Adenosine deaminase 2 deficiency with a novel variant of CECR1 gene mutation: Responding to tumor necrosis factor antagonist therapy

Deficiency of Adenosine deaminase 2 (DADA2) syndrome is a chronic, systemic, and inflammatory disorder, characterized by early-onset recurrent strokes, fever, livedo reticularis, and immunodeficiency. We report the case of a 4-year-old child, a product of consanguineous marriage, who presented with...

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Main Authors: Zakiya Saleh Al Mosawi, Hiba Omar Abduljawad, Maryam Yusuf Busehail, Barrak Mahmood Al Moosawi
Format: Article
Language:English
Published: SAGE Publishing 2019-01-01
Series:Indian Journal of Rheumatology
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Online Access:http://www.indianjrheumatol.com/article.asp?issn=0973-3698;year=2019;volume=14;issue=3;spage=236;epage=240;aulast=Al
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author Zakiya Saleh Al Mosawi
Hiba Omar Abduljawad
Maryam Yusuf Busehail
Barrak Mahmood Al Moosawi
author_facet Zakiya Saleh Al Mosawi
Hiba Omar Abduljawad
Maryam Yusuf Busehail
Barrak Mahmood Al Moosawi
author_sort Zakiya Saleh Al Mosawi
collection DOAJ
description Deficiency of Adenosine deaminase 2 (DADA2) syndrome is a chronic, systemic, and inflammatory disorder, characterized by early-onset recurrent strokes, fever, livedo reticularis, and immunodeficiency. We report the case of a 4-year-old child, a product of consanguineous marriage, who presented with three episodes of hemiparesis within 1 year. She also manifested skin discoloration in the form of livedo reticularis. Workup with magnetic resonance imaging (MRI) of the brain revealed acute infarction in the right aspect of the cerebral peduncle and chronic lacunars infarct in the right thalamus with diffusion restriction. Repeated MRI after 5 months revealed diffuse loss of brain volume. The blood workup showed high inflammatory markers and significantly low adenosine deaminase 2 (ADA2) level. After being on corticosteroid and anticoagulant treatments, she suffered from a recurrent episode of cerebral infarction, after which she was commenced on tumor necrosis factor (TNF)-antagonist therapy in addition to monthly fresh plasma infusion. Thereafter, there was no cerebral insult reported for >18 months. The genetic study of the child and her parents revealed a homozygous mutation c. 336C>A, p. (His112Gln) in the CECR1 gene, and her parents were heterozygous for the same variant. This variant was not previously reported in literature. We would suggest to link this novel variant c. 336C>A, p. (His112Gln) of CECR1 gene mutation with the clinical picture, along with the positive response to TNF-antagonist therapy in the era of ADA2 deficiency syndrome.
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spelling doaj-art-e010d10b7566404f9e94704bab925be52025-08-20T01:47:42ZengSAGE PublishingIndian Journal of Rheumatology0973-36980973-37012019-01-0114323624010.4103/injr.injr_36_19Adenosine deaminase 2 deficiency with a novel variant of CECR1 gene mutation: Responding to tumor necrosis factor antagonist therapyZakiya Saleh Al MosawiHiba Omar AbduljawadMaryam Yusuf BusehailBarrak Mahmood Al MoosawiDeficiency of Adenosine deaminase 2 (DADA2) syndrome is a chronic, systemic, and inflammatory disorder, characterized by early-onset recurrent strokes, fever, livedo reticularis, and immunodeficiency. We report the case of a 4-year-old child, a product of consanguineous marriage, who presented with three episodes of hemiparesis within 1 year. She also manifested skin discoloration in the form of livedo reticularis. Workup with magnetic resonance imaging (MRI) of the brain revealed acute infarction in the right aspect of the cerebral peduncle and chronic lacunars infarct in the right thalamus with diffusion restriction. Repeated MRI after 5 months revealed diffuse loss of brain volume. The blood workup showed high inflammatory markers and significantly low adenosine deaminase 2 (ADA2) level. After being on corticosteroid and anticoagulant treatments, she suffered from a recurrent episode of cerebral infarction, after which she was commenced on tumor necrosis factor (TNF)-antagonist therapy in addition to monthly fresh plasma infusion. Thereafter, there was no cerebral insult reported for >18 months. The genetic study of the child and her parents revealed a homozygous mutation c. 336C>A, p. (His112Gln) in the CECR1 gene, and her parents were heterozygous for the same variant. This variant was not previously reported in literature. We would suggest to link this novel variant c. 336C>A, p. (His112Gln) of CECR1 gene mutation with the clinical picture, along with the positive response to TNF-antagonist therapy in the era of ADA2 deficiency syndrome.http://www.indianjrheumatol.com/article.asp?issn=0973-3698;year=2019;volume=14;issue=3;spage=236;epage=240;aulast=Aladenosine deaminase deficiencyanti-tumor necrosis factor therapycat eye syndrome chromosome regioncandidate 1 mutationlivedo reticularis
spellingShingle Zakiya Saleh Al Mosawi
Hiba Omar Abduljawad
Maryam Yusuf Busehail
Barrak Mahmood Al Moosawi
Adenosine deaminase 2 deficiency with a novel variant of CECR1 gene mutation: Responding to tumor necrosis factor antagonist therapy
Indian Journal of Rheumatology
adenosine deaminase deficiency
anti-tumor necrosis factor therapy
cat eye syndrome chromosome region
candidate 1 mutation
livedo reticularis
title Adenosine deaminase 2 deficiency with a novel variant of CECR1 gene mutation: Responding to tumor necrosis factor antagonist therapy
title_full Adenosine deaminase 2 deficiency with a novel variant of CECR1 gene mutation: Responding to tumor necrosis factor antagonist therapy
title_fullStr Adenosine deaminase 2 deficiency with a novel variant of CECR1 gene mutation: Responding to tumor necrosis factor antagonist therapy
title_full_unstemmed Adenosine deaminase 2 deficiency with a novel variant of CECR1 gene mutation: Responding to tumor necrosis factor antagonist therapy
title_short Adenosine deaminase 2 deficiency with a novel variant of CECR1 gene mutation: Responding to tumor necrosis factor antagonist therapy
title_sort adenosine deaminase 2 deficiency with a novel variant of cecr1 gene mutation responding to tumor necrosis factor antagonist therapy
topic adenosine deaminase deficiency
anti-tumor necrosis factor therapy
cat eye syndrome chromosome region
candidate 1 mutation
livedo reticularis
url http://www.indianjrheumatol.com/article.asp?issn=0973-3698;year=2019;volume=14;issue=3;spage=236;epage=240;aulast=Al
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AT maryamyusufbusehail adenosinedeaminase2deficiencywithanovelvariantofcecr1genemutationrespondingtotumornecrosisfactorantagonisttherapy
AT barrakmahmoodalmoosawi adenosinedeaminase2deficiencywithanovelvariantofcecr1genemutationrespondingtotumornecrosisfactorantagonisttherapy