Department of Pediatrics, Shimane University Faculty of Medicine, 89-1, Ennya, Izumo, Shimane, 693-8501, Japan.
J Hum Genet. 2019 Feb;64(2):73-85. doi: 10.1038/s10038-018-0527-7. Epub 2018 Nov 6.
Mitochondrial fatty acid oxidation disorders (FAODs) are caused by defects in β-oxidation enzymes, including very long-chain acyl-CoA dehydrogenase (VLCAD), trifunctional protein (TFP), carnitine palmitoyltransferase-2 (CPT2), carnitine-acylcarnitine translocase (CACT) and others. During prolonged fasting, infection, or exercise, patients with FAODs present with hypoglycemia, rhabdomyolysis, cardiomyopathy, liver dysfunction, and occasionally sudden death. This article describes the diagnosis, newborn screening, and treatment of long-chain FAODs with a focus on VLCAD deficiency. VLCAD deficiency is generally classified into three phenotypes based on onset time, but the classification should be comprehensively determined based on genotype, residual enzyme activity, and clinical course, due to a lack of apparent genotype-phenotype correlation. With the expansion of newborn screening for FAODs, several issues have arisen, such as missed detection, overdiagnosis (including detection of benign/asymptomatic type), and poor prognosis of the neonatal-onset form. Meanwhile, dietary management and restriction of exercise have been unnecessary for patients with the benign/asymptomatic type of VLCAD deficiency with a high fatty acid oxidation flux score. Although L-carnitine therapy for VLCAD/TFP deficiency has been controversial, supplementation with L-carnitine may be accepted for CPT2/CACT and multiple acyl-CoA dehydrogenase deficiencies. Recently, a double-blind, randomized controlled trial of triheptanoin (seven-carbon fatty acid triglyceride) versus trioctanoin (regular medium-chain triglyceride) was conducted and demonstrated improvement of cardiac functions on triheptanoin. Additionally, although the clinical efficacy of bezafibrate remains controversial, a recent open-label clinical trial showed efficacy of this drug in improving quality of life. These drugs may be promising for the treatment of FAODs, though further studies are required.
线粒体脂肪酸氧化障碍(FAODs)是由β-氧化酶缺陷引起的,包括长链酰基辅酶 A 脱氢酶(VLCAD)、三功能蛋白(TFP)、肉碱棕榈酰转移酶-2(CPT2)、肉碱酰基肉碱移位酶(CACT)等。在长时间禁食、感染或运动期间,FAOD 患者会出现低血糖、横纹肌溶解、心肌病、肝功能障碍,偶尔还会突然死亡。本文主要介绍长链 FAOD 的诊断、新生儿筛查和治疗,重点介绍 VLCAD 缺乏症。VLCAD 缺乏症通常根据发病时间分为三种表型,但由于缺乏明显的基因型-表型相关性,分类应综合考虑基因型、残余酶活性和临床过程。随着 FAOD 新生儿筛查的扩大,出现了一些问题,如漏检、过度诊断(包括良性/无症状型的检测)和新生儿发病形式的不良预后。同时,对于具有高脂肪酸氧化通量评分的良性/无症状型 VLCAD 缺乏症患者,饮食管理和运动限制已不再必要。虽然 L-肉碱治疗 VLCAD/TFP 缺乏症存在争议,但对于 CPT2/CACT 和多种酰基辅酶 A 脱氢酶缺乏症,补充 L-肉碱可能被接受。最近,一项关于三庚酸(七碳脂肪酸三酯)与三辛酸(常规中链甘油三酯)的双盲、随机对照试验表明,三庚酸可改善心脏功能。此外,尽管 bezafibrate 的临床疗效仍存在争议,但最近的一项开放标签临床试验表明,该药可有效提高生活质量。这些药物可能是 FAODs 治疗的有前途的药物,但仍需要进一步研究。