Evidence map›Paper›PMID 38833157›Full record

ArticleCancer immunology, immunotherapy : CII2024

Combined use of tyrosine kinase inhibitors with PD-(L)1 blockade increased the risk of thyroid dysfunction in PD-(L)1 blockade: a prospective study.

Tomoko Kobayashi, Shintaro Iwama, Ayana Yamagami, Tetsushi Izuchi, Koji Suzuki, Koki Otake, Yoshinori Yasuda, Masahiko Ando, Takeshi Onoue, Takashi Miyata and 17 more

Abstract read
In one paragraph

Article in Cancer immunology, immunotherapy : CII, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing 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

6 citing papers in PubMed.

  1. Article
  2. Observational
  3. Review
  4. Review
  5. Article
  6. 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

27 authors.

Tomoko KobayashiDepartment of Endocrinology and Diabetes, Nagoya University Graduate School of Medicine, 65 Tsurumai-Cho, Showa-Ku, Nagoya, 466-8550, Japan.
Shintaro IwamaDepartment of Endocrinology and Diabetes, Nagoya University Graduate School of Medicine, 65 Tsurumai-Cho, Showa-Ku, Nagoya, 466-8550, Japan. iwama.shintaro.m1@f.mail.nagoya-u.ac.jp.
Ayana YamagamiDepartment of Endocrinology and Diabetes, Nagoya University Graduate School of Medicine, 65 Tsurumai-Cho, Showa-Ku, Nagoya, 466-8550, Japan.
Tetsushi IzuchiDepartment of Endocrinology and Diabetes, Nagoya University Graduate School of Medicine, 65 Tsurumai-Cho, Showa-Ku, Nagoya, 466-8550, Japan.
Koji SuzukiDepartment of Endocrinology and Diabetes, Nagoya University Graduate School of Medicine, 65 Tsurumai-Cho, Showa-Ku, Nagoya, 466-8550, Japan.
Koki OtakeDepartment of Endocrinology and Diabetes, Nagoya University Graduate School of Medicine, 65 Tsurumai-Cho, Showa-Ku, Nagoya, 466-8550, Japan.
Yoshinori YasudaDepartment of Endocrinology and Diabetes, Nagoya University Graduate School of Medicine, 65 Tsurumai-Cho, Showa-Ku, Nagoya, 466-8550, Japan.
Masahiko AndoCenter for Advanced Medicine and Clinical Research, Nagoya University Hospital, Nagoya, Japan.
Takeshi OnoueDepartment of Endocrinology and Diabetes, Nagoya University Graduate School of Medicine, 65 Tsurumai-Cho, Showa-Ku, Nagoya, 466-8550, Japan.
Takashi MiyataDepartment of Endocrinology and Diabetes, Nagoya University Graduate School of Medicine, 65 Tsurumai-Cho, Showa-Ku, Nagoya, 466-8550, Japan.
Mariko SugiyamaDepartment of Endocrinology and Diabetes, Nagoya University Graduate School of Medicine, 65 Tsurumai-Cho, Showa-Ku, Nagoya, 466-8550, Japan.
Daisuke HagiwaraDepartment of Endocrinology and Diabetes, Nagoya University Graduate School of Medicine, 65 Tsurumai-Cho, Showa-Ku, Nagoya, 466-8550, Japan.
Hidetaka SugaDepartment of Endocrinology and Diabetes, Nagoya University Graduate School of Medicine, 65 Tsurumai-Cho, Showa-Ku, Nagoya, 466-8550, Japan.
Ryoichi BannoPhysical Fitness and Sports, Research Center of Health, Nagoya University, Nagoya, Japan.
Tetsunari HaseDepartment of Respiratory Medicine, Nagoya University Graduate School of Medicine, Nagoya, Japan.
Naoki NishioDepartment of Otorhinolaryngology, Nagoya University Graduate School of Medicine, Nagoya, Japan.
Shoichiro MoriDepartment of Dermatology, Nagoya University Graduate School of Medicine, Nagoya, Japan.
Tomoya ShimokataDepartment of Clinical Oncology and Chemotherapy, Nagoya University Hospital, Nagoya, Japan.
Tomoyasu SanoDepartment of Urology, Nagoya University Graduate School of Medicine, Nagoya, Japan.
Kaoru NiimiDepartment of Obstetrics and Gynecology, Nagoya University Graduate School of Medicine, Nagoya, Japan.
Nobuhisa YoshikawaDepartment of Obstetrics and Gynecology, Nagoya University Graduate School of Medicine, Nagoya, Japan.
Shusuke AkamatsuDepartment of Urology, Nagoya University Graduate School of Medicine, Nagoya, Japan.
Yuichi AndoDepartment of Clinical Oncology and Chemotherapy, Nagoya University Hospital, Nagoya, Japan.
Masashi AkiyamaDepartment of Dermatology, Nagoya University Graduate School of Medicine, Nagoya, Japan.
Michihiko SoneDepartment of Otorhinolaryngology, Nagoya University Graduate School of Medicine, Nagoya, Japan.
Makoto IshiiDepartment of Respiratory Medicine, Nagoya University Graduate School of Medicine, Nagoya, Japan.
Hiroshi ArimaDepartment of Endocrinology and Diabetes, Nagoya University Graduate School of Medicine, 65 Tsurumai-Cho, Showa-Ku, Nagoya, 466-8550, Japan.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundAnti-programmed cell death-1 (ligand-1) antibody [PD-(L)1-Ab] can cause destructive thyroiditis and/or hypothyroidism. In addition, tyrosine kinase inhibitors (TKIs) frequently induce hypothyroidism. The aim of this prospective study is to examine the incidence and clinical characteristics of thyroid dysfunction induced by combination therapy of a PD-(L)1-Ab and TKI [PD-(L)1-Ab/TKI].

methodsA total of 757 patients treated with PD-(L)1-Ab or PD-(L)1-Ab/TKI were evaluated for anti-thyroid antibodies (ATAs) at baseline and for thyroid function for 48 weeks after treatment initiation and then observed until the last visit.

resultsThe cumulative incidences of destructive thyroiditis [4/23 (17.4%) vs. 45/734 (6.1%) patients, p < 0.001], isolated hypothyroidism [10/23 (43.5%) vs. 29/734 (4.0%) patients, p < 0.001], and all thyroid dysfunction [14/23 (60.9%) vs. 74/734 (10.1%) patients, p < 0.001] were significantly higher in the PD-(L)1-Ab/TKI group than PD-(L)1-Ab group, respectively. All patients positive for ATAs at baseline developed thyroid dysfunction after PD-(L)1-Ab/TKI treatment, a significantly higher incidence than that in those negative for ATAs at baseline [4/4 (100%) vs. 10/19 (52.6%) patients, p = 0.026].

conclusionsThe addition of TKIs increased the risk of thyroid dysfunction induced by PD-(L)1-Ab, with the risk being higher in patients positive for baseline ATAs.

Indexed as

B7-H1 AntigenImmune Checkpoint InhibitorsProtein Kinase InhibitorsAdultAgedAged, 80 and overFemaleHumansHypothyroidismIncidenceMaleMiddle AgedNeoplasmsProspective StudiesThyroid DiseasesTyrosine Kinase InhibitorsB7-H1 AntigenCD274 protein, humanImmune Checkpoint InhibitorsProtein Kinase InhibitorsTyrosine Kinase InhibitorsHypothyroidismirAEPD-1PD-L1ThyroiditisTKI

Identifiers

PMID38833157
PMCPMC11150211

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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.