Clinical, biochemical, and molecular overview of transaldolase deficiency and evaluation of the endocrine function: Update of 34 patients.


Journal

Journal of inherited metabolic disease
ISSN: 1573-2665
Titre abrégé: J Inherit Metab Dis
Pays: United States
ID NLM: 7910918

Informations de publication

Date de publication:
01 2019
Historique:
entrez: 12 2 2019
pubmed: 12 2 2019
medline: 2 4 2020
Statut: ppublish

Résumé

Transaldolase deficiency (TALDO-D) is a rare autosomal recessive inborn error of the pentose phosphate pathway. Since its first description in 2001, several case reports have been published, but there has been no comprehensive overview of phenotype, genotype, and phenotype-genotype correlation. We performed a retrospective questionnaire and literature study of clinical, biochemical, and molecular data of 34 patients from 25 families with proven TALDO-D. In some patients, endocrine abnormalities have been found. To further evaluate these abnormalities, we performed biochemical investigations on blood of 14 patients. Most patients (n = 22) had an early-onset presentation (prenatally or before 1 month of age); 12 patients had a late-onset presentation (3 months to 9 years). Main presenting symptoms were intrauterine growth restriction, dysmorphic facial features, congenital heart disease, anemia, thrombocytopenia, and hepato(spleno)megaly. An older sib of two affected patients was asymptomatic until the age of 9 years, and only after molecular diagnosis was hepatomegaly noted. In some patients, there was gonadal dysfunction with low levels of testosterone and secondary luteinizing hormone (LH) and follicle-stimulating hormone (FSH) abnormalities later in life. This overview provides information that can be helpful for managing patients and counseling families regarding prognosis. Diagnostic guidelines, possible genotype-phenotype correlations, treatment options, and pathophysiological disease mechanisms are proposed.

Sections du résumé

BACKGROUND
Transaldolase deficiency (TALDO-D) is a rare autosomal recessive inborn error of the pentose phosphate pathway. Since its first description in 2001, several case reports have been published, but there has been no comprehensive overview of phenotype, genotype, and phenotype-genotype correlation.
METHODS
We performed a retrospective questionnaire and literature study of clinical, biochemical, and molecular data of 34 patients from 25 families with proven TALDO-D. In some patients, endocrine abnormalities have been found. To further evaluate these abnormalities, we performed biochemical investigations on blood of 14 patients.
RESULTS AND CONCLUSIONS
Most patients (n = 22) had an early-onset presentation (prenatally or before 1 month of age); 12 patients had a late-onset presentation (3 months to 9 years). Main presenting symptoms were intrauterine growth restriction, dysmorphic facial features, congenital heart disease, anemia, thrombocytopenia, and hepato(spleno)megaly. An older sib of two affected patients was asymptomatic until the age of 9 years, and only after molecular diagnosis was hepatomegaly noted. In some patients, there was gonadal dysfunction with low levels of testosterone and secondary luteinizing hormone (LH) and follicle-stimulating hormone (FSH) abnormalities later in life. This overview provides information that can be helpful for managing patients and counseling families regarding prognosis. Diagnostic guidelines, possible genotype-phenotype correlations, treatment options, and pathophysiological disease mechanisms are proposed.

Identifiants

pubmed: 30740741
doi: 10.1002/jimd.12036
doi:

Substances chimiques

Hormones 0
Transaldolase EC 2.2.1.2

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

147-158

Informations de copyright

© 2018 The Authors. Journal of Inherited Metabolic Disease published by John Wiley & Sons Ltd on behalf of SSIEM.

Auteurs

Monique Williams (M)

Metabolic Laboratory, Department of Clinical Chemistry, Amsterdam Neuroscience, VU University Medical Center, Amsterdam, The Netherlands.

Vassili Valayannopoulos (V)

Sanofi Genzyme, Cambridge, Massachusetts, USA.
Reference Center for Inherited Metabolic Disease, Institut IMAGINE, Hopital Universitaire Necker - Enfants Malades, Paris, France.

Ruqaiah Altassan (R)

King Abdulaziz Medical City-Riyadh, National Guard Health Affairs, King Abdullah International Medical Research Center (KAIMRC), King Saud Bin Abdulaziz University for Health Sciences, Riyadh, Saudi Arabia.

Wendy K Chung (WK)

Departments of Pediatrics and Medicine, Columbia University, New York, New York, USA.

Annemieke C Heijboer (AC)

Endocrine Laboratory, Department of Clinical Chemistry, VU University Medical Center, Amsterdam, The Netherlands.
Laboratory of Endocrinology, Academic Medical Center, Amsterdam, the Netherlands.

Wei Teik Keng (WT)

Genetic Department, Hospital Kuala Lumpur, Kuala Lumpur, Malaysia.

Risto Lapatto (R)

Children's Hospital, University of Helsinki and Helsinki University Central Hospital, Helsinki, Finland.

Patricia McClean (P)

Children's Liver Unit, Leeds Teaching Hospitals NHS Trust, Leeds, UK.

Margot F Mulder (MF)

Department of Pediatrics, VU University Medical Center, Amsterdam, The Netherlands.

Anna Tylki-Szymańska (A)

Department of Pediatric, Nutrition and Metabolic Disease, The Children's Memorial Health Institute, Warsaw, Poland.

Marie-Jose E Walenkamp (ME)

Department of Pediatrics, VU University Medical Center, Amsterdam, The Netherlands.

Majid Alfadhel (M)

King Abdulaziz Medical City-Riyadh, National Guard Health Affairs, King Abdullah International Medical Research Center (KAIMRC), King Saud Bin Abdulaziz University for Health Sciences, Riyadh, Saudi Arabia.

Hajar Alakeel (H)

King Abdulaziz Medical City-Riyadh, National Guard Health Affairs, King Abdullah International Medical Research Center (KAIMRC), King Saud Bin Abdulaziz University for Health Sciences, Riyadh, Saudi Arabia.

Gajja S Salomons (GS)

Metabolic Laboratory, Department of Clinical Chemistry, Amsterdam Neuroscience, VU University Medical Center, Amsterdam, The Netherlands.

Wafaa Eyaid (W)

King Abdulaziz Medical City-Riyadh, National Guard Health Affairs, King Abdullah International Medical Research Center (KAIMRC), King Saud Bin Abdulaziz University for Health Sciences, Riyadh, Saudi Arabia.

Mirjam M C Wamelink (MMC)

Metabolic Laboratory, Department of Clinical Chemistry, Amsterdam Neuroscience, VU University Medical Center, Amsterdam, The Netherlands.

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Classifications MeSH