Department of Paediatric Neurology, University Hospitals Bristol NHS Foundation Trust, 6th Floor Education Centre, Upper Maudlin St, Bristol BS2 8BJ, United Kingdom.
Department of Neuropathology, North Bristol Hospital NHS Foundation Trust, Bristol, United Kingdom.
Neuromuscul Disord. 2020 Feb;30(2):159-164. doi: 10.1016/j.nmd.2019.11.014. Epub 2019 Dec 1.
We describe the presentation and follow-up of a three-year-old girl with nemaline myopathy due to a de-novo variant in ACTA1 (encoding skeletal alpha actin) and moderately low enzyme level of Complex I of the mitochondrial respiratory chain. She presented in the neonatal period with hypotonia, followed by weakness in the facial, bulbar, respiratory and neck flexors muscles. A biopsy of her quadriceps muscle at the age of one year showed nemaline rods. Based on her clinical presentation of a congenital myopathy and histopathological features on a muscle biopsy, ACTA1 was sequenced, and this revealed a novel sequence variant, c.760 A>C p. (Asn254His). In addition, mitochondrial respiratory chain enzymatic activity of skeletal muscle biopsy showed a moderately low activity of complex I (nicotinamide adenine dinucleotide (NADH): ubiquinone oxidoreductase). Disturbances of Complex I of the respiratory chain have been reported in patients with nemaline myopathy, although the mechanism remains unclear.
我们描述了一位三岁女孩的临床表现和随访情况,她患有肌原纤维性肌病,是由 ACTA1(编码骨骼肌α肌动蛋白)中的从头变异和线粒体呼吸链复合物 I 的酶水平中度降低引起的。她在新生儿期表现为肌张力低下,随后出现面部、球部、呼吸和颈部屈肌无力。她在一岁时进行的股四头肌活检显示有杆状肌纤维。根据她先天性肌病的临床表现和肌肉活检的组织病理学特征,对 ACTA1 进行了测序,结果显示了一个新的序列变异,c.760 A>C p.(Asn254His)。此外,骨骼肌活检的线粒体呼吸链酶活性显示复合物 I(烟酰胺腺嘌呤二核苷酸(NADH):泛醌氧化还原酶)的活性中度降低。尽管机制尚不清楚,但已有报道称,在肌原纤维性肌病患者中存在呼吸链复合物 I 的紊乱。