Division of Clinical and Metabolic Genetics, The Hospital for Sick Children, Toronto, Ontario, Canada.
National Metabolic Service, Starship Children's Hospital, Auckland, New Zealand.
J Inherit Metab Dis. 2021 Jul;44(4):903-915. doi: 10.1002/jimd.12371. Epub 2021 Mar 29.
Carnitine acyl-carnitine translocase deficiency (CACTD) is a rare autosomal recessive disorder of mitochondrial long-chain fatty-acid transport. Most patients present in the first 2 days of life, with hypoketotic hypoglycaemia, hyperammonaemia, cardiomyopathy or arrhythmia, hepatomegaly and elevated liver enzymes. Multi-centre international retrospective chart review of clinical presentation, biochemistry, treatment modalities including diet, subsequent complications, and mode of death of all patients. Twenty-three patients from nine tertiary metabolic units were identified. Seven attenuated patients of Pakistani heritage, six of these homozygous c.82G>T, had later onset manifestations and long-term survival without chronic hyperammonemia. Of the 16 classical cases, 15 had cardiac involvement at presentation comprising cardiac arrhythmias (9/15), cardiac arrest (7/15), and cardiac hypertrophy (9/15). Where recorded, ammonia levels were elevated in all but one severe case (13/14 measured) and 14/16 had hypoglycaemia. Nine classical patients survived longer-term-most with feeding difficulties and cognitive delay. Hyperammonaemia appears refractory to ammonia scavenger treatment and carglumic acid, but responds well to high glucose delivery during acute metabolic crises. High-energy intake seems necessary to prevent decompensation. Anaplerosis utilising therapeutic d,l-3-hydroxybutyrate, Triheptanoin and increased protein intake, appeared to improve chronic hyperammonemia and metabolic stability where trialled in individual cases. CACTD is a rare disorder of fatty acid oxidation with a preponderance to severe cardiac dysfunction. Long-term survival is possible in classical early-onset cases with long-chain fat restriction, judicious use of glucose infusions, and medium chain triglyceride supplementation. Adjunctive therapies supporting anaplerosis may improve longer-term outcomes.
肉碱酰基肉碱转位酶缺乏症(CACTD)是一种罕见的常染色体隐性线粒体长链脂肪酸转运缺陷。大多数患者在出生后前 2 天内发病,表现为低酮低血糖、高血氨、心肌病或心律失常、肝肿大和肝酶升高。对所有患者的临床表现、生化特征、治疗方式(包括饮食)、后续并发症和死亡模式进行了来自 9 个三级代谢单位的 23 名患者的多中心国际回顾性图表审查。确定了 7 名具有巴基斯坦血统的轻度患者,其中 6 名患者为纯合 c.82G>T,发病较晚,且长期生存,无慢性高血氨。在 16 例经典病例中,15 例在发病时存在心脏受累,包括心律失常(9/15)、心脏骤停(7/15)和心脏肥大(9/15)。在有记录的病例中,除 1 例重度病例外(14/16 例测量),所有病例的血氨水平均升高,14/16 例出现低血糖。9 例经典患者存活时间较长——大多数存在喂养困难和认知延迟。高血糖输注可有效缓解急性代谢危象期间的高氨血症,但对氨清除剂治疗和卡谷氨酸的治疗效果较差。似乎需要高能量摄入来防止代偿失调。在个别病例中试用的治疗性 d,l-3-羟基丁酸、三己酸甘油酯和增加蛋白质摄入的氨同化作用,似乎可以改善慢性高血氨和代谢稳定性。CACTD 是一种罕见的脂肪酸氧化缺陷疾病,其特征为严重的心脏功能障碍。对于经典的早发型病例,通过限制长链脂肪摄入、合理使用葡萄糖输注和补充中链甘油三酯,长期生存是可能的。支持氨同化作用的辅助治疗可能会改善长期预后。