Evidence map›Paper›PMID 37106270›Full record

ArticleDrug safety2023

Cardiovascular Toxicities Associated with Anaplastic Lymphoma Kinase Inhibitors: A Disproportionality Analysis of the WHO Pharmacovigilance Database (VigiBase).

Takahiro Niimura, Koji Miyata, Hirofumi Hamano, Yuuki Nounin, Hiroto Unten, Masaki Yoshino, Satoru Mitsuboshi, Fuka Aizawa, Kenta Yagi, Toshihiro Koyama and 5 more

Abstract read
PubMed Publisher
In one paragraph

Article in Drug safety, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
3.1field-weighted citation impact, top 8% 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

10 citing papers in PubMed, 12 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Review
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. 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

15 authors at 8 institutions in 1 country.

Takahiro NiimuraDepartment of Clinical Pharmacology and Therapeutics, Tokushima University Graduate School of Biomedical Sciences, 3-18-15 Kuramoto, Tokushima, 770-8503, Japan. niimura@tokushima-u.ac.jp.ORCID 0000-0003-2033-4246
Koji MiyataDepartment of Clinical Pharmacology and Therapeutics, Tokushima University Graduate School of Biomedical Sciences, 3-18-15 Kuramoto, Tokushima, 770-8503, Japan.
Hirofumi HamanoClinical Research Center for Developmental Therapeutics, Tokushima University Hospital, Tokushima, Japan.
Yuuki NouninDepartment of Clinical Pharmacology and Therapeutics, Tokushima University Graduate School of Biomedical Sciences, 3-18-15 Kuramoto, Tokushima, 770-8503, Japan.
Hiroto UntenDepartment of Clinical Pharmacology and Therapeutics, Tokushima University Graduate School of Biomedical Sciences, 3-18-15 Kuramoto, Tokushima, 770-8503, Japan.
Masaki YoshinoDepartment of Pharmacy, Niigata Prefectural Cancer Center Hospital, Niigata, Japan.
Satoru MitsuboshiDepartment of Pharmacy, Kaetsu Hospital, Niigata, Japan.
Fuka AizawaDepartment of Clinical Pharmacology and Therapeutics, Tokushima University Graduate School of Biomedical Sciences, 3-18-15 Kuramoto, Tokushima, 770-8503, Japan.
Kenta YagiDepartment of Clinical Pharmacology and Therapeutics, Tokushima University Graduate School of Biomedical Sciences, 3-18-15 Kuramoto, Tokushima, 770-8503, Japan.
Toshihiro KoyamaDepartment of Health Data Science, Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences, Okayama University, Okayama, Japan.
Mitsuhiro GodaDepartment of Clinical Pharmacology and Therapeutics, Tokushima University Graduate School of Biomedical Sciences, 3-18-15 Kuramoto, Tokushima, 770-8503, Japan.
Yasunari KandaDivision of Pharmacology, National Institute of Health Sciences, Kawasaki, Japan.
Yuki Izawa-IshizawaDepartment of Clinical Pharmacology and Therapeutics, Tokushima University Graduate School of Biomedical Sciences, 3-18-15 Kuramoto, Tokushima, 770-8503, Japan.
Yoshito ZamamiDepartment of Clinical Pharmacology and Therapeutics, Tokushima University Graduate School of Biomedical Sciences, 3-18-15 Kuramoto, Tokushima, 770-8503, Japan.
Keisuke IshizawaDepartment of Clinical Pharmacology and Therapeutics, Tokushima University Graduate School of Biomedical Sciences, 3-18-15 Kuramoto, Tokushima, 770-8503, Japan.
Tokushima University Hospital · JPOkayama University Hospital · JPTokushima University · JPKaetsu University · JPNational Institute of Health Sciences · JPNiigata Cancer Center Hospital · JPOkayama University · JPTaoka Hospital · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

introductionRecently, cases of cardiovascular toxicities, such as pericarditis, caused by anaplastic lymphoma kinase (ALK) inhibitors have been reported; however, whether these adverse events are common among all ALK inhibitors remains unclear.

aimsThis study aimed to clarify the cardiovascular toxicity profile of ALK inhibitors using an adverse event spontaneous report database.

methodsWe analyzed data from VigiBase, the WHO global database of individual safety reports, from its inception in 1968 to December 2021. We calculated the reporting odds ratio to evaluate the association between ALK inhibitors (crizotinib, ceritinib, alectinib, brigatinib, and lorlatinib) and 21 cardiovascular adverse events. Time to onset of pericarditis from ALK inhibitor administration was analyzed.

resultsOf the 27,994,584 reports, 19,911 involved treatment with ALK inhibitors. Among the 21 cardiovascular toxicities, only pericarditis signals were detected with all five ALK inhibitors (crizotinib [reporting odds ratios (ROR), 4.7; 95% CI 3.63-6.15], ceritinib [ROR, 12.9; 95% CI 9.37-17.79], alectinib [ROR, 4.8; 95% CI 3.15-7.42], brigatinib [ROR, 3.5; 95% CI 1.33-9.46], and lorlatinib [ROR, 6.4; 95% CI 3.60-11.22]). For torsade de pointes/QT prolongation, signals were detected with crizotinib (ROR, 5.0; 95% CI 3.72-6.77) and ceritinib (ROR, 4.2; 95% CI 2.17-8.05), whereas for hypertension, they were identified only with brigatinib (ROR, 3.9; 95% CI 2.88-5.20), and for heart failure, they were detected with alectinib (ROR, 2.2; 95% CI 1.60-2.90), crizotinib (ROR, 2.1; 95% CI 1.72-2.48), and lorlatinib (ROR, 2.0; 95% CI 1.27-3.23). Regarding time-to-onset analysis from drug administration to adverse event reporting, for pericarditis, it ranged from 52.5 days for alectinib to 166.5 days for crizotinib.

conclusionsSystematic evaluation of ALK inhibitor-associated adverse events revealed differences in the cardiotoxicity profiles among ALK inhibitors. Understanding the differences in the cardiovascular toxicity profile of each ALK inhibitor will contribute to safe drug therapy when switching between ALK inhibitors.

Indexed as

Carcinoma, Non-Small-Cell LungLung NeoplasmsPericarditisAminopyridinesAnaplastic Lymphoma KinaseCrizotinibHumansLactamsOrganophosphorus CompoundsPharmacovigilanceProtein Kinase InhibitorsPyrazolesPyrimidinesSulfonesWorld Health OrganizationAminopyridinesAnaplastic Lymphoma KinasebrigatinibceritinibCrizotinibLactamslorlatinibOrganophosphorus CompoundsProtein Kinase InhibitorsPyrazolesPyrimidinesSulfones

Identifiers

PMID37106270
OpenAlexW4367176798

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.