Evidence map›Paper›PMID 28506261›Full record

ArticleBMC neurology2017

A possible role of low regulatory T cells in anti-acetylcholine receptor antibody positive myasthenia gravis after bone marrow transplantation.

Masahiko Fukatsu, Takenobu Murakami, Hiroshi Ohkawara, Shunichi Saito, Kazuhiko Ikeda, Suguru Kadowaki, Itaru Sasaki, Mari Segawa, Tomoko Soeda, Akihiko Hoshi and 8 more

Open access · goldAbstract readCase Reports
In one paragraph

Article in BMC neurology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
0.5field-weighted citation impact, top 32% 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

1 citing paper in PubMed, 5 citations in OpenAlex.

  1. Article
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 at 1 institution in 1 country.

Masahiko FukatsuDepartment of Neurology, Fukushima Medical University, 1 Hikariga-oka, Fukushima, Fukushima, 960-1295, Japan.
Takenobu MurakamiDepartment of Neurology, Fukushima Medical University, 1 Hikariga-oka, Fukushima, Fukushima, 960-1295, Japan. takebou@fmu.ac.jp.
Hiroshi OhkawaraDepartment of Hematology, Fukushima Medical University, Fukushima, Japan.
Shunichi SaitoDepartment of Blood Transfusion and Transplantation Immunology, Fukushima Medical University, Fukushima, Japan.
Kazuhiko IkedaDepartment of Hematology, Fukushima Medical University, Fukushima, Japan.
Suguru KadowakiDepartment of Neurology, Fukushima Medical University, 1 Hikariga-oka, Fukushima, Fukushima, 960-1295, Japan.
Itaru SasakiDepartment of Neurology, Fukushima Medical University, 1 Hikariga-oka, Fukushima, Fukushima, 960-1295, Japan.
Mari SegawaDepartment of Neurology, Fukushima Medical University, 1 Hikariga-oka, Fukushima, Fukushima, 960-1295, Japan.
Tomoko SoedaDepartment of Neurology, Fukushima Medical University, 1 Hikariga-oka, Fukushima, Fukushima, 960-1295, Japan.
Akihiko HoshiDepartment of Neurology, Fukushima Medical University, 1 Hikariga-oka, Fukushima, Fukushima, 960-1295, Japan.
Hiroshi TakahashiDepartment of Hematology, Fukushima Medical University, Fukushima, Japan.
Akiko Shichishima-NakamuraDepartment of Hematology, Fukushima Medical University, Fukushima, Japan.
Kazuei OgawaDepartment of Hematology, Fukushima Medical University, Fukushima, Japan.
Yoshihiro SugiuraDepartment of Neurology, Fukushima Medical University, 1 Hikariga-oka, Fukushima, Fukushima, 960-1295, Japan.
Hitoshi OhtoDepartment of Blood Transfusion and Transplantation Immunology, Fukushima Medical University, Fukushima, Japan.
Yasuchika TakeishiDepartment of Cardiovascular Medicine, Fukushima Medical University, Fukushima, Japan.
Takayuki IkezoeDepartment of Hematology, Fukushima Medical University, Fukushima, Japan.
Yoshikazu UgawaDepartment of Neurology, Fukushima Medical University, 1 Hikariga-oka, Fukushima, Fukushima, 960-1295, Japan.
Fukushima Medical University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundChronic graft-versus-host disease (GVHD) appears several months following allogenic hematopoietic stem cell transplantation (HSCT) and is clinically analogous to autoimmune disorder. Polymyositis is a common neuromuscular disorder in chronic GVHD, but myasthenia gravis (MG) is extremely rare. Hence, its pathophysiology and treatment have not been elucidated. CASE PRESENTATION: A 63-year-old man with a history of chronic GVHD presented with ptosis, dropped head, and dyspnea on exertion, which had worsened over the previous several months. He showed progressive decrement of compound muscle action potential in the deltoid muscle evoked by 3-Hz repetitive nerve stimulation, a positive edrophonium test, and elevated levels of serum anti-acetylcholine receptor antibodies, which suggested a diagnosis of generalized MG. No thymoma was found. Flow cytometric analysis revealed a remarkable depletion of peripheral Tregs (CD4

conclusionsMyasthenic symptoms appeared in the process of tapering prednisolone for the treatment of chronic GVHD, supporting the diagnosis of MG associated with chronic GVHD. The present case proposes a possibility that reduction of Tregs might contribute to the pathogenesis of MG underlying chronic GVHD. Immunotherapy with rituximab is beneficial for treatment of refractory MG and GVHD.

Indexed as

AutoantibodiesBone Marrow TransplantationCholinergic AntagonistsGraft vs Host DiseaseMyasthenia GravisHumansMaleMiddle AgedT-Lymphocytes, RegulatoryAutoantibodiesCholinergic AntagonistsAnti-acetylcholine receptor antibodyGraft-versus-host diseaseHematopoietic cell transplantationMyasthenia gravisRegulatory T cellsRituximab

Identifiers

PMID28506261
PMCPMC5433011
OpenAlexW2616065860

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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.