The role of tyrosine kinase inhibitor “Lapatinib‿in pulmonary hypertension

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• 作者：Yaser Alkhatib^a ; ^{Yalkhat1@hfhs.org" class="auth_mail" title="E-mail the corresponding author} ; Derar Albashaireh^b ; Tameem Al-Aqtash^c ; Rana Awdish^d
• 关键词：Pulmonary hypertension ; Lapatinib ; Tyrosine kinase inhibitors
• 刊名：Pulmonary Pharmacology & Therapeutics
• 出版年：2016
• 出版时间：April 2016
• 年：2016
• 卷：37
• 期：Complete
• 页码：81-84
• 全文大小：224 K

文摘

Pulmonary Arterial Hypertension (PAH) and cancer share growth factor and protein kinase signaling pathways that result in smooth muscle cell proliferation and vasculopathy. There is little known about the impact of Lapatinib on the pulmonary vasculature. After reporting a case of Lapatinib-induced PAH we investigated the association of Lapatinib with the development of PAH in our institution.

Methods

We reviewed charts for all patients treated with Lapatinib at our institution between 2008 and 2013. Patients who had undergone 2D-echocardiogram both prior to and after treatment were included in the analysis. Increase in Pulmonary artery systolic pressure (PASP) was assessed. Patients were also evaluated in terms of risk factors for non-Group 1 PAH.

Results

A total of 27 patients were found to have 2-D echo done before and after starting treatment with Lapatinib. Six patients were found to have significant increase in their PASP after starting treatment. Right heart catheterization before and after stopping the medication was available in three patient, confirming the diagnosis of PAH with complete resolution after stopping the medication. The median pre-treatment and post treatment PASP in those 6 patients was 29 mmHg and 65.5 mmHg respectively (N = 6; p = 0.027).

Conclusion

Lapatinib might be associated with the development of PAH. PASP should be evaluated in patients who become short of breath while on treatment, and stopping the drug in cases where no other reasons are identified could be associated with reversibility of the elevated pulmonary artery pressure.