Bosutinib induced pleural effusions: Case report and review of tyrosine kinase inhibitors induced pulmonary toxicity

Abstract

Tyrosine kinase inhibitors are known to cause pulmonary complications. We report a case of bosutinib related bilateral pleural effusions in a patient with chronic myeloid leukemia. Characteristics of the pleural fluid are presented. We also discuss other tyrosine kinase inhibitors induced pulmonary toxicities, including pulmonary hypertension and interstitial lung disease.

Bosutinib‐associated interstitial lung disease and pleural effusion: A case report and literature review

“…17 Moguillansky et al reported a case of bosutinib-associated pleural effusions that resolved after discontinuation of the medication. 7 Jutant et al reported a case of bosutinib-related pneumonitis. 12 As in the case we are presenting, bosutinib may also be associated with interstitial lung disease and pleural effusion; a spectrum of lung complications previously described with other TKIs.…”

“…The most common side effects are gastrointestinal, followed by thrombocytopenia and abnormal liver function tests 6 . However, there have been cases reporting pulmonary injury related to bosutinib 7 . Here, we discuss a case of bosutinib‐induced interstitial lung disease and pleural effusion.…”

“…6 However, there have been cases reporting pulmonary injury related to bosutinib. 7 Here, we discuss a case of bosutinib-induced interstitial lung disease and pleural effusion.…”

Bosutinib – related pleural effusion in patients with chronic myeloid leukemia

“…It is a dual Src/Abl TKI, and it exhibits minimal inhibitory activity against c-KIT or PDGFR [21]. Diarrhea is the most common AE of bosutinib therapy, and PE can also be observed in patients receiving bosutinib [22], but rarely when bosutinib is used in newly diagnosed cases and as second-line treatment following imatinib failure.…”

Pulmonary hypertension: Molecular aspects of current therapeutic intervention and future direction

“…Vascular adverse events are an evolving dilemma in patients with chronic pulmonary disorders and tyrosine kinase inhibitors can directly cause pulmonary endothelial cell toxicity via the production of mitochondrial reactive oxygen species (Moguillansky, Fakih, & Wingard, 2017). Platelet-derived growth factors (PDGFs) and their receptors (PDGFRs) have served as prototypes for growth factor and receptor tyrosine kinase (Andrae, Gallini, & Betsholtz, 2008).…”