ArticleCureus2026
Rapidly Progressive Triple M Overlap Syndrome After Immune Checkpoint Inhibitor Therapy.
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
7 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Immune checkpoint inhibitors (ICIs) are widely used in cancer treatment, but can cause immune-related adverse events affecting multiple organ systems. Triple M overlap syndrome (TMOS) is a rare and often fatal complication, consisting of the triad of ICI-mediated myositis, myocarditis, and myasthenia gravis. An 85-year-old man with metastatic renal cell carcinoma was initiated on combination ICI-based therapy with pembrolizumab and lenvatinib. Approximately four weeks after initiation of immunotherapy, he presented to the emergency department following a two-week history of progressive neck extensor weakness, downward gaze, worsening proximal upper and lower extremity weakness, recurrent falls, dysphagia, and dysphonia. On evaluation, myositis, myocarditis, and clinical evidence of a myasthenia gravis-like syndrome were noted, and TMOS was diagnosed. Initial treatment with high-dose intravenous corticosteroids and intravenous immunoglobulin was started, yet the patient's condition deteriorated. Despite aggressive treatment, due to hemodynamic instability and liver injury, he could not be started on plasmapheresis or second-line immunosuppression. With progressive multiorgan failure, the patient's management was shifted to comfort-based measures. Although an increasing number of immunosuppressive agents have shown efficacy in TMOS management, this case illustrates how the multiorgan injury inherent to TMOS can itself create contraindications to the very therapies required for definitive treatment. This self-reinforcing cycle of therapeutic limitation highlights the importance of early recognition and aggressive management of TMOS prior to end-organ damage, narrowing the treatment window.
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.