Evidence map›Paper›PMID 41333914›Full record

ReviewJugan geon-gang gwa jilbyeong2025

[A Comprehensive Review on Glycogen Storage Disease: Molecular Mechanisms, Diagnosis, and Treatment Strategies].

Hong Koh

Abstract readEnglish AbstractReview
In one paragraph

Review in Jugan geon-gang gwa jilbyeong, 2025. 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

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

1 citing paper in PubMed.

  1. Article
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

1 author.

Hong Koh연세대학교 의과대학 소아과학교실.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Glycogen storage disease (GSD) is a hereditary metabolic disorder caused by defective enzymes involved in carbohydrate metabolism. GSD leads to abnormal glycogen accumulation in tissues, such as the liver, muscles, and heart, resulting in various clinical symptoms, including hypoglycemia, hepatomegaly, muscle weakness, and heart dysfunction. There are several types of GSD. Each type of GSD is caused by a deficiency of a specific enzyme, and its clinical symptoms can vary significantly depending on the affected enzyme and organ systems. Advances in molecular genetics have elucidated the genetic basis of GSD, improving its diagnostic accuracy, and enhancing our understanding of its pathophysiology. This review focused on the molecular mechanisms, clinical symptoms, diagnostic approaches, and current treatment strategies for all types of GSD, including dietary management, enzyme replacement therapy, and emerging genetic therapies. It also addressed challenges relating to treatment adherence, long-term outcomes, and future research directions. Early diagnosis and personalized treatment plans are essential for improving the prognosis of patients with GSD. Continued research to discover more effective treatment options, and ultimately, cure the disease is crucial.

Indexed as

Diet therapyEnzyme replacement therapyGlycogen storage diseaseHepatitis

Identifiers

PMID41333914
PMCPMC12480407

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
Read underepoch 390

Registered trials

None linked

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.