Havali Cengiz, Dorum Sevil, Akbaş Yılmaz, Görükmez Orhan, Hirfanoglu Tugba
Bursa Yuksek İhtisas Training and Research Hospital, Department of Pediatrics, Division of Neurology, Yıldırım/Bursa 16310, Turkey.
Department of Pediatrics, Division of Neurology, Bursa Yuksek İhtisas Training and Research Hospital, Bursa, Turkey.
J Pediatr Endocrinol Metab. 2020 Mar 26;33(3):437-441. doi: 10.1515/jpem-2019-0194.
Background Peroxisomal biogenesis disorders (PBDs) include a miscellaneous group of diseases which cause serious multisystem disease. Mutations of 13 different PEX genes lead to PBDs including Zellweger syndrome (ZS). Different types of mutations of PEX1 and PEX10 genes are correlated with broad-range phenotypes of PBDs. Case presentation Patient 1 is a 4-month-old boy who was affected by myoclonic seizures, poor oral feeding since birth. The patient was hypotonic and had hepatosplenomegaly. Patient 2 is a 2-month-old boy who presented with decreased movement, severe hypotonia and failure to thrive. The laboratory studies of the patients revealed increased plasma very-long-chain fatty acids (VLCFAs). The genetic analyses of patient 1 demonstrated the first homozygous missense mutation in the PEX10 gene. A novel homozygous missense mutation was found in the PEX1 gene in patient 2. Conclusions This report highlights that the detected homozygous missense mutations of PEX10 and PEX1 genes and the substitutions of specific amino acids lead to the severe form of PBDs.
背景 过氧化物酶体生物发生障碍(PBDs)包括一组导致严重多系统疾病的杂合性疾病。13种不同的PEX基因突变会导致PBDs,包括泽尔韦格综合征(ZS)。PEX1和PEX10基因的不同类型突变与PBDs的广泛表型相关。病例报告 患者1是一名4个月大的男孩,自出生以来受肌阵挛性癫痫发作、经口喂养困难影响。该患者肌张力减退且有肝脾肿大。患者2是一名2个月大的男孩,表现为活动减少、严重肌张力减退和发育不良。患者的实验室检查显示血浆极长链脂肪酸(VLCFAs)升高。患者1的基因分析显示PEX10基因中首次出现纯合错义突变。在患者2的PEX1基因中发现了一种新的纯合错义突变。结论 本报告强调,检测到的PEX10和PEX1基因纯合错义突变以及特定氨基酸的替代导致了严重形式的PBDs。