Bruno Claudio, Cassandrini Denise, Martinuzzi Andrea, Toscano Antonio, Moggio Maurizio, Morandi Lucia, Servidei Serena, Mongini Tiziana, Angelini Corrado, Musumeci Olimpia, Comi Giacomo P, Lamperti Costanza, Filosto Massimiliano, Zara Federico, Minetti Carlo
Neuromuscular Disease Unit, Department of Pediatrics, University of Genova, Giannina Gaslini Institute, Genova, Italy.
Hum Mutat. 2006 Jul;27(7):718. doi: 10.1002/humu.9434.
Deficiency of the muscle isozyme of glycogen phosphorylase is causative of McArdle disease or Glycogen storage disease type V (GSD-V), the most common autosomal recessive disorder of glycogen metabolism. The typical clinical presentation is characterized by exercise intolerance with cramps, and recurrent myoglobinuria. To date, 46 mutations in the PYGM gene have been detected in GSD-V patients. We report the mutational spectrum in 68 Italian patients. We identified 30 different mutations in the PYGM gene, including 19 mutations that have not been reported previously. The novel mutations include: eight missense mutations (c.475G>A, p.G159R; c.689C>G, p.P230R; c.1094C>T, p.A365E; c.1151C>A, p.A384D; c.1182C>T, p.R428C; c.1471C>T, p.R491C; c.2444A>C, p.D815A; c.2477G>C, p.W826S), two nonsense mutations (c.1475G>A, p.W492X; c.1627A>T, p.K543X), five splice site mutations (c.855 +1G>C; c.1092 +1G>A; c. 1093-1G>T; c.1239 +1G>A; c.2380 +1G>A), and four deletions (c.715_717delGTC, p.V239del; c.304delA, p.N102DfsX4; c.1970_2177del, p.V657_G726; c.2113_2114delGG, p.G705RfsX16). Whereas we confirmed lack of direct correlation between the clinical phenotype and the genotype, we also found that the so-called 'common mutation' (p.R50X) accounted for about 43% of alleles in our cohort and that no population-related mutations are clearly identified in Italian patients.
糖原磷酸化酶肌肉同工酶缺乏是麦卡德尔病或糖原贮积病V型(GSD-V)的病因,这是糖原代谢最常见的常染色体隐性疾病。典型的临床表现为运动不耐受伴痉挛和复发性肌红蛋白尿。迄今为止,在GSD-V患者中已检测到PYGM基因的46种突变。我们报告了68例意大利患者的突变谱。我们在PYGM基因中鉴定出30种不同的突变,包括19种以前未报告过的突变。新突变包括:8种错义突变(c.475G>A,p.G159R;c.689C>G,p.P230R;c.1094C>T,p.A365E;c.1151C>A,p.A384D;c.1182C>T,p.R428C;c.1471C>T,p.R491C;c.2444A>C,p.D815A;c.2477G>C,p.W826S),2种无义突变(c.1475G>A,p.W492X;c.1627A>T,p.K543X),5种剪接位点突变(c.855 +1G>C;c.1092 +1G>A;c. 1093-1G>T;c.1239 +1G>A;c.2380 +1G>A),以及4种缺失(c.715_717delGTC,p.V239del;c.304delA,p.N102DfsX4;c.1970_2177del,p.V657_G726;c.2113_2114delGG,p.G705RfsX16)。虽然我们证实临床表型与基因型之间缺乏直接相关性,但我们也发现所谓的“常见突变”(p.R50X)在我们的队列中约占43%的等位基因,并且在意大利患者中未明确鉴定出与人群相关的突变。