Gregersen N, Christensen M F, Christensen E, Kølvraa S
Acta Paediatr Scand. 1986 Jul;75(4):676-81. doi: 10.1111/j.1651-2227.1986.tb10272.x.
A boy with riboflavin-responsive beta-oxidation deficiency (multiple acyl-CoA dehydrogenation deficiency) was assessed clinically and biochemically after 3 years of continuous riboflavin medication. He was diagnosed at the age of three years after an attack of a Reye's syndrome-like disease. During the 3 years of assessment he has experienced no serious disease; although short episodes of fatigue and loss of appetite have been noted. His mental and physical development has been normal. Biochemically the abnormal excretion of organic acid metabolites, characteristic of the acyl-CoA dehydrogenation deficiency, has been continuously present. Quantitatively there has been a trend to a more simple picture with ethylmalonic acid as the predominant metabolite. However, because of the large within-day variation in the excretion of all the metabolites, changes following diet and riboflavin trials must be interpreted with caution in these patients.
一名患有核黄素反应性β-氧化缺陷(多种酰基辅酶A脱氢酶缺乏症)的男孩在连续服用核黄素3年后接受了临床和生化评估。他在三岁时因一次类似瑞氏综合征的疾病发作后被确诊。在评估的3年中,他没有经历过严重疾病;尽管注意到有短暂的疲劳和食欲不振发作。他的智力和身体发育一直正常。生化方面,酰基辅酶A脱氢酶缺乏症特有的有机酸代谢产物异常排泄一直存在。从数量上看,以乙基丙二酸为主要代谢产物的情况有趋于更简单的趋势。然而,由于所有代谢产物的排泄在一天内变化很大,在这些患者中,饮食和核黄素试验后的变化必须谨慎解释。