Evidence map›Paper›PMID 39092009›Full record

ArticleMedicine international

Clinical and genetic analysis of children with glucose transporter type 1 deficiency syndrome.

Hao Qian, Guohuan Ying, Haifeng Xu, Shangyu Wang, Bing Wu, Xin Wang, Hongdan Qi, Mingying He, M Jalal Ud Din, Tingting Huang and 2 more

Abstract read
In one paragraph

Article in Medicine international. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

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3 · Its place in the literature

Who cites it

1 citing paper in PubMed.

  1. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

12 authors.

Hao QianDepartment of Neurology, Children's Hospital of Nanjing Medical University, Nanjing, Jiangsu 210006, P.R. China.
Guohuan YingDepartment of Neurology, Children's Hospital of Nanjing Medical University, Nanjing, Jiangsu 210006, P.R. China.
Haifeng XuDepartment of Neurology, Children's Hospital of Nanjing Medical University, Nanjing, Jiangsu 210006, P.R. China.
Shangyu WangDepartment of Neurology, Children's Hospital of Nanjing Medical University, Nanjing, Jiangsu 210006, P.R. China.
Bing WuDepartment of Neurology, Children's Hospital of Nanjing Medical University, Nanjing, Jiangsu 210006, P.R. China.
Xin WangDepartment of Neurology, Children's Hospital of Nanjing Medical University, Nanjing, Jiangsu 210006, P.R. China.
Hongdan QiDepartment of Neurology, Children's Hospital of Nanjing Medical University, Nanjing, Jiangsu 210006, P.R. China.
Mingying HeDepartment of Neurology, Children's Hospital of Nanjing Medical University, Nanjing, Jiangsu 210006, P.R. China.
M Jalal Ud DinDepartment of Neurology, Children's Hospital of Nanjing Medical University, Nanjing, Jiangsu 210006, P.R. China.
Tingting HuangDepartment of Neurology, Children's Hospital of Nanjing Medical University, Nanjing, Jiangsu 210006, P.R. China.
Yimei WuDepartment of Neurology, Children's Hospital of Nanjing Medical University, Nanjing, Jiangsu 210006, P.R. China.
Gang ZhangDepartment of Neurology, Children's Hospital of Nanjing Medical University, Nanjing, Jiangsu 210006, P.R. China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Glucose transporter type 1 deficiency syndrome (GLUT1-DS) is a rare metabolic encephalopathy with a wide variety of clinical phenotypes. In the present study, 15 patients diagnosed with GLUT1-DS were selected, all of whom had obvious clinical manifestations and complete genetic testing. Their clinical data and genetic reports were collated. All patients were provided with a ketogenic diet (KD) and an improvement in their symptoms was observed during a follow-up period of up to 1 year. The results revealed that the 15 cases had clinical symptoms, such as convulsions or dyskinesia. Although none had a cerebrospinal fluid/glucose ratio <0.4, the genetic report revealed that all had the solute carrier family 2 member 1 gene variant, and their clinical symptoms basically improved following the use of the KD. GLUT1-DS is a genetic metabolic disease that causes a series of neurological symptoms due to glucose metabolism disorders in the brain. Low glucose levels in cerebrospinal fluid and genetic testing are key diagnostic criteria, and the KD is a highly effective treatment option. By summarizing and analyzing patients with GLUT1-DS, summarizing clinical characteristics and expanding their gene profile, the findings of the present study may be of clinical significance for the early recognition and diagnosis of the disease, so as to conduct early treatment and shorten the duration of brain energy deficiency. This is of utmost importance for improving the prognosis and quality of life of affected children.

Indexed as

childrenepilepsyglucose transporter type 1 deficiency syndromeketogenic dietsolute carrier family 2 member 1

Identifiers

PMID39092009
PMCPMC11289861

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.