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Atypical PEX16 peroxisome biogenesis disorder with mild biochemical disruptions and long survival.
Zaabi, Nuha Al; Kendi, Anoud; Al-Jasmi, Fatma; Takashima, Shigeo; Shimozawa, Nobuyuki; Al-Dirbashi, Osama Y.
Afiliación
  • Zaabi NA; Departments of Pediatrics, College of Medicine and Health Sciences, United Arab Emirates University, Al-Ain, United Arab Emirates; Departments of Pediatrics, Tawam Hospital, Al-Ain, United Arab Emirates.
  • Kendi A; Departments of Pediatrics, Tawam Hospital, Al-Ain, United Arab Emirates.
  • Al-Jasmi F; Departments of Pediatrics, College of Medicine and Health Sciences, United Arab Emirates University, Al-Ain, United Arab Emirates; Departments of Pediatrics, Tawam Hospital, Al-Ain, United Arab Emirates.
  • Takashima S; Division of Genomics Research, Life Science Research Center, Gifu University, Japan.
  • Shimozawa N; Division of Genomics Research, Life Science Research Center, Gifu University, Japan.
  • Al-Dirbashi OY; Departments of Pediatrics, College of Medicine and Health Sciences, United Arab Emirates University, Al-Ain, United Arab Emirates; Research Institute, Children's Hospital of Eastern Ontario, Ottawa, Ontario K1H 5B2, Canada. Electronic address: dirbashios@uaeu.ac.ae.
Brain Dev ; 41(1): 57-65, 2019 Jan.
Article en En | MEDLINE | ID: mdl-30078639
BACKGROUND: Mutations in PEX16 cause peroxisome biogenesis disorder (PBD). Zellweger syndrome characterized by neurological dysfunction, dysmorphic features, liver disease and early death represents the severe end of this clinical spectrum. Here we discuss the diagnostic challenge of atypical PEX16 related PBD in 3 patients from highly inbred kindred and describe the role of specific metabolites analyses, fibroblasts studies, whole-exome sequencing (WES) and metabolomics profiling to establish the diagnosis. METHODS AND PATIENTS: The proband is a 12-year-old male born to consanguineous parents. Despite normal development in the first year, regression and progressive spastic diplegia, poor coordination and dysarthria occurred thereafter. Patient 2 (3-year old female) and Patient 3 (19-month old female) shared similar clinical course with the proband. Biochemical studies on plasma and fibroblasts, WES and global metabolomics analyses were performed. RESULTS: Very-long-chain fatty acids analysis showed subtle elevations in C26 and C26/C22. Global Metabolomics-Assisted Pathway profiling was not remarkable. Immunocytochemical investigations on fibroblasts revealed fewer catalase and PMP70-containing particles indicating aberrant peroxisomal assembly. Complementation studies were inconclusive. WES revealed a novel homozygous variant in PEX16 (c.859C>T). The biochemical profiles of Patient 2 and Patient 3 were similar to the proband and the same genotype was confirmed. CONCLUSION: This paper highlights the diagnostic challenge of PEX16 patients due to the widely variable clinical and biochemical phenotypes. It also emphasizes the important roles of combined biochemical assays with next generation sequencing techniques in reaching diagnosis in the context of atypical clinical presentations, subtle biomarker abnormalities and consanguinity.
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Trastorno Peroxisomal / Proteínas de la Membrana Tipo de estudio: Diagnostic_studies Límite: Child / Child, preschool / Female / Humans / Infant / Male Idioma: En Revista: Brain Dev Año: 2019 Tipo del documento: Article País de afiliación: Emiratos Árabes Unidos Pais de publicación: Países Bajos

Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Trastorno Peroxisomal / Proteínas de la Membrana Tipo de estudio: Diagnostic_studies Límite: Child / Child, preschool / Female / Humans / Infant / Male Idioma: En Revista: Brain Dev Año: 2019 Tipo del documento: Article País de afiliación: Emiratos Árabes Unidos Pais de publicación: Países Bajos