Lee Eun-Ha, Ahn Mi-Sun, Hwang Jin-Soon, Ryu Kyung-Hwa, Kim Sun-Jun, Kim Sung-Hwan
Department of Pediatrics and Research Laboratory for Human Mitochondrial Disorders, Ajou University School of Medicine, Suwon, Korea.
J Korean Med Sci. 2006 Oct;21(5):800-4. doi: 10.3346/jkms.2006.21.5.800.
Pyruvate dehydrogenase complex (PDHC) deficiency is mostly due to mutations in the X-linked E1alpha subunit gene (PDHA1). Some of the patients with PDHC deficiency showed clinical improvements with thiamine treatment. We report the results of biochemical and molecular analysis in a female patient with lactic acidemia. The PDHC activity was assayed at different concentrations of thiamine pyrophosphate (TPP). The PDHC activity showed null activity at low TPP concentration (1 x 10(-3) mM), but significantly increased at a high TPP concentration (1 mM). Sequencing analysis of PDHA1 gene of the patient revealed a substitution of cysteine for tyrosine at position 161 (Y161C). Thiamine treatment resulted in reduction of the patient's serum lactate concentration and dramatic clinical improvement. Biochemical, molecular, and clinical data suggest that this patient has a thiamine-responsive PDHC deficiency due to a novel mutation, Y161C. Therefore, to detect the thiamine responsiveness it is necessary to measure activities of PDHC not only at high but also at low concentration of TPP.
丙酮酸脱氢酶复合体(PDHC)缺乏症主要归因于X连锁E1α亚基基因(PDHA1)的突变。一些PDHC缺乏症患者经硫胺素治疗后临床症状有所改善。我们报告了一名患有乳酸性血症女性患者的生化和分子分析结果。在不同浓度的硫胺素焦磷酸(TPP)下测定了PDHC活性。在低TPP浓度(1×10⁻³ mM)时,PDHC活性显示为零,但在高TPP浓度(1 mM)时显著增加。对该患者的PDHA1基因进行测序分析发现,第161位的酪氨酸被半胱氨酸取代(Y161C)。硫胺素治疗使患者血清乳酸浓度降低,临床症状显著改善。生化、分子和临床数据表明,该患者由于一种新的突变Y161C而患有硫胺素反应性PDHC缺乏症。因此,为了检测硫胺素反应性,不仅需要在高浓度TPP下,还需要在低浓度TPP下测量PDHC的活性。