Center for Pediatric Liver Diseases, Children's Hospital of Fudan University, Shanghai 201102, China.
World J Gastroenterol. 2012 Dec 21;18(47):7113-7. doi: 10.3748/wjg.v18.i47.7113.
Aldo-keto reductase 1D1 (AKR1D1) deficiency, a rare but life-threatening form of bile acid deficiency, has not been previously described in China. Here, we describe the first two primary ∆4-3-oxosteroid 5β-reductase deficiency patients in Mainland China diagnosed by fast atom bombardment-mass spectroscopy of urinary bile acids and confirmed by genetic analysis. A high proportion of atypical 3-oxo-∆4-bile acids in the urine indicated a deficiency in ∆4-3-oxosteroid 5β-reductase. All of the coding exons and adjacent intronic sequence of the AKR1D1 gene were sequenced using peripheral lymphocyte genomic DNA of two patients and one of the patient's parents. One patient exhibited compound heterozygous mutations: c.396C>A and c.722A>T, while the other was heterozygous for the mutation c.797G>A. Based on these mutations, a diagnosis of primary ∆4-3-oxosteroid 5β-reductase deficiency could be confirmed. With ursodeoxycholic acid treatment and fat-soluble vitamin supplements, liver function tests normalized rapidly, and the degree of hepatomegaly was markedly reduced in both patients.
醛酮还原酶 1D1(AKR1D1)缺乏症是一种罕见但危及生命的胆汁酸缺乏症,在中国尚未有过相关描述。在此,我们报告了中国大陆首例经尿胆汁酸的快原子轰击质谱分析和基因分析确诊的 2 例原发性 4Δ-3-酮类固醇 5β-还原酶缺乏症患者。尿液中存在大量非典型的 3-氧代-Δ4-胆汁酸,提示 4Δ-3-酮类固醇 5β-还原酶缺乏。我们对 2 名患者和 1 名患者的父母外周血淋巴细胞基因组 DNA 进行 AKR1D1 基因所有外显子和相邻内含子序列的测序。一名患者表现为复合杂合突变:c.396C>A 和 c.722A>T,另一名患者则为 c.797G>A 的杂合突变。基于这些突变,可以确诊为原发性 4Δ-3-酮类固醇 5β-还原酶缺乏症。经过熊去氧胆酸治疗和脂溶性维生素补充,两名患者的肝功能迅速恢复正常,肝肿大程度明显减轻。