Dasatinib-Induced Pulmonary Arterial Hypertension<\/a><\/h1>\nCan J Cardiol.\u00a02019 Nov;35(11):1604.e1-1604.e3.<\/span>\u00a0doi: 10.1016\/j.cjca.2019.08.002.\u00a0<\/span>Epub 2019 Aug 8.<\/span><\/div>\n\n\n\nAuthors<\/h3>\nEvan Orlikow<\/a>\u00a0\u00a01\u00a0<\/sup>,\u00a0<\/span>Jason Weatherald<\/a>\u00a0\u00a02\u00a0<\/sup>,\u00a0<\/span>Naushad Hirani<\/a> \u00a03<\/sup><\/span><\/div>\n<\/div>\n<\/div>\n<\/div>\n\n- PMID:\u00a031590985<\/a><\/span><\/li>\n
- DOI:\u00a010.1016\/j.cjca.2019.08.002<\/a><\/span><\/li>\n<\/ul>\n<\/header>\n\n
Abstract<\/h2>\n\nA 73-year-old woman with chronic myeloid leukemia developed severe pulmonary arterial hypertension (PAH) and pleural effusions after treatment with dasatinib. During workup, partial anomalous pulmonary venous connection and a sinus venosus atrial septal defect were found; these anomalies may have predisposed her to developing this rare and life-threatening condition. Fortunately, her PAH was completely reversible by discontinuation of dasatinib. This case highlights dasatinib’s ability to cause PAH in patients predisposed to pulmonary vascular disease.<\/p>\n<\/div>\n<\/div>\n
Copyright \u00a9 2019 Canadian Cardiovascular Society. Published by Elsevier Inc. All rights reserved.<\/p>\n\nFull text links<\/h3>\n![\"Elsevier](\"https:\/\/ci3.googleusercontent.com\/proxy\/o_kRcBR6vJxq3Z80xpxgtw7rbzb7yl4aFEeyQc-3qG5wZB3fpqcDdylHlPHYznJjJMjWy1pdXaifxRfCSwOcp8ORo1i1QKQdZvT0iVFQbZbVTQi6RKEJh38DLl9vbdP3mxUbfirLWL0U1uyPgtga0WG2TpD2f17h4jV5XCRgUw=s0-d-e1-ft#https:\/\/cdn.ncbi.nlm.nih.gov\/corehtml\/query\/egifs\/https:--linkinghub.elsevier.com-ihub-images-PubMedLink.gif\")
<\/a><\/div>\n<\/section>\n<\/div>\n<\/td>\n<\/tr>\n\n\n3.<\/div>\n<\/td>\n\n\n\nDasatinib-induced pulmonary arterial hypertension – A rare late complication<\/a><\/h1>\nJ Oncol Pharm Pract.\u00a02019 Apr;25(3):727-730.<\/span>\u00a0doi: 10.1177\/1078155217753740.\u00a0<\/span>Epub 2018 Jan 17.<\/span><\/div>\n\n\n\nAuthors<\/h3>\nUroosa Ibrahim<\/a>\u00a0\u00a01\u00a0<\/sup>,\u00a0<\/span>Amina Saqib<\/a>\u00a0\u00a02\u00a0<\/sup>,\u00a0<\/span>Vidhya Dhar<\/a>\u00a0\u00a03\u00a0<\/sup>,\u00a0<\/span>Marcel Odaimi<\/a>\u00a0\u00a01<\/sup><\/span><\/div>\n<\/div>\n\nAffiliations<\/h3>\n\n- 1<\/sup>\u00a0<\/span>1 Department of Hematology\/Oncology, Staten Island University Hospital, Staten Island, New York, USA.<\/li>\n
- 2<\/sup>\u00a0<\/span>2 Department of Pulmonary\/Critical Care, Staten Island University Hospital, Staten Island, New York, USA.<\/li>\n
- 3<\/sup>\u00a0<\/span>3 Department of Medicine, Staten Island University Hospital, Staten Island, New York, USA.<\/li>\n<\/ul>\n<\/div>\n<\/div>\n<\/div>\n
\n- PMID:\u00a029343154<\/a><\/span><\/li>\n
- DOI:\u00a010.1177\/1078155217753740<\/a><\/span><\/li>\n<\/ul>\n<\/header>\n\n
Abstract<\/h2>\n\nDasatinib is a dual Src\/Abl tyrosine kinase inhibitor approved for frontline and second line treatment of chronic phase chronic myelogenous leukemia. Pulmonary arterial hypertension is defined by an increase in mean pulmonary arterial pressure >25 mmHg at rest. Dasatinib-induced pulmonary hypertension has been reported in less than 1% of patients on chronic dasatinib treatment for chronic myelogenous leukemia. The pulmonary arterial hypertension from dasatinib may be categorized as either group 1 (drug-induced) or group 5 based on various mechanisms that may be involved including the pathogenesis of the disease process of chronic myelogenous leukemia. There have been reports of dasatinib-induced pulmonary arterial hypertension being reversible. We report a case of pulmonary arterial hypertension in a 46-year-old female patient with chronic phase chronic myelogenous leukemia on dasatinib treatment for over 10 years. She had significant improvement in symptoms after discontinuation of dasatinib and initiation of vasodilators. Several clinical questions arise once patients experience significant adverse effects as discussed in our case.<\/p>\n<\/div>\n
