| Literature DB >> 29383513 |
Eduardo de Paula Estephan1, Cláudia Ferreira da Rosa Sobreira2, André Clériston José Dos Santos2, Pedro José Tomaselli2, Wilson Marques2, Roberta Paiva Magalhães Ortega3, Marcela Câmara Machado Costa4, André Macedo Serafim da Silva1, Rodrigo Holanda Mendonça1, Vitor Marques Caldas1, Antonio Alberto Zambon1, Osório Abath Neto1, Paulo Eurípedes Marchiori1, Carlos Otto Heise1, Umbertina Conti Reed1, Yoshiteru Azuma5, Ana Töpf5, Hanns Lochmüller5, Edmar Zanoteli6.
Abstract
The most common causes of congenital myasthenic syndromes (CMS) are CHRNE mutations, and some pathogenic allelic variants in this gene are especially frequent in certain ethnic groups. In the southern region of Brazil, a study found the c.130dupG CHRNE mutation in up to 33% of families with CMS. Here, we aimed to verify the frequency of this mutation among individuals with CMS in a larger cohort of CMS patients from different areas of Brazil and to characterize clinical features of these patients. Eighty-four patients with CMS, from 72 families, were clinically evaluated and submitted to direct sequencing of the exon 2 of CHRNE. The c.130dupG mutation was found in 32 patients (23 families), with 26 patients (19 families, 26.3%) in homozygosis, confirming its high prevalence in different regions of Brazil. Among the homozygous patients, the following characteristics were frequent: onset of symptoms before 2 years of age (92.3%), little functional restriction (92.3%), fluctuating symptoms (100%), ocular muscle impairment (96.1%), ptosis (100%), limb weakness (88.4%), response to pyridostigmine (100%), facial involvement (77%), and bulbar symptoms (70.8%). The pretest probability of finding at least one allele harbouring the c.130dupG mutation was 38.1%. Selecting only patients with impaired eye movement together with limb weakness and improvement with pyridostigmine, the probability increases to 72.2%. This clinical pre-selection of patients is likely a useful tool for regions where CHRNE mutations have a founder effect. In conclusion, the CHRNE mutation c.130dupG leads to fairly benign natural course of the disease with relative homogeneity.Entities:
Keywords: Acetylcholine receptor; CHRNE; Congenital myasthenic syndrome; Neuromuscular junction; Pyridostigmine
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Year: 2018 PMID: 29383513 PMCID: PMC7115868 DOI: 10.1007/s00415-018-8736-8
Source DB: PubMed Journal: J Neurol ISSN: 0340-5354 Impact factor: 4.849