Evidence map›Paper›PMID 32902816›Full record

ArticleCEN case reports2021

A classic variant of Fabry disease in a family with the M296I late-onset variant.

Shuma Hirashio, Reiko Kagawa, Go Tajima, Takao Masaki

Open access · bronzeAbstract readCase Reports
In one paragraph

Article in CEN case reports, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
0.4field-weighted citation impact, top 39% of its field
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

3 citing papers in PubMed, 5 citations in OpenAlex.

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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

4 authors at 2 institutions in 1 country.

Shuma HirashioDepartment of Nephrology, Hiroshima University Hospital, Hiroshima, 1-2-3 Kasumi, Hiroshima, 734-8551, Japan.
Reiko KagawaDepartment of Pediatrics, Hiroshima University Hospital, Hiroshima, Hiroshima, 1-2-3 Kasumi, 734-8551, Japan.
Go TajimaDivision of Neonatal Screening, Research Institute, National Center for Child Health and Development, 2-10-1 Okura, Setagaya-ku, Tokyo, 157-8535, Japan.
Takao MasakiDepartment of Nephrology, Hiroshima University Hospital, Hiroshima, 1-2-3 Kasumi, Hiroshima, 734-8551, Japan. masakit@hiroshima-u.ac.jp.ORCID 0000-0003-4271-9964
Hiroshima University Hospital · JPNational Center For Child Health and Development · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Fabry disease is an X-linked recessive disease of glycosphingolipid metabolism caused by deficiency or reduced activity of α-galactosidase A. Fabry disease phenotypes are known to consist of a classic variant and a late-onset variant. In patients with Fabry disease, the phenotype is generally considered to be defined (at least partially) by the genotype. However, patients with the classic variant have been encountered in families with mutations that are expected to produce the late-onset variant. Here, we describe a 4-year-old boy with a classic variant of Fabry disease in a family with the M296I late-onset variant. The patient's grandfather, mother, and aunt experienced late-onset disease, characteristic of the M296I variant. Conversely, the patient experienced typical disease symptoms in childhood. He had symptoms of hypohidrosis and associated heat accumulation. He cried at night due to the occurrence of severe acroparaesthesia. This symptom became more pronounced in warmer climates. Although the patient's family had a late-onset variant mutation of Fabry disease, we determined that the patient's symptoms were similar to those of classic Fabry disease. Therefore, the patient began enzyme replacement therapy, which alleviated his symptoms. Notably, enzyme replacement therapy led to rapid improvement of the patient's subjective symptoms. Thus, we presumed that the patient's symptoms supported a diagnosis of classic Fabry disease. These findings suggest that childhood symptoms may occur in patients with Fabry disease, even in families with late-onset variant mutations. The genotype-phenotype correlation in Fabry disease remains controversial.

Indexed as

alpha-GalactosidaseChild, PreschoolEnzyme Replacement TherapyFabry DiseaseHumansHypohidrosisMaleMutationPhenotypeTreatment Outcomealpha-GalactosidaseClassic variantFabry diseaseGenotypeLate-onset variantM296I mutationPhenotype

Identifiers

PMID32902816
PMCPMC7829310
OpenAlexW3086227795

What OpenQuestion holds

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Registered trials

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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.