Gold June-Anne, Mahmoud Ranim, Cassidy Suzanne B, Kimonis Virginia
Division of Genetics and Genomic Medicine, Department of Pediatrics, University of California, Irvine, California.
Division of Genetics and Metabolism, Department of Pediatrics, Loma Linda University, Loma Linda, California.
Am J Med Genet A. 2018 May;176(5):1161-1165. doi: 10.1002/ajmg.a.38679.
Prader-Willi syndrome (PWS) is caused by a deficiency of imprinted genes in the 15q11-q13 region and is characterized by prenatal onset of hypotonia, poor feeding, childhood-onset obesity, hyperphagia, short stature, facial dysmorphism, intellectual disability, and behavioral problems. We studied perinatal factors in a cohort of 64 people with PWS resulting from paternal deletion of 15q11-q13 and maternal uniparental disomy (UPD) for chromosome 15. We recruited 34 individuals with deletion and 30 with UPD. We compared the frequency of multiple prenatal and neonatal factors with the general population as well as between the two genetic subtypes. Of the 64 individuals with PWS, fetal movements were decreased in 82.8%, 31.7% were born prematurely, 42.1% by Cesarean section, and 35.9% required oxytocin induction. Apgar scores were low in 34.6%, 96.8% had feeding difficulty, 50% needed tube feeding, and 6.2% subsequently had gastrostomy tube placement. On comparing findings in the deletion versus the UPD groups, we did not find many significant differences. We, however, found a higher maternal age, and also later age at diagnosis in the UPD versus the deletion group. PWS subjects have higher rates of perinatal complications, especially Cesarean section rate, hypotonia, and low Apgar scores compared to the general population. We did not find many differences between the genetic subtypes, except for later age of diagnosis of the UPD 15 group suggesting a milder phenotype. We also found that the mothers in the UPD were older, supporting the hypothesis that UPD results from nondisjunction associated trisomy rescue.
普拉德-威利综合征(PWS)由15q11-q13区域印迹基因缺陷引起,其特征为产前出现肌张力减退、喂养困难、儿童期起病的肥胖、食欲亢进、身材矮小、面部畸形、智力残疾和行为问题。我们研究了一组64例因父源15q11-q13缺失和母源15号染色体单亲二倍体(UPD)导致的PWS患者的围产期因素。我们招募了34例缺失型个体和30例UPD型个体。我们将多种产前和新生儿因素的发生频率与普通人群进行了比较,也在两种遗传亚型之间进行了比较。在这64例PWS患者中,82.8%的胎儿胎动减少,31.7%早产,42.1%通过剖宫产出生,35.9%需要催产素引产。34.6%的患者阿氏评分低,96.8%有喂养困难,50%需要鼻饲,6.2%随后进行了胃造瘘管置入。比较缺失型与UPD型组的结果时,我们未发现许多显著差异。然而,我们发现UPD型组的母亲年龄较大,诊断年龄也较晚。与普通人群相比,PWS患者围产期并发症发生率更高,尤其是剖宫产率、肌张力减退和低阿氏评分。除了UPD 15组诊断年龄较晚提示表型较轻外,我们在遗传亚型之间未发现许多差异。我们还发现UPD型组的母亲年龄较大,支持UPD由与三体挽救相关的不分离所致这一假说。