Keywords:\u00a0<\/span><\/strong>CML; Chronic myeloid leukemia; dasatinib; pulmonary arterial hypertension; tyrosine kinase inhibitor.<\/p>\n<\/div>\n\nFull text links<\/h3>\n![\"Atypon\"](\"https:\/\/ci5.googleusercontent.com\/proxy\/mfr0dHF3AMRagWqDuybIT4rtMPQBopOtKNg-QtojWJfV6ag0Cqa4far8lq2Pi1l8FWAG7x1bcdDGtS13WNYa4spxd1F0jJh_GbXEH1TZWv72o5JYQPSWVcf2VYFYdSd67ONdo_WPCDNE4jBWTayYYoRmedf2h63Qrqx51FARZaQ=s0-d-e1-ft#https:\/\/cdn.ncbi.nlm.nih.gov\/corehtml\/query\/egifs\/https:--journals.sagepub.com-pb-assets-sage-pubmed-sage.png\")
<\/a><\/div>\n<\/section>\n<\/div>\n<\/td>\n<\/tr>\n\n\n4.<\/div>\n<\/td>\n\n\n\n[Reversible dasatinib-related pulmonary arterial hypertension in a CML patient]<\/a><\/h1>\nRinsho Ketsueki.\u00a02016 May;57(5):618-23.<\/span>\u00a0doi: 10.11406\/rinketsu.57.618.<\/span><\/div>\n[Article in Japanese]<\/div>\n\n\n\nAuthors<\/h3>\nJoji Nagasaki<\/a>\u00a0\u00a01\u00a0<\/sup>,\u00a0<\/span>Yasutaka Aoyama<\/a>,\u00a0<\/span>Yuta Nomoto<\/a>,\u00a0<\/span>Kentaro Ido<\/a>,\u00a0<\/span>Hiroyoshi Ichihara<\/a>,\u00a0<\/span>Atsuko Mugitani<\/a><\/span><\/div>\n<\/div>\n\nAffiliation<\/h3>\n\n- 1<\/sup>\u00a0<\/span>Department of Hematology, Seichokai Fuchu Hospital.<\/li>\n<\/ul>\n<\/div>\n<\/div>\n<\/div>\n
\n- PMID:\u00a027263788<\/a><\/span><\/li>\n
- DOI:\u00a010.11406\/rinketsu.57.618<\/a><\/span><\/li>\n<\/ul>\n<\/header>\n\n
Abstract<\/h2>\n\nA 59-year-old man diagnosed with the chronic phase of chronic myeloid leukemia (CML) in June 2011 was started on dasatinib (100 mg\/day). He had no signs of pleural effusion (PE) or right heart failure before treatment, but symptoms of PE and dyspnea (New York Heart Association class III) appeared in January 2013 and May 2014, respectively. Doppler transthoracic echocardiography and right heart catheterization revealed pulmonary arterial hypertension (PAH) with an estimated pulmonary artery systolic pressure (PASP) of 80 mmHg and estimated mean pulmonary artery pressure of 29 mmHg. Rheumatoid factor, antinuclear antibody, dsDNA antibody, and SCL70 were not elevated, and computed tomography confirmed the absence of a pulmonary embolism. Therefore, dasatinib-related PAH was diagnosed and treatment with this agent was discontinued. The PASP had decreased to 51 and 40 mmHg at one month and one year, respectively, after dasatinib discontinuation. This patient developed PAH while receiving dasatinib administration and only discontinuation of this agent improved his symptoms. The possibility that dasatinib can cause PAH must be considered before administering this agent to patients with CML.<\/p>\n<\/div>\n<\/div>\n\nFull text links<\/h3>\n![\"J-STAGE,](\"https:\/\/ci5.googleusercontent.com\/proxy\/bjU41InZkhOfBtqRj-JbUt0jYpXUHU8vtKx568viKuOmSLYFbS8U6G7HmP-1Ou7f4kaIv3znqsUH-Zp_XoYp03IClxKDTDdevo1Iqy65HOv9UJFvmvncVBa0sLBb7kwMV6sH_mcm2fUQTSqgO7NRnNbAt4ka=s0-d-e1-ft#https:\/\/cdn.ncbi.nlm.nih.gov\/corehtml\/query\/egifs\/http:--linkout.jstage.jst.go.jp-logo_nonfree.gif\")
