Homozygous pArg610del Mutation Unusually Associated With Severe Delay of Growth in 2 Acid Sphingomyelinase Deficiency-affected Sibs.


Journal

Journal of pediatric hematology/oncology
ISSN: 1536-3678
Titre abrégé: J Pediatr Hematol Oncol
Pays: United States
ID NLM: 9505928

Informations de publication

Date de publication:
08 2020
Historique:
pubmed: 15 3 2019
medline: 1 1 2021
entrez: 15 3 2019
Statut: ppublish

Résumé

Typically, patients with Acid Sphingomyelinase Deficiency (ASMD) because of p.Arg610del mutation, have mild phenotype with normal linear growth. We reported the case of 2 Tunisian brothers who have been referred for splenomegaly, polyadenopathies, pubertal, and growth delay. Molecular testing of SMPD1 gene revealed the presence of a homozygous p.Arg610del mutation. Lysosphingomyelin and its isoform-509 were both increased confirming ASMD for both cases. Growth hormone deficiency was highly suspected but growth hormone response after stimulating tests was acceptable for both patients. There is no correlation between phenotype-genotype in case of p.Arg610del mutation that could be associated to a severe delay of growth.

Sections du résumé

BACKGROUND
Typically, patients with Acid Sphingomyelinase Deficiency (ASMD) because of p.Arg610del mutation, have mild phenotype with normal linear growth.
OBSERVATION
We reported the case of 2 Tunisian brothers who have been referred for splenomegaly, polyadenopathies, pubertal, and growth delay. Molecular testing of SMPD1 gene revealed the presence of a homozygous p.Arg610del mutation. Lysosphingomyelin and its isoform-509 were both increased confirming ASMD for both cases. Growth hormone deficiency was highly suspected but growth hormone response after stimulating tests was acceptable for both patients.
CONCLUSIONS
There is no correlation between phenotype-genotype in case of p.Arg610del mutation that could be associated to a severe delay of growth.

Identifiants

pubmed: 30870388
doi: 10.1097/MPH.0000000000001447
pii: 00043426-202008000-00034
doi:

Substances chimiques

Sphingomyelin Phosphodiesterase EC 3.1.4.12

Types de publication

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

Langues

eng

Sous-ensembles de citation

IM

Pagination

e499-e502

Références

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Auteurs

Manel Naifar (M)

Biochemistry Laboratory, Habib Bourguiba Hospital and UR12ES17 Sfax Medicine School.

Faten Kallel (F)

Department of Hematology, Hedi Chaker Hospital.

Faten HadjKacem (F)

Endocrine Department, Hedi Chaker Hospital.

Hela Boudabous (H)

Pediatric Department, La Rabta Hospital.

Rim Kallel (R)

Pathological Laboratory, Habib Bourguiba Hospital, Sfax.

Tahia Boudawara (T)

Pathological Laboratory, Habib Bourguiba Hospital, Sfax.

Olfa Messaoud (O)

Biomedical Genomics and Oncogenetics Laboratory, Institut Pasteur de Tunis, University Tunis El Manar, Tunis, Tunisia.

Neji Tbib (N)

Pediatric Department, La Rabta Hospital.

Nadia Charfi (N)

Endocrine Department, Hedi Chaker Hospital.

Mohamed Abid (M)

Endocrine Department, Hedi Chaker Hospital.

Roseline Froissart (R)

Service de Biochimie et Biologie Moléculaire Grand Est, Unité Médicale Pathologies Métaboliques, Erythrocytaires et Dépistage Périnatal, Centre de Biologie et de Pathologie Est, Hospices Civils de Lyon, Bron, France.

Sondes Hdiji Messedi (SH)

Department of Hematology, Hedi Chaker Hospital.

Fatma Ayedi (F)

Biochemistry Laboratory, Habib Bourguiba Hospital and UR12ES17 Sfax Medicine School.

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