Reichmann H, Schalke B, Seibel P, Naumann M, Toyka K
Department of Neurology, University of Würzburg, Germany.
Neuromuscul Disord. 1995 Jul;5(4):277-83. doi: 10.1016/0960-8966(94)00060-m.
We report on a 33-yr-old female patient with myalgia, CK values up to 3500 Ul-1 and proximal weakness. An initial muscle biopsy showed myositis. One year later an enlarged lymph node was investigated and sarcoidosis diagnosed. In a second muscle biopsy inflammatory cells and morphological characteristics of mitochondrial myopathy were found. Biochemical analyses indicated a 50% reduction in complex II activity of the respiratory chain. Due to failure in clinical improvement a third muscle biopsy was performed in 1990 where only 19% of normal complex II activity was present. Southern blot analysis of the mitochondrial genome was normal. Thus for the first time we describe a patient with sarcoid myopathy and a complex II deficiency. Our interpretation is that a pre-existing complex II defect became clinically relevant because of additional sarcoid myopathy.
我们报告了一名33岁女性患者,她患有肌痛,肌酸激酶(CK)值高达3500 U/L-1且近端肌无力。最初的肌肉活检显示为肌炎。一年后,对一个肿大的淋巴结进行检查并诊断为结节病。在第二次肌肉活检中发现了炎症细胞和线粒体肌病的形态学特征。生化分析表明呼吸链复合体II活性降低了50%。由于临床症状未改善,1990年进行了第三次肌肉活检,此时复合体II活性仅为正常水平的19%。线粒体基因组的Southern印迹分析结果正常。因此,我们首次描述了一名患有结节病性肌病和复合体II缺陷的患者。我们的解释是,由于额外的结节病性肌病,先前存在的复合体II缺陷变得具有临床相关性。