方法需要有怀疑的指标来考虑针对尿多元醇的靶向检测。为了确定广谱生化检测是否可以准确识别定义非氧化 PPP 中 IEM 的特定代谢模式,我们采用了临床代谢组学分析作为一种新颖的诊断方法。本研究纳入了经分子证实的 PPP 中 IEM 患者。通过色谱法和质谱法对尿和血浆样本中的多元醇进行靶向定量分析。通过液相色谱和高分辨率质谱评估小分子,对半定量非靶向和代谢组学分析对尿和/或血浆样本进行分析。然后比较和分析未靶向和靶向分析的结果以确定诊断准确性。确定了两名患有转酮醇酶 (TKT) 缺乏症的兄弟姐妹和三名患有 transaldolase (TALDO) 缺乏症的无关个体参加该研究。对于这两种 IEM,针对尿和/或血浆样本中的多元醇进行的靶向和非靶向代谢组学检测确定了各自疾病的典型扰动。此外,非靶向代谢组学检测还显示,其他 PPP 代谢物的水平升高,这些代谢物通常无法通过靶向多元醇检测测量,包括 TKT 缺乏症中的核糖醇、核糖和赤藓糖 7-磷酸,以及 TALDO 缺乏症中的核糖醇、赤藓糖和 sedoheptulose 7-磷酸。对于 TKT 和 TALDO 缺乏症患者,还观察到非 PPP 改变涉及色氨酸、嘌呤和嘧啶代谢。靶向多元醇检测和非靶向代谢组学检测方法均能够在血浆和尿液样本中识别出指示 TKT 和 TALDO 缺乏的特定生化模式。此外,非靶向代谢组学能够识别新的生物标志物,从而扩展了这两种疾病的现有知识,并为潜在的潜在病理生理机制提供了进一步的见解。此外,非靶向代谢组学检测为识别罕见的 IEM(如 TKT 和 TALDO 缺乏症)提供了一种有效的单一生化筛选测试,否则由于其通常非特异性的临床表现,这些 IEM 可能会被漏诊。