Evidence map›Paper›PMID 25778939›Full record

ReviewJournal of inherited metabolic disease2015

Acute rhabdomyolysis and inflammation.

Yamina Hamel, Asmaa Mamoune, François-Xavier Mauvais, Florence Habarou, Laetitia Lallement, Norma Beatriz Romero, Chris Ottolenghi, Pascale de Lonlay

Abstract readReview
PubMed Publisher
In one paragraph

Review in Journal of inherited metabolic disease, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
3.3field-weighted citation impact, top 8% 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

33 citing papers in PubMed, 62 citations in OpenAlex.

  1. Rhabdomyolysis: a narrative review.Arquivos de neuro-psiquiatria · 2026
    Review
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  10. Use of dexamethasone in acute rhabdomyolysis inMolecular genetics and metabolism reports · 2023
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  18. SARS-CoV-2 Infection with Associated Rhabdomyolysis and Probable Myocarditis.European journal of case reports in internal medicine · 2020
    Article
  19. Article
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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

8 authors at 5 institutions in 1 country.

Yamina HamelInstitut Imagine, Institut National de la Santé et de la Recherche Médicale, Unité 1163, 75015, Paris, France.
Asmaa Mamoune
François-Xavier Mauvais
Florence Habarou
Laetitia Lallement
Norma Beatriz Romero
Chris Ottolenghi
Pascale de Lonlay
Délégation Paris 5 · FRHôpital Necker-Enfants Malades · FRInserm · FRInstitut des Maladies Génétiques Imagine · FRSorbonne Paris Cité · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Rhabdomyolysis results from the rapid breakdown of skeletal muscle fibers, which leads to leakage of potentially toxic cellular content into the systemic circulation. Acquired causes by direct injury to the sarcolemma are most frequent. The inherited causes are: i) metabolic with failure of energy production, including mitochondrial fatty acid ß-oxidation defects, LPIN1 mutations, inborn errors of glycogenolysis and glycolysis, more rarely mitochondrial respiratory chain deficiency, purine defects and peroxysomal α-methyl-acyl-CoA-racemase defect (AMACR), ii) structural causes with muscle dystrophies and myopathies, iii) calcium pump disorder with RYR1 gene mutations, iv) inflammatory causes with myositis. Irrespective of the cause of rhabdomyolysis, the pathology follows a common pathway, either by the direct injury to sarcolemma by increased intracellular calcium concentration (acquired causes) or by the failure of energy production (inherited causes), which leads to fiber necrosis. Rhabdomyolysis are frequently precipitated by febrile illness or exercise. These conditions are associated with two events, elevated temperature and high circulating levels of pro-inflammatory mediators such as cytokines and chemokines. To illustrate these points in the context of energy metabolism, protein thermolability and the potential benefits of arginine therapy, we focus on a rare cause of rhabdomyolysis, aldolase A deficiency. In addition, our studies on lipin-1 (LPIN1) deficiency raise the possibility that several diseases involved in rhabdomyolysis implicate pro-inflammatory cytokines and may even represent primarily pro-inflammatory diseases. Thus, not only thermolability of mutant proteins critical for muscle function, but also pro-inflammatory cytokines per se, may lead to metabolic decompensation and rhabdomyolysis.

Indexed as

Acute DiseaseCytokinesHumansInflammationPhosphatidate PhosphataseRhabdomyolysisCytokinesLPIN1 protein, humanPhosphatidate Phosphatase

Identifiers

PMID25778939
OpenAlexW2005454521

What OpenQuestion holds

Textmetadata
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.