Evidence map›Paper›PMID 42809155›Full record

ReviewJournal of neurology2026

Scleromyxedema-Associated Myopathy and Vacuolar Myopathy with Monoclonal Gammopathy and Stiffness (VAMMGAS) as manifestations of Monoclonal Gammopathy of Clinical Significance (MGCS): a disease spectrum between autophagy dysfunction and inflammation.

Tommaso Nicoletti, Olivier Benveniste, Maxime Battistella, Thibault Mahevas, Bertrand Arnulf, Tanya Stojkovic, Katia Staedler, Thierry Maisonobe, Franck Letournel, Pierre Romero and 8 more

Abstract readCase ReportsReview
PubMed Publisher
In one paragraph

Review in Journal of neurology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing 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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

18 authors.

Tommaso NicolettiDepartment of Neuropathology, Sorbonne Université, AP-HP, Institut du Cerveau-Paris Brain Institute-ICM, Inserm, CNRS, Hôpitaux Universitaires La Pitié Salpêtrière-Charles Foix, 75013, Paris, France. tommasof.nicoletti@gmail.com.ORCID http://orcid.org/0000-0002-9335-1218
Olivier BenvenisteDépartement de Médecine Interne et Immunologie Clinique, Groupe Hospitalier Pitié-Salpêtrière, Centre National de Référence des Myopathies Inflammatoires, Assistance Publique-Hôpitaux de Paris, Paris, France.
Maxime BattistellaPathology Department, Hôpital Saint-Louis AP-HP, INSERM U1342, Université Paris Cité, Paris, France.
Thibault MahevasDermatology Department, Hôpital Saint-Louis AP-HP, Université Paris Cité, Paris, France.
Bertrand ArnulfImmuno-Hematology Department, Saint-Louis Hospital, Assistance Publique Hôpitaux de Paris, UMR 1342, Université Paris Cité, Paris, France.
Tanya StojkovicNeuromuscular Reference Center Nord/Est/Ile de France, Neuromyology Department, Pitié-Salpêtrière Hospital, Assistance Publique des Hôpitaux de Paris, Sorbonne University, Paris, France.
Katia StaedlerNeuromuscular Reference Center Nord/Est/Ile de France, Neuromyology Department, Pitié-Salpêtrière Hospital, Assistance Publique des Hôpitaux de Paris, Sorbonne University, Paris, France.
Thierry MaisonobeDépartement de Neurophysiologie Clinique, Hôpitaux Universitaires la Pitié Salpêtrière-Charles Foix, AP-HP, Sorbonne Université, Paris, France.
Franck LetournelCHU Angers, Inserm, CNRS, MINT, SFR ICAT, Univ Angers, 49000, Angers, France.
Pierre RomeroPathology Department, Centre Hospitalo-Universitaire de Pitié Salpétrière, CIMI, U11-35 Assistance Publique-Hôpitaux de Paris, Paris, France.
Edoardo MalfattiReference Center for Neuromuscular Disorders, APHP Henri Mondor University Hospital, Créteil, France.
Marguerite VignonDepartment of Hematology, GHU Paris Centre- Cochin-, AP-HP, Paris, France.
Aleksandra Nadaj-PaklezaNeurology Department, Reference Center for Neuromuscular Diseases 'Nord-Est-Ile de France', University Hospitals of Strasbourg, and European Reference Network for Rare Neuromuscular Diseases (ERN EURO-NMD), 67000, Strasbourg, France.
Beatrice LabellaNeuromuscular Functional Unit, Department of Neuropathology, Groupe Hospitalier Universitaire La Pitié-Salpêtrière-Sorbonne University, 75013, Paris, France.
Emmanuelle LaceneNeuromuscular Morphology Unit, Myology Institute, Paris, France.
Guy BrochierNeuromuscular Morphology Unit, Myology Institute, Paris, France.
Teresinha EvangelistaNeuromuscular Functional Unit, Department of Neuropathology, Groupe Hospitalier Universitaire La Pitié-Salpêtrière-Sorbonne University, 75013, Paris, France.
Sarah Leonard-LouisNeuromuscular Reference Center Nord/Est/Ile de France, Neuromyology Department, Pitié-Salpêtrière Hospital, Assistance Publique des Hôpitaux de Paris, Sorbonne University, Paris, France. sarah.leonard-louis@aphp.fr.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Scleromyxedema-Associated Myopathy (SAM) and Vacuolar Myopathy with Monoclonal Gammopathy and Stiffness (VAMMGAS) are rare clinical entities associated with Monoclonal Gammopathy of Clinical Significance (MGCS). We compared the clinical, neurophysiological, histopathological, and ultrastructural features of three patients (two with SAM and one with VAMMGAS), together with a review of the available literature, to further characterize the similarities and differences between these two conditions. Our analysis suggests that SAM and VAMMGAS may represent part of a clinical spectrum characterized by progressive proximal muscle weakness and prominent pathological spontaneous activity on electromyography. By definition, SAM is associated with scleromyxedema, which may occasionally develop after the onset of myopathy, whereas VAMMGAS is characterized by muscle stiffness. The underlying monoclonal gammopathy is most commonly IgG ? in SAM, while IgG ? appears to be more frequent in VAMMGAS. Histopathologically, both conditions show a myopathy with features suggestive of impaired autophagy and evidence of immune activation (abnormal HLA-I expression and sarcolemmal C5b-9 deposits), although inflammatory infiltrates appear to be more characteristic of SAM, providing insights into potentially shared pathogenic mechanisms. Taken together, these findings support the concept that SAM and VAMMGAS may represent related manifestations within the spectrum of MGCS-associated muscle disease. Recognition of their overlapping clinical, neurophysiological, and histological features may facilitate diagnosis and broaden our understanding of the underlying pathophysiological mechanisms, potentially informing therapeutic strategies. Importantly, both conditions appear to be treatable with immunomodulatory approaches (including intravenous immunoglobulins and plasma exchange) as well as clone-directed therapies.

Indexed as

AutophagyLysosomal Storage DiseasesMuscular DiseasesParaproteinemiasScleromyxedemaAdultAgedFemaleHumansInflammationMaleMiddle AgedMuscle, SkeletalAutophagyMGUSMonoclonal gammopathyScleromyxedemaVacuolar myopathyVAMMGAS

Identifiers

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.