A 3-Year-Old Boy with an Xp21 Deletion Syndrome: A Case Report.

Contiguous deletion syndromes adrenal insufficiency chromosome xp21 deletion syndrome complex glycerol kinase deficiency hypoaldosteronism next generation sequencing

Journal

Endocrine, metabolic & immune disorders drug targets
ISSN: 2212-3873
Titre abrégé: Endocr Metab Immune Disord Drug Targets
Pays: United Arab Emirates
ID NLM: 101269157

Informations de publication

Date de publication:
2022
Historique:
received: 05 09 2021
revised: 08 11 2021
accepted: 01 12 2021
pubmed: 3 2 2022
medline: 31 8 2022
entrez: 2 2 2022
Statut: ppublish

Résumé

Chromosome Xp21 deletion syndrome is a rare X-linked recessive defect that occurs as a result of multiple gene deletions, including Glycerol kinase (GK) and its neighboring genes, dystrophin, which causes Duchenne muscular dystrophy (DMD), and NR0B1, which causes congenital adrenal hypoplasia (CAHhttps://www.omim.org/entry/300200). Patients usually present with glycerol kinase deficiency, congenital adrenal hypoplasia, Duchenne muscular dystrophy, hyperglycerolemia, and glyceroluria, associated with DMD and/or CAH, growth failure, myopathy, osteoporosis, mental retardation, and psychomotor retardation. Herein, we report a 3-year- old boy from Iraq who had bloody diarrhea, food intolerance and abdominal cramp, adrenal insufficiency, recurrent fevers, tuberculosis (TB) infection, cervical abscess, oral thrush, cervical and mediastinal lymphadenopathies, developmental delay, and undescended testis. His parents are non-consanguine and had no family history of diseases. Next generation sequencing demonstrated a hemizygote deletion in chromosome X. Loss of a large part of the X-chromosome most likely can explain the clinical findings of this patient. Contiguous gene deletion syndrome in Xp21 should be considered after diagnosing adrenal insufficiency to treat metabolic complications efficiently.

Sections du résumé

BACKGROUND BACKGROUND
Chromosome Xp21 deletion syndrome is a rare X-linked recessive defect that occurs as a result of multiple gene deletions, including Glycerol kinase (GK) and its neighboring genes, dystrophin, which causes Duchenne muscular dystrophy (DMD), and NR0B1, which causes congenital adrenal hypoplasia (CAHhttps://www.omim.org/entry/300200). Patients usually present with glycerol kinase deficiency, congenital adrenal hypoplasia, Duchenne muscular dystrophy, hyperglycerolemia, and glyceroluria, associated with DMD and/or CAH, growth failure, myopathy, osteoporosis, mental retardation, and psychomotor retardation.
CASE PRESENTATION METHODS
Herein, we report a 3-year- old boy from Iraq who had bloody diarrhea, food intolerance and abdominal cramp, adrenal insufficiency, recurrent fevers, tuberculosis (TB) infection, cervical abscess, oral thrush, cervical and mediastinal lymphadenopathies, developmental delay, and undescended testis. His parents are non-consanguine and had no family history of diseases. Next generation sequencing demonstrated a hemizygote deletion in chromosome X.
CONCLUSION CONCLUSIONS
Loss of a large part of the X-chromosome most likely can explain the clinical findings of this patient. Contiguous gene deletion syndrome in Xp21 should be considered after diagnosing adrenal insufficiency to treat metabolic complications efficiently.

Identifiants

pubmed: 35105298
pii: EMIDDT-EPUB-120607
doi: 10.2174/1871530322666220201143656
doi:

Substances chimiques

Glycerol Kinase EC 2.7.1.30

Types de publication

Case Reports

Langues

eng

Sous-ensembles de citation

IM

Pagination

881-887

Informations de copyright

Copyright© Bentham Science Publishers; For any queries, please email at epub@benthamscience.net.

Auteurs

Shaghayegh Sadeghmousavi (S)

School of Medicine, Shahid Beheshti University of Medical Sciences, Tehran, Iran.
Medical Genetics Network (MeGeNe), Universal Scientific Education and Research Network (USERN), Tehran, Iran.

Sepideh Shahkarami (S)

Department of Pediatrics, Dr. von Hauner Children\'s Hospital, University Hospital, Ludwig-Maximilians-Universität München (LMU), Munich, Germany.
Research Center for Immunodeficiencies, Children's Medical Center, Tehran University of Medical Sciences, Tehran, Iran.

Elham Rayzan (E)

Research Center for Immunodeficiencies, Children's Medical Center, Tehran University of Medical Sciences, Tehran, Iran.
International Hematology/Oncology of Pediatric Experts (IHOPE), Universal Scientific Education and Research Network (USERN), Tehran, Iran.

Souran Ahmed (S)

Kurdistan Pediatric Society, Department of Medicine, University of Sulaimani, Sulaimani, Iraq.

Farzaneh Hosseini Gharalari (FH)

Department of Pathology, School of Medicine, Urmia University of Medical Sciences, Urmia, Iran.

Meino Rohlfs (M)

Department of Pediatrics, Dr. von Hauner Children\'s Hospital, University Hospital, Ludwig-Maximilians-Universität München (LMU), Munich, Germany.

Christoph Klein (C)

Department of Pediatrics, Dr. von Hauner Children\'s Hospital, University Hospital, Ludwig-Maximilians-Universität München (LMU), Munich, Germany.

Nima Rezaei (N)

Research Center for Immunodeficiencies, Children's Medical Center, Tehran University of Medical Sciences, Tehran, Iran.
Network of Immunity in Infection, Malignancy and Autoimmunity (NIIMA), Universal Scientific Education and Research Network (USERN), Tehran, Iran.

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Classifications MeSH