Evidence map›Paper›PMID 36544095›Full record

ArticleBMC cancer2022

Clinicopathological findings, prognosis, and Epstein-Barr virus infection in rheumatoid arthritis patients with other iatrogenic immunodeficiency-associated T- and NK-cell lymphoproliferative disorders.

Shoichi Kimura, Yumi Oshiro, Hiromi Iwasaki, Masanori Kadowaki, Masao Ogata, Tsutomu Daa, Toshifumi Sakata, Shigeto Kawauchi, Ziyao Wang, Yasushi Takamatsu and 1 more

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in BMC cancer, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
0.4field-weighted citation impact, top 35% 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

2 citing papers in PubMed, 4 citations in OpenAlex.

  1. Review
  2. Review
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

11 authors at 4 institutions in 1 country.

Shoichi KimuraGraduate School of Medical Sciences, Division of Pathomorphology, Fukuoka University, 7-45-1 Nanakuma, Jonan-ku, Fukuoka, 8140180, Japan.
Yumi OshiroDepartment of Pathology, Matsuyama Red Cross Hospital, 1 Bunkyo-cho, Matsuyama, 7910000, Japan.
Hiromi IwasakiDepartment of Haematology, Clinical Research Centre, National Hospital Organization Kyushu Medical Centre, 1-8-1 Jigyohama, Chuo-ku, Fukuoka, 8108563, Japan.
Masanori KadowakiDepartment of Haematology, Clinical Research Centre, National Hospital Organization Kyushu Medical Centre, 1-8-1 Jigyohama, Chuo-ku, Fukuoka, 8108563, Japan.
Masao OgataDepartment of Hematology, Faculty of Medicine, Oita University, Idaigaoka, Hazama-machi, Yufushi, Oita, 8795593, Japan.
Tsutomu DaaDepartment of Pathology, Faculty of Medicine, Oita University, Idaigaoka, Hazama-machi, Yufushi, Oita, 8795593, Japan.
Toshifumi SakataDepartment of Otolaryngology, Faculty of Medicine, and Fukuoka University, 7-45-1 Nanakuma, Jonan-ku, Fukuoka, 8140180, Japan.
Shigeto KawauchiDepartment of Pathology, Clinical Research Centre, National Hospital Organization Kyushu Medical Centre, 1-8-1 Jigyohama, Chuo-ku, Fukuoka, 8108563, Japan.
Ziyao WangGraduate School of Medical Sciences, Division of Pathomorphology, Fukuoka University, 7-45-1 Nanakuma, Jonan-ku, Fukuoka, 8140180, Japan.
Yasushi TakamatsuDepartment of Internal Medicine, Division of Medical Oncology, Hematology and Infectious Disease, Faculty of Medicine, Fukuoka University, 7-45-1 Nanakuma, Jonan-ku, Fukuoka, 8140180, Japan.
Morishige TakeshitaGraduate School of Medical Sciences, Division of Pathomorphology, Fukuoka University, 7-45-1 Nanakuma, Jonan-ku, Fukuoka, 8140180, Japan. m-take@adm.fukuoka-u.ac.jp.ORCID http://orcid.org/0000-0003-0267-2081
Fukuoka University · JPNational Kyushu Medical Center · JPOita University · JPMatsuyama Red Cross Hospital · JP

Funding

the Ministry of Education, Science, and Culture of Japan Grant-in-Aid for Scientific Research (17K08732)
6 · The paper itself

Abstract

backgroundOther iatrogenic immunodeficiency-associated (OIIA) T- and natural killer (NK)-cell lymphoproliferative disorders (TNK-LPDs) are rare in patients with rheumatoid arthritis (RA).

methodsWe investigated the clinicopathological characteristics, Epstein-Barr virus (EBV) infection, genetic findings, therapeutic response, and prognostic factors in 21 RA patients with OIIA TNK-LPDs and compared these with those of 39 with OIIA B-cell LPDs (B-LPDs) and 22 with non-OIIA B-LPDs.

resultsImmunohistologically, 11 patients (52%) showed CD4+ T-LPDs, and 7 had a T follicular helper (TFH) phenotype. The other nine patients (43%) showed CD8+ T-LPDs, and the remaining one (5%) had features of CD3+ CD4- CD8- nasal type TNK-cell lymphoma. CD30+, p53+, and CMYC+ atypical lymphocytes were identified in seven (33%), eight (38%), and five (24%) patients, respectively. In situ hybridisation detected EBV-encoded RNA (EBER) + large atypical lymphocytes in five patients (24%). Nine of 17 patients (53%) showed clonal peaks of TCRγ by polymerase chain reaction. Withdrawal of MTX and biologic drugs was effective in 12 patients (57%), and 8 (38%) received chemotherapies. Two patients with TFH+ or EBV+ CD4+ CD30+ large cell peripheral T-cell lymphoma, one with CD8+ systemic anaplastic large cell lymphoma, and two with systemic EBV+ CD8+ T-cell lymphoma of childhood showed a lethal progressive clinical course within 13 months. Moreover, > 500 U/L LDH, large atypical lymphocytes, expression of CD30, p53, and CMYC, and EBER+ atypical lymphocytes were significantly poor prognostic factors for overall survival (p < 0.05). Median interval from RA onset to OIIA TNK-LPDs was 72 months, which was shorter than 166 months in OIIA B-LPDs (p = 0.003). EBV+ atypical and reactive lymphocytes were frequently found in 15 patients with OIIA TNK-LPDs (71%), in 27 with OIIA B-LPDs (69%), and only in 3 with non-OIIA B-LPDs (14%).

conclusionsOIIA TNK-LPDs occurred in early phase of RA, compared with OIIA B-LPDs, and occasionally showed a lethal progressive clinical course. Detection of OIIA TNK-LPD patients with poor prognostic factors is necessary. EBV infection in immunosuppressed patients due to persistent RA, MTX, and biologic drugs may play a role in forming the tumour microenvironment and lymphomagenesis of TNK-LPDs.

Indexed as

Arthritis, RheumatoidEpstein-Barr Virus InfectionsLymphoproliferative DisordersDisease ProgressionHerpesvirus 4, HumanHumansIatrogenic DiseaseKiller Cells, NaturalMethotrexatePrognosisTumor Suppressor Protein p53MethotrexateTumor Suppressor Protein p53Epstein–Barr virusIatrogenic immunodeficiencyMethotrexateRheumatoid arthritisT cells, NK cells, lymphoproliferative disorders

Identifiers

PMID36544095
PMCPMC9773610
OpenAlexW4312129162

What OpenQuestion holds

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LicenceCC BY
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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.