Evidence map›Paper›PMID 39198174›Full record

ArticleInternal medicine (Tokyo, Japan)2025

Nilotinib-induced Diabetes in Japanese Patients with Chronic Myeloid Leukemia.

Yuichiro Iwamoto, Tomohiko Kimura, Hideyuki Iwamoto, Junpei Sanada, Yoshiro Fushimi, Yukino Katakura, Masashi Shimoda, Toshinori Kondo, Shuhei Nakanishi, Tomoatsu Mune and 3 more

Abstract read
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In one paragraph

Article in Internal medicine (Tokyo, Japan), 2025. 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
–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

1 citing paper in PubMed.

  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

13 authors.

Yuichiro IwamotoDepartment of Diabetes, Endocrinology and Metabolism, Kawasaki Medical School, Japan.
Tomohiko KimuraDepartment of Diabetes, Endocrinology and Metabolism, Kawasaki Medical School, Japan.
Hideyuki IwamotoDepartment of Diabetes, Endocrinology and Metabolism, Kawasaki Medical School, Japan.
Junpei SanadaDepartment of Diabetes, Endocrinology and Metabolism, Kawasaki Medical School, Japan.
Yoshiro FushimiDepartment of Diabetes, Endocrinology and Metabolism, Kawasaki Medical School, Japan.
Yukino KatakuraDepartment of Diabetes, Endocrinology and Metabolism, Kawasaki Medical School, Japan.
Masashi ShimodaDepartment of Diabetes, Endocrinology and Metabolism, Kawasaki Medical School, Japan.
Toshinori KondoDepartment of Hematology, Kawasaki Medical School, Japan.
Shuhei NakanishiDepartment of Diabetes, Endocrinology and Metabolism, Kawasaki Medical School, Japan.
Tomoatsu MuneDepartment of Diabetes, Endocrinology and Metabolism, Kawasaki Medical School, Japan.
Kohei KakuDepartment of Diabetes, Endocrinology and Metabolism, Kawasaki Medical School, Japan.
Hideho WadaDepartment of Hematology, Kawasaki Medical School, Japan.
Hideaki KanetoDepartment of Diabetes, Endocrinology and Metabolism, Kawasaki Medical School, Japan.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Objective This study aimed to examine the risk of diabetes mellitus induced by nilotinib, a second-generation tyrosine kinase inhibitor. Methods This retrospective study included 25 patients with chronic myeloid leukemia (CML) treated with nilotinib at our hospital. Four patients had diabetes mellitus at the start of nilotinib administration (prior DM group), and five patients were newly diagnosed with diabetes mellitus after the start of nilotinib administration (new DM group). Sixteen patients who were not diagnosed with diabetes mellitus were classified into the non-DM group. Changes in the blood glucose and HbA1c levels were evaluated in each group at the time of nilotinib administration and two years later. Results Molecular genetic remission of CML was achieved in 81.8% of patients with diabetes and 72.2% of patients without non-DM group. There were no cases in this study in which nilotinib was changed or discontinued owing to hyperglycemia. There was no difference in the blood glucose levels at the start of nilotinib treatment among the groups. Two years after starting nilotinib, the blood glucose levels in the new DM group [232 (186-296) mg/dL] and prior DM group [168 (123-269) mg/dL] were significantly higher than those in the non-DM group [100 (91-115) mg/dL]. ΔHbA1c levels in the new DM group [1.3 (0.9-2.2) %] and prior DM group [1.6 (0.7-1.7) %] were significantly higher than those in the non-DM group [-0.2 (-0.3-0.1) %]. Conclusion Nilotinib caused diabetes in 23.8% of the participants, but there were no hyperglycemia-related severe adverse events. Therefore, nilotinib may be safely continued with regular monitoring for the development of diabetes after nilotinib administration.

Indexed as

Antineoplastic AgentsDiabetes MellitusLeukemia, Myelogenous, Chronic, BCR-ABL PositiveProtein Kinase InhibitorsPyrimidinesAdultAgedBlood GlucoseEast Asian PeopleFemaleGlycated HemoglobinHumansJapanMaleMiddle AgedRetrospective StudiesAntineoplastic AgentsBlood GlucoseGlycated HemoglobinnilotinibProtein Kinase InhibitorsPyrimidineschronic myeloid leukemiadiabetes mellitusdyslipidemianilotinibtyrosine kinase inhibitor

Identifiers

PMID39198174
PMCPMC11986321

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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.