Genotype-phenotype studies in a large cohort of Brazilian patients with Hunter syndrome.
Juliana Alves JosahkianAna Carolina Brusius FacchinAlice Brinckmann Oliveira NettoSandra Leistner-SegalDiana Rojas MálagaMaira Graeff BurinKristiane Michelin-TirelliFranciele Barbosa TrappAugusto César Cardoso Dos SantosErlane Marques RibeiroChong Ae KimAna Cecília Menezes de SiqueiraMara Lucia Schmitz Ferreira SantosDaniel Almeida do ValleRaquel Tavares Boy da SilvaDafne Dain Gandelman HorovitzPaula Frassinetti Vasconcelos de MedeirosCarolina Fischinger Moura de SouzaLiane de Rosso GiulianiDiego Santana Chaves Geraldo MiguelLuiz Carlos Santana da SilvaMarcial Francis GaleraRoberto GiuglianiPublished in: American journal of medical genetics. Part C, Seminars in medical genetics (2021)
Mucopolysaccharidosis type II (MPS II) is an X-linked inherited disease caused by pathogenic variants in the IDS gene, leading to deficiency of the lysosomal enzyme iduronate-2-sulfatase and consequent widespread storage of glycosaminoglycans, leading to several clinical consequences, with progressive manifestations which most times includes cognitive decline. MPS II has wide allelic and clinical heterogeneity and a complex genotype-phenotype correlation. We evaluated data from 501 Brazilian patients diagnosed with MPS II from 1982 to 2020. We genotyped 280 of these patients (55.9%), which were assigned to 206 different families. Point mutations were present in 70% of our patients, being missense variants the most frequent. We correlated the IDS pathogenic variants identified with the phenotype (neuronophatic or non-neuronopathic). Except for two half-brothers, there was no discordance in the genotype-phenotype correlation among family members, nor among MPS II patients from different families with the same single base-pair substitution variant. Mothers were carriers in 82.0% of the cases. This comprehensive study of the molecular profile of the MPS II cases in Brazil sheds light on the genotype-phenotype correlation and helps the better understanding of the disease and the prediction of its clinical course, enabling the provision of a more refined genetic counseling to the affected families.