<\/a><\/div>\n<\/section>\n<\/div>\n<\/td>\n<\/tr>\n\n\n5.<\/div>\n<\/td>\n\n\n\nBeneficial Effects of Imatinib in a Patient with Suspected Pulmonary Veno-Occlusive Disease<\/a><\/h1>\nTohoku J Exp Med.\u00a02019 Feb;247(2):69-73.<\/span>\u00a0doi: 10.1620\/tjem.247.69.<\/span><\/div>\n\n\n\nAuthors<\/h3>\nHaruka Sato<\/a>\u00a0\u00a01\u00a0<\/sup>,\u00a0<\/span>Koichiro Sugimura<\/a>\u00a0\u00a01\u00a0<\/sup>,\u00a0<\/span>Masanobu Miura<\/a>\u00a0\u00a01\u00a0<\/sup>,\u00a0<\/span>Ryo Konno<\/a>\u00a0\u00a01\u00a0<\/sup>,\u00a0<\/span>Katsuya Kozu<\/a>\u00a0\u00a01\u00a0<\/sup>,\u00a0<\/span>Nobuhiro Yaoita<\/a>\u00a0\u00a01\u00a0<\/sup>,\u00a0<\/span>Toru Shimizu<\/a>\u00a0\u00a01\u00a0<\/sup>,\u00a0<\/span>Saori Yamamoto<\/a>\u00a0\u00a01\u00a0<\/sup>,\u00a0<\/span>Tatsuo Aoki<\/a>\u00a0\u00a01\u00a0<\/sup>,\u00a0<\/span>Shunsuke Tatebe<\/a>\u00a0\u00a01\u00a0<\/sup>,\u00a0<\/span>Kimio Satoh<\/a>\u00a0\u00a01\u00a0<\/sup>,\u00a0<\/span>Hiroaki Shimokawa<\/a>\u00a0\u00a01<\/sup><\/span><\/div>\n<\/div>\n\nAffiliation<\/h3>\n\n- 1<\/sup>\u00a0<\/span>Department of Cardiovascular Medicine, Tohoku University Graduate School of Medicine.<\/li>\n<\/ul>\n<\/div>\n<\/div>\n<\/div>\n
\n- PMID:\u00a030700638<\/a><\/span><\/li>\n
- DOI:\u00a010.1620\/tjem.247.69<\/a><\/span><\/li>\n<\/ul>\n
Free article<\/span><\/p>\n<\/header>\n\nAbstract<\/h2>\n\nPulmonary veno-occlusive disease (PVOD) is a rare form of pulmonary hypertension (PH). The prognosis of PVOD patients remains poor, since no effective medical therapy is yet available. Imatinib is a tyrosine kinase inhibitor specific for platelet-derived growth factor receptor and is expected as a treatment option for pulmonary arterial hypertension (PAH). Recently, it has been reported that imatinib improved functional capacity of a patient with PVOD. We here report a patient with suspected PVOD who has been successfully treated with imatinib and is alive for 6 years after diagnosis. A 57-year-old woman was admitted to a hospital for severe dyspnea. Echocardiography suggested the presence of PH, because tricuspid regurgitation pressure gradient was elevated. The patient was then transferred to our hospital by an ambulance ahead of schedule due to fever and worsening dyspnea. Because the patient had no left heart disease, we diagnosed that she had PAH associated with severe right heart failure. We immediately started treatment with nitric oxide (NO) for her severe hypoxia; however, it caused pulmonary edema. We suspected PVOD from CT characteristics and pulmonary edema after PAH-targeted vasodilator therapy, and then started oral imatinib treatment. In response to imatinib, her pulmonary edema gradually improved. Since then, the patient has been alive for 6 years with imatinib and pulmonary vasodilators. At present, lung transplantation is the only effective therapy for PVOD with limited availability. We therefore propose that imatinib may be a treatment option for PVOD and a bridge to lung transplantation.<\/p>\n<\/div>\n
Keywords:\u00a0<\/span><\/strong>imatinib; pulmonary arterial hypertension; pulmonary hypertension; pulmonary veno-occlusive disease; transplantation.<\/p>\n<\/div>\n\n
Authors<\/h3>\nEvan Orlikow<\/a>\u00a0\u00a01\u00a0<\/sup>,\u00a0<\/span>Jason Weatherald<\/a>\u00a0\u00a02\u00a0<\/sup>,\u00a0<\/span>Naushad Hirani<\/a> \u00a03<\/sup><\/span><\/div>\n<\/div>\n<\/div>\n<\/div>\n\n- PMID:\u00a031590985<\/a><\/span><\/li>\n
- DOI:\u00a010.1016\/j.cjca.2019.08.002<\/a><\/span><\/li>\n<\/ul>\n<\/header>\n\n
Abstract<\/h2>\n\nA 73-year-old woman with chronic myeloid leukemia developed severe pulmonary arterial hypertension (PAH) and pleural effusions after treatment with dasatinib. During workup, partial anomalous pulmonary venous connection and a sinus venosus atrial septal defect were found; these anomalies may have predisposed her to developing this rare and life-threatening condition. Fortunately, her PAH