Ridova Nevenka, Trajkova Sanja, Chonevska Biljana, Stojanoski Zlate, Ivanovski Martin, Popova-Labachevska Marija, Stojanovska-Jakimovska Simona, Filipche Venko, Sofijanova Aspazija, Panovska-Stavridis Irina
Faculty of Medicine, Ss. Cyril and Methodius University in Skopje, University Clinic for Hematology, 1000 Skopje, Republic of North Macedonia.
Acibadem Sistina Hospital - Skopje, Department of pediatric Hematology/Oncology, Skupi 5A, 1000 Skopje, Macedonia.
Mol Genet Metab Rep. 2022 Jul 8;32:100895. doi: 10.1016/j.ymgmr.2022.100895. eCollection 2022 Sep.
The majority of Gaucher Disease (GD) cases result from pathologic mutations in the GBA1 gene. A rich mutational spectrum of about 500 identified variants has been recognized. The disease is characterized by phenotypic diversity. Data regarding the genotype-phenotype correlation are scanty and inconclusive. Here, we summarize the genetic and phenotypic "portraits" of 14 patients with GD type 1 in the Republic of North Macedonia, 4 of Macedonian and 10 of Albanian origin. Altogether, 6 variants were detected, compounding 6 different genotypes. All genotypes contained the N370S variant, which was detected with an overall prevalence of 60.7%. Other frequent variants included the 1263del55 deletion and the double mutant allele D409H;H255Q, each with a prevalence of 14.2%. We detected two rare mutations: W92* - a pathogenic nonsense mutation and D399N - a single nucleotide variant of uncertain pathogenicity. The most common genotypes were N370S/1263del55 and H255Q;D409H/N370S, both present in 4/14 patients, followed by N370S homozygosity (3/14). Splenomegaly was the most common clinical manifestation, identified in all patients. Hepatomegaly was less frequent and was present in 50% of cases. Thrombocytopenia was present in 9/14, while half of the patients had anemia. Bone pathology was demonstrated in 8 patients. Patients with different genotypes displayed a high degree of phenotypic heterogeneity, suggesting that the other allele determines the onset and severity of the disease in patients with the N370S mutation. Longer follow-up, bigger cohorts of patients and multicentric studies should be conducted to further define the association between the genotypic and phenotypic expression in GD.
大多数戈谢病(GD)病例是由GBA1基因的病理性突变引起的。已识别出约500种变异的丰富突变谱。该疾病具有表型多样性的特征。关于基因型-表型相关性的数据很少且尚无定论。在此,我们总结了北马其顿共和国14例1型戈谢病患者的遗传和表型“画像”,其中4例为马其顿裔,10例为阿尔巴尼亚裔。共检测到6种变异,构成6种不同的基因型。所有基因型均包含N370S变异,其总体患病率为60.7%。其他常见变异包括1263del55缺失和双突变等位基因D409H;H255Q,每种的患病率均为14.2%。我们检测到两种罕见突变:W92*——一种致病性无义突变和D399N——一种致病性不确定的单核苷酸变异。最常见的基因型是N370S/1263del55和H255Q;D409H/N370S,均在4/14例患者中出现,其次是N370S纯合子(3/14)。脾肿大是最常见的临床表现,在所有患者中均有发现。肝肿大较少见,50%的病例中存在。9/14例患者有血小板减少症,而一半患者有贫血。8例患者有骨骼病变。不同基因型的患者表现出高度的表型异质性,这表明另一个等位基因决定了N370S突变患者疾病的发病和严重程度。应进行更长时间的随访、更大规模的患者队列研究和多中心研究,以进一步明确戈谢病基因型和表型表达之间的关联。