Marczak-Hałupka Anna, Kalina Maria A, Tańska Anna, Chrzanowska Krystyna H
Department of Infants and Newborn Pathology, Paediatric Centre, Sosnowiec, Poland.
Katedra i Klinika Pediatrii, Endokrynologii i Diabetologii Dziecięcej, Śląski Uniwersytet Medyczny, Katowice, Polska.
Pediatr Endocrinol Diabetes Metab. 2015;20(3):101-6. doi: 10.18544/PEDM-20.03.0009.
Silver-Russell syndrome (SRS) is a rare, clinically and genetically heterogeneous entity, caused by (epi)genetic alternations. It is characterized by prenatal and postnatal growth retardation, relative macrocephaly, the triangular face and body asymmetry. About 40-60% of cases are caused by hypomethylation of 11p.15.5 Imprinting Centre Region 1 (ICR1) on the paternal chromosome, and maternal uniparental disomy for chromosome 7 (UPD(7)mat) is found in 5-10% of cases. There are suggested correlations between genotype and the phenotype. Psychomotor development may be delayed, usually mildly, with school difficulties and speech delay more common in patients with UPD(7)mat. Children with 11p15 hypomethylation are shorter and lighter at birth in comparison to children with UPD(7)mat, however further deceleration tends to be more apparent in the latter group. The onset of puberty tends to occur early, with acceleration of bone age, resulting in less apparent growth spurt. Failure to thrive and feeding problems are characteristic for the infant period, and further development of a child may be conditioned by additional congenital defects.
Silver-Russell综合征(SRS)是一种罕见的、临床和基因异质性疾病,由(表观)遗传改变引起。其特征为产前和产后生长发育迟缓、相对巨头畸形、三角形脸和身体不对称。约40%-60%的病例由父源染色体11p.15.5印记中心区域1(ICR1)低甲基化引起,5%-10%的病例存在母源7号染色体单亲二体(UPD(7)mat)。基因型与表型之间存在相关性。精神运动发育可能延迟,通常为轻度延迟,在UPD(7)mat患者中上学困难和语言延迟更为常见。与UPD(7)mat儿童相比,11p15低甲基化儿童出生时更矮小、体重更轻,然而,后一组的进一步生长减速往往更明显。青春期往往提前开始,骨龄加速,导致生长突增不明显。生长发育不良和喂养问题是婴儿期的特征,儿童的进一步发育可能受其他先天性缺陷影响。