Stable clinical course in three siblings with late-onset isolated sulfite oxidase deficiency: a case series and literature review.


Journal

BMC pediatrics
ISSN: 1471-2431
Titre abrégé: BMC Pediatr
Pays: England
ID NLM: 100967804

Informations de publication

Date de publication:
23 12 2019
Historique:
received: 03 03 2019
accepted: 15 12 2019
entrez: 25 12 2019
pubmed: 25 12 2019
medline: 3 11 2020
Statut: epublish

Résumé

Isolated sulfite oxidase deficiency (ISOD) is an autosomal recessive disorder caused by a deficiency of sulfite oxidase, which is encoded by the sulfite oxidase gene (SUOX). Clinically, the disorder is classified as one of two forms: the late-onset mild form or the classic early-onset form. The latter is life-threatening and always leads to death during early childhood. Mild ISOD cases are rare and may benefit from dietary therapy. To date, no cases of ISOD have been reported to recover spontaneously. Here, we present three mild ISOD cases in one family, each with a stable clinical course and spontaneous recovery. All three siblings had two novel compound heterozygous mutations in the SUOX gene (NM_000456; c.1096C > T [p.R366C] and c.1376G > A [p.R459Q]). The siblings included two males and one female with late ages of onset (12-16 months) and presented with specific neuroimaging abnormalities limited to the bilateral globus pallidus and substantia nigra. The three patients had decreased plasma homocysteine levels. They exhibited a monophasic clinical course continuing up to 8.5 years even without dietary therapy. This is the first report of mild ISOD cases with a stable clinical course and spontaneous recovery without dietary therapy. Our study provides an expansion for the clinical spectrum of ISOD. Furthermore, we highlight the importance of including ISOD in the differential diagnosis for patients presenting with late-onset symptoms, bilaterally symmetric regions of abnormal intensities in the basal ganglia, and decreased plasma homocysteine levels.

Sections du résumé

BACKGROUND
Isolated sulfite oxidase deficiency (ISOD) is an autosomal recessive disorder caused by a deficiency of sulfite oxidase, which is encoded by the sulfite oxidase gene (SUOX). Clinically, the disorder is classified as one of two forms: the late-onset mild form or the classic early-onset form. The latter is life-threatening and always leads to death during early childhood. Mild ISOD cases are rare and may benefit from dietary therapy. To date, no cases of ISOD have been reported to recover spontaneously. Here, we present three mild ISOD cases in one family, each with a stable clinical course and spontaneous recovery.
CASE PRESENTATION
All three siblings had two novel compound heterozygous mutations in the SUOX gene (NM_000456; c.1096C > T [p.R366C] and c.1376G > A [p.R459Q]). The siblings included two males and one female with late ages of onset (12-16 months) and presented with specific neuroimaging abnormalities limited to the bilateral globus pallidus and substantia nigra. The three patients had decreased plasma homocysteine levels. They exhibited a monophasic clinical course continuing up to 8.5 years even without dietary therapy.
CONCLUSION
This is the first report of mild ISOD cases with a stable clinical course and spontaneous recovery without dietary therapy. Our study provides an expansion for the clinical spectrum of ISOD. Furthermore, we highlight the importance of including ISOD in the differential diagnosis for patients presenting with late-onset symptoms, bilaterally symmetric regions of abnormal intensities in the basal ganglia, and decreased plasma homocysteine levels.

Identifiants

pubmed: 31870341
doi: 10.1186/s12887-019-1889-5
pii: 10.1186/s12887-019-1889-5
pmc: PMC6927172
doi:

Substances chimiques

Sulfite Oxidase EC 1.8.3.1

Types de publication

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

Langues

eng

Sous-ensembles de citation

IM

Pagination

510

Références

Proc Natl Acad Sci U S A. 1998 May 26;95(11):6394-8
pubmed: 9600976
Neuropediatrics. 1996 Dec;27(6):299-304
pubmed: 9050047
N Engl J Med. 1977 Nov 10;297(19):1022-8
pubmed: 302914
Eur J Pediatr. 1991 Jan;150(3):196-7
pubmed: 2044591
J Child Neurol. 2007 Oct;22(10):1214-21
pubmed: 17940249
J Inherit Metab Dis. 2000 Feb;23(1):45-53
pubmed: 10682307
Genet Med. 2015 May;17(5):405-24
pubmed: 25741868
Can J Neurol Sci. 2014 Jan;41(1):42-8
pubmed: 24384336
J Inherit Metab Dis. 2018 Jan;41(1):101-108
pubmed: 28980090
Pediatrics. 2005 Sep;116(3):757-66
pubmed: 16140720
Mol Genet Metab. 2013 Apr;108(4):263-6
pubmed: 23414711
Brain Dev. 2014 Feb;36(2):176-9
pubmed: 23452914
Cell. 1997 Dec 26;91(7):973-83
pubmed: 9428520
Neuropediatrics. 1995 Dec;26(6):322-4
pubmed: 8719749

Auteurs

Maoqiang Tian (M)

Department of Pediatrics, West China Second University Hospital, Sichuan University, Chengdu, 610041, China.
Key Laboratory of Birth Defects and Related Diseases of Women and Children, (Sichuan University), Ministry of Education, Chengdu, 610041, China.
Department of Pediatrics, Affiliated Hospital of Zunyi Medical University, Zunyi, 563003, China.

Yi Qu (Y)

Department of Pediatrics, West China Second University Hospital, Sichuan University, Chengdu, 610041, China. quyi712002@163.com.
Key Laboratory of Birth Defects and Related Diseases of Women and Children, (Sichuan University), Ministry of Education, Chengdu, 610041, China. quyi712002@163.com.

Lingyi Huang (L)

West China College of Stomatology, Sichuan University, Chengdu, 610041, China.

Xiaojuan Su (X)

Department of Pediatrics, West China Second University Hospital, Sichuan University, Chengdu, 610041, China.
Key Laboratory of Birth Defects and Related Diseases of Women and Children, (Sichuan University), Ministry of Education, Chengdu, 610041, China.

Shiping Li (S)

Department of Pediatrics, West China Second University Hospital, Sichuan University, Chengdu, 610041, China.
Key Laboratory of Birth Defects and Related Diseases of Women and Children, (Sichuan University), Ministry of Education, Chengdu, 610041, China.

Junjie Ying (J)

Department of Pediatrics, West China Second University Hospital, Sichuan University, Chengdu, 610041, China.
Key Laboratory of Birth Defects and Related Diseases of Women and Children, (Sichuan University), Ministry of Education, Chengdu, 610041, China.

Fengyan Zhao (F)

Department of Pediatrics, West China Second University Hospital, Sichuan University, Chengdu, 610041, China.
Key Laboratory of Birth Defects and Related Diseases of Women and Children, (Sichuan University), Ministry of Education, Chengdu, 610041, China.

Dezhi Mu (D)

Department of Pediatrics, West China Second University Hospital, Sichuan University, Chengdu, 610041, China.
Key Laboratory of Birth Defects and Related Diseases of Women and Children, (Sichuan University), Ministry of Education, Chengdu, 610041, China.

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