[Nemaline myopathy as a cause of neonatal hypotonia - with emphasis on personal experiences. Report of a family with two brothers affected].

丝状体肌病 先天性肌病 医学 张力减退 星云素 肌张力过低 肌肉活检 肌肉无力 肌病 弱点 病理 内科学 活检 解剖 肌节 心肌细胞 提丁
作者
Agata Bojdo,Ewa Obersztyn,Carina Wallgren‐Pettersson,Vilma‐Lotta Lehtokari,Nigel G. Laing,Mark R. Davis,Zofia Kułakowska
出处
期刊:PubMed 卷期号:13 (1): 5-10 被引量:3
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Nemaline myopathy is a heterogenous form of congenital myopathy characterised by a variable spectrum of clinical features, predominated in the severe form by profound muscle hypotonia and weakness accompanied by respiratory insufficiency. The clinical variability, with differing age of onset and severity of symptoms makes the diagnosis of nemaline myopathy difficult in some cases. Severe forms of nemaline myopathy may be caused by mutation of a number of different genes: skeletal muscle actin (ACTA1), nebulin (NEB) and alpha-tropomyosin (TPM3), all of which encode components of the sarcomeric thin filaments of skeletal muscle. We describe the severe form of nemaline myopathy diagnosed in two brothers who died at the age of 12 days and 9 months, due to respiratory insufficiency caused by severe muscle weakness. Polyhydramnios and weakness of foetal movements in the IIIrd trimester of pregnancy, as well as variable clinical severity were noted in both cases. Microscopically visible significant immaturity of muscle fibers was found in the skeletal muscle biopsy performed in one of the brothers. The diagnosis of nemaline myopathy was confirmed by the presence of nemaline bodies (rods) in sections stained using the Gomori trichrome method. Molecular studies of DNA isolated from blood leucocytes showed no mutation in the ACTA1 or the TPM3 genes. Linkage analysis with polymorphic markers did not rule out linkage to part of the NEB gene locus. Results of the clinical evaluation and the investigations performed in the family members confirm that it is essential to consider congenital myopathies in the differential diagnosis of neonatal and infantile hypotonia with respiratory insufficiency. Molecular verification of the clinical diagnosis is also important for genetic counselling of the families.

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