Atypical phenotype of a patient with Bardet-Biedl syndrome type 4.


Journal

Molecular genetics & genomic medicine
ISSN: 2324-9269
Titre abrégé: Mol Genet Genomic Med
Pays: United States
ID NLM: 101603758

Informations de publication

Date de publication:
05 2022
Historique:
revised: 16 06 2021
received: 06 06 2020
accepted: 14 12 2021
pubmed: 24 3 2022
medline: 27 4 2022
entrez: 23 3 2022
Statut: ppublish

Résumé

Bardet-Biedl syndrome (BBS) is a multisystemic disorder characterized by rod-cone dystrophy, truncal obesity, postaxial polydactyly, cognitive impairment, male hypogonadotropic hypogonadism, complex female genitourinary malformations, and renal abnormalities. There is a large clinical and also genetic heterogeneity in BBS. Here, we report a patient with polydactyly, hyperechogenic kidneys increased in size with normal corticomedullary differentiation, anal imperforation, and malformation of genitals with presence of a genital tubercle with ventral urethral meatus associated with two unfused lateral genital swelling and absent urethral folds, in the context of 46, XY karyotype. Karyotype and solo exome sequencing were performed to look for a genetic etiology for the features described in our patient. We identified a homozygous in-frame deletion of exons 4 to 6 in the BBS4 gene (NM-033028 (BBS4-i001): c.[(157-?)_(405 +?)del] p.(Ala53-Trp135del), which is classified as pathogenic variant. This analysis allowed the molecular diagnosis of BBS type 4 in this patient. Complex genital malformations are only reported in female BBS6 patients yet, and genital abnormalities and anal imperforation are not reported in male BBS4 patients to date. We discuss the possible hypotheses for this phenotype, including the phenotypic overlap between ciliopathies.

Sections du résumé

BACKGROUND
Bardet-Biedl syndrome (BBS) is a multisystemic disorder characterized by rod-cone dystrophy, truncal obesity, postaxial polydactyly, cognitive impairment, male hypogonadotropic hypogonadism, complex female genitourinary malformations, and renal abnormalities. There is a large clinical and also genetic heterogeneity in BBS. Here, we report a patient with polydactyly, hyperechogenic kidneys increased in size with normal corticomedullary differentiation, anal imperforation, and malformation of genitals with presence of a genital tubercle with ventral urethral meatus associated with two unfused lateral genital swelling and absent urethral folds, in the context of 46, XY karyotype.
METHODS
Karyotype and solo exome sequencing were performed to look for a genetic etiology for the features described in our patient.
RESULTS
We identified a homozygous in-frame deletion of exons 4 to 6 in the BBS4 gene (NM-033028 (BBS4-i001): c.[(157-?)_(405 +?)del] p.(Ala53-Trp135del), which is classified as pathogenic variant. This analysis allowed the molecular diagnosis of BBS type 4 in this patient.
CONCLUSION
Complex genital malformations are only reported in female BBS6 patients yet, and genital abnormalities and anal imperforation are not reported in male BBS4 patients to date. We discuss the possible hypotheses for this phenotype, including the phenotypic overlap between ciliopathies.

Identifiants

pubmed: 35318824
doi: 10.1002/mgg3.1869
pmc: PMC9034675
doi:

Types de publication

Case Reports Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

e1869

Informations de copyright

© 2022 The Authors. Molecular Genetics & Genomic Medicine published by Wiley Periodicals LLC.

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Auteurs

Natacha Sloboda (N)

Service de Génétique Clinique, CHRU Nancy, Nancy, France.

Laetitia Lambert (L)

Service de Génétique Clinique, CHRU Nancy, Nancy, France.

Viorica Ciorna (V)

Service de Génétique, CHR Metz-Thionville, France.

Ange-Line Bruel (AL)

Laboratoire de génétique, Innovation en diagnostic génomique des maladies rares UF6254, Plate-forme de Biologie Hospitalo-Universitaire, CHU Dijon, Dijon, France.

Frédéric Tran Mau-Them (F)

Laboratoire de génétique, Innovation en diagnostic génomique des maladies rares UF6254, Plate-forme de Biologie Hospitalo-Universitaire, CHU Dijon, Dijon, France.
INSERM U1231, LNC UMR1231 GAD, Université de Bourgogne, Dijon, France.

Vladimir Gomola (V)

Service de Chirurgie Viscérale Infantile, CHRU Nancy, Nancy, France.

Jean-Louis Lemelle (JL)

Service de Chirurgie Viscérale Infantile, CHRU Nancy, Nancy, France.

Olivier Klein (O)

Service de Neurochirurgie Pédiatrique, CHRU Nancy, Nancy, France.

Marie-Christine Camoin-Schweitzer (MC)

Service de néphrologie pédiatrique, dialyse, transplantation rénale, CHRU Nancy, Nancy, France.

Marie Magnavacca (M)

Service de néphrologie pédiatrique, dialyse, transplantation rénale, CHRU Nancy, Nancy, France.

Carole Legagneur (C)

Unité d'Endocrinologie Pédiatrique et Diabétologie, CHRU Nancy, Nancy, France.

Marie-Laure Ezsto (ML)

Service de Gynécologie-Obstétrique, CHR Metz-Thionville, France.

Céline Bonnet (C)

Laboratoire de Génétique, CHRU Nancy, Nancy, France.

Christophe Philippe (C)

Laboratoire de génétique, Innovation en diagnostic génomique des maladies rares UF6254, Plate-forme de Biologie Hospitalo-Universitaire, CHU Dijon, Dijon, France.
INSERM U1231, LNC UMR1231 GAD, Université de Bourgogne, Dijon, France.

Bruno Leheup (B)

Service de Génétique Clinique, CHRU Nancy, Nancy, France.

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