Dasatinib-Induced Recurrent Pleural Effusion in Chronic Myeloid Leukemia: A Case Report and Review of Management Strategies
Dr. Amit Kumar Pandey*, Dr. Krishan Kumar1, Dr. Darshak Mehul Patel2, Dr. Anubha Tiwari3
Correspondence to: Dr. Amit Kumar Pandey
Copyright
© 2026 Dr Amit Kumar Pandey. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
Received: 02 March 2026
Published: 01 April 2026
DOI: https://doi.org/10.5281/zenodo.19430832
Dasatinib is a second-generation tyrosine kinase inhibitor widely used in the management of chronic myeloid leukemia (CML). Pleural effusion is a well-recognised but incompletely understood adverse effect of dasatinib therapy. We report a case of a 34-year-old man with BCR::ABL1-positive CML who developed recurrent bilateral pleural effusion during first-line dasatinib treatment. Extensive evaluation excluded infectious, cardiac, malignant, and thromboembolic causes. The pleural effusion recurred despite therapeutic thoracentesis, prompting permanent discontinuation of dasatinib and transition to nilotinib, following which there was complete clinical and radiological resolution. This case highlights the importance of recognising dasatinib-induced pleural effusion even in young patients without conventional risk factors and discusses current management strategies.
Keywords: Chronic myeloid leukemia; Dasatinib; Pleural effusion; Tyrosine kinase inhibitors; Nilotinib; Drug toxicity
Introduction
ABL1 tyrosine kinase inhibitors (TKIs) has transformed chronic myeloid leukemia (CML) into a chronic, manageable condition with near-normal life expectancy. However, TKIs are associated with off-target toxicities that may significantly impact morbidity and treatment adherence.
Among available TKIs, dasatinib is uniquely associated with pleural effusion, with reported incidences ranging from 14% to 30%. The mechanism is thought to involve immune-mediated serosal inflammation and kinase inhibition beyond BCR::ABL1. Despite increasing clinical recognition, uncertainty remains regarding optimal management, particularly in cases of recurrence. This report contributes to the growing literature on dasatinib-induced pleural effusion and supports early drug switching in severe or recurrent cases.
Case Presentation
A 34-year-old man presented with progressively worsening exertional dyspnea, intermittent non-productive cough, fatigue, bilateral lower limb edema, and abdominal distension. Symptoms had been present for approximately two months, with significant worsening over the preceding 15 days.
He had been diagnosed with chronic myeloid leukemia at 26 years of age and was receiving dasatinib 75 mg twice daily as first-line therapy. He had no history of cardiovascular disease, pulmonary illness, autoimmune disorders, hypertension, or smoking. There was no history of tuberculosis or occupational exposure.
On examination, breath sounds were reduced bilaterally with dullness to percussion over the lower lung fields. Other systemic examination findings were unremarkable.
Investigations
Chest radiography revealed bilateral massive pleural effusions. Diagnostic and therapeutic thoracentesis yielded approximately 2 litres of hemorrhagic fluid.
Pleural fluid analysis showed:
• Total leukocyte count: 1100 cells/mm³
• Differential count: lymphocytes 80%, polymorphs 20%
• Protein: 5.37 g/dL
• LDH: 240 IU/L
• Glucose: 141 mg/dL
• pH: 7.5
• ADA: 21 U/L
Cytological examination was negative for malignant cells. Microbiological evaluation, including acid-fast bacilli staining, was negative. Echocardiography showed normal cardiac function. There was no evidence of renal or hepatic dysfunction.
Differential Diagnosis
• Tuberculous pleural effusion
• Malignant pleural effusion
• Cardiac failure–related effusion
• Pulmonary embolism
• Drug-induced pleural effusion (dasatinib)
Given the lymphocyte-predominant exudate, negative workup, and temporal association with dasatinib therapy, a diagnosis of dasatinib-induced pleural effusion was made.
Treatment
Initial management included therapeutic thoracentesis and supportive care. Despite transient symptomatic improvement, the patient re-presented with recurrent dyspnea, and repeat imaging confirmed re-accumulation of bilateral pleural effusion.
In view of recurrence and severity, dasatinib was permanently discontinued. The patient was switched to nilotinib, considering its lower incidence of pleural toxicity.
Outcome and Follow-Up
Following the change in therapy, the patient experienced complete resolution of symptoms. Follow-up chest radiography showed near-complete resolution of pleural effusion. At subsequent visits, there was no recurrence of effusion, and the patient remained clinically stable on nilotinib with continued hematological response.
Discussion
Pleural effusion is a distinctive adverse effect of dasatinib and is uncommon with other TKIs. Proposed mechanisms include platelet-derived growth factor receptor-β inhibition, SRC kinase inhibition, and immune-mediated lymphocytic serositis. Dasatinib-induced effusions are typically exudative, lymphocyte-predominant, and non-malignant.
While older age and comorbidities are considered risk factors, this case demonstrates that pleural effusion may occur in young, otherwise healthy individuals and during first-line therapy. Recurrence rates are high, and repeated dose interruptions or reductions may be insufficient.
Switching to an alternative TKI such as nilotinib or bosutinib has been shown to be effective in preventing recurrence and maintaining disease control, as illustrated in this case.
Learning Points
• Dasatinib-induced pleural effusion should be considered in any CML patient presenting with unexplained dyspnea.
• Pleural effusion may occur early, recur frequently, and affect patients without traditional risk factors.
• Recurrent pleural effusion often necessitates permanent discontinuation of dasatinib.
• Switching to an alternative TKI such as nilotinib can lead to sustained resolution without compromising disease control.
Patient Perspective
The patient reported significant improvement in breathing and overall quality of life after the change in medication and expressed relief at the resolution of recurrent symptoms.
Conclusion
This case underscores that dasatinib-induced pleural effusion can occur early, recur rapidly, and affect patients without conventional risk factors. Permanent discontinuation of dasatinib with transition to nilotinib resulted in sustained resolution without recurrence. Clinicians should maintain a high index of suspicion for this adverse event and tailor management strategies based on severity, recurrence, and overall disease response.
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