Department of Neurology, Rigshospitalet, Copenhagen Neuromuscular Center, University of Copenhagen, Copenhagen, Denmark.
Department of Neurology, Medical University of Vienna, Vienna, Austria.
Hum Mutat. 2022 Sep;43(9):1234-1238. doi: 10.1002/humu.24415. Epub 2022 Jul 16.
Emery-Dreifuss muscular dystrophy (EDMD) is a hereditary muscle disease, characterized by the clinical triade of early-onset joint contractures, progressive muscle weakness, and cardiac involvement. Pathogenic variants in FHL1 can cause a rare X-linked recessive form of EDMD, type 6. We report three men with novel variants in FHL1 leading to EDMD6. The onset of muscle symptoms was in late adulthood and muscle weakness was not prominent in either of the patients. All patients had hypertrophic cardiomyopathy and one of them also had cardiac arrhythmias. Western blot performed on muscle biopsies from two of the patients showed no FHL1 protein expression. We predict that the variant in the third patient also leads to the absence of FHL1 protein. Complete loss of all FHL1 isoforms combined with mild muscle involvement supports the hypothesis that loss of all FHL1 isoforms is more benign than the cytotoxic effects of expressed FHL1 protein with pathogenic missense variants.
先天性肌营养不良症(EDMD)是一种遗传性肌肉疾病,其临床三联征为早发性关节挛缩、进行性肌肉无力和心脏受累。FHL1 中的致病性变异可导致罕见的 X 连锁隐性遗传型 EDMD,即 6 型。我们报道了 3 名男性患者,他们携带导致 EDMD6 的 FHL1 新变异。肌肉症状的发病年龄为成年后期,且两名患者的肌肉无力均不明显。所有患者均患有肥厚型心肌病,其中 1 名患者还患有心律失常。对两名患者的肌肉活检进行的 Western blot 显示,FHL1 蛋白表达缺失。我们预测第三位患者的变异也导致 FHL1 蛋白缺失。所有 FHL1 同工型完全缺失,同时肌肉受累较轻,这支持这样一种假说,即所有 FHL1 同工型的缺失比具有致病性错义变异的表达型 FHL1 蛋白的细胞毒性作用更为良性。