ArticleCureus2026
A Diagnostic Conundrum: Atypical McArdle Disease Mimic With Heterozygous PYGM Mutation and Cytochrome C Oxidase (COX)-Negative Fibers.
Article in Cureus, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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.
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.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
McArdle disease is inherited in an autosomal recessive pattern, with classical disease manifesting with biallelic pathogenic variants in the PYGM (myophosphorylase) gene. Here, we present a case of a 77-year-old man with a paraspinal myopathy and head drop with cytochrome c oxidase (COX)-negative fibers who is a heterozygous carrier of a pathogenic c.148C>T (p.Arg50*) nonsense variant in PYGM as identified on a comprehensive glycogen storage disease gene panel through Mayo Clinic Laboratories. Two findings complicate a confident diagnosis of classical McArdle disease. They are explicitly addressed: a single (heterozygous) pathogenic allele for an autosomal recessive disorder, and COX-negative fibers in the absence of frank glycogen accumulation on periodic acid-Schiff staining. The case is presented as suggestive of an atypical metabolic-mitochondrial phenotype, and we discuss the diagnostic limitations of a blood-based targeted gene panel, as well as further testing, including muscle RNA sequencing and tissue-specific mitochondrial DNA analysis, that could resolve a potentially undetected second variant or a tissue-restricted mitochondrial etiology.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.