Aledo R, Mir C, Dalton R N, Turner C, Pié J, Hegardt F G, Casals N, Champion M P
Unit of Biochemistry and Molecular Biology, School of Health Sciences, International University of Catalonia, Spain.
J Inherit Metab Dis. 2006 Feb;29(1):207-11. doi: 10.1007/s10545-006-0214-2.
Mitochondrial HMG-CoA synthase deficiency is an inherited metabolic disorder caused by a defect in the enzyme that regulates the formation of ketone bodies. Patients present with hypoketotic hypoglycaemia, encephalopathy and hepatomegaly, usually precipitated by an intercurrent infection or prolonged fasting. The diagnosis may easily be missed as previously reported results of routine metabolic investigations, urinary organic acids and plasma acylcarnitines may be nonspecific or normal, and a high index of suspicion is required to proceed to further confirmatory tests. We describe a further acute case in which the combination of urinary organic acids, low free carnitine and changes in the plasma acylcarnitine profile on carnitine supplementation were very suggestive of a defect in ketone synthesis. The diagnosis of mitochondrial HMG-CoA synthase deficiency was confirmed on genotyping, revealing two novel mutations: c.614G > A (R188H) and c.971T > C (M307T). A further sibling, in whom the diagnosis had not been made acutely, was also found to be affected. The possible effects of these mutations on enzyme activity are discussed.
线粒体HMG-CoA合酶缺乏症是一种遗传性代谢紊乱疾病,由调节酮体形成的酶缺陷引起。患者表现为低酮性低血糖、脑病和肝肿大,通常由并发感染或长期禁食诱发。由于之前常规代谢检查、尿有机酸和血浆酰基肉碱的结果可能不具特异性或正常,诊断可能容易被漏诊,因此需要高度怀疑才能进行进一步的确诊检查。我们描述了另一例急性病例,其中尿有机酸、低游离肉碱以及补充肉碱后血浆酰基肉碱谱的变化强烈提示酮体合成存在缺陷。基因分型确诊为线粒体HMG-CoA合酶缺乏症,发现了两个新的突变:c.614G > A(R188H)和c.971T > C(M307T)。还发现另一个未急性确诊的同胞也受影响。讨论了这些突变对酶活性可能产生的影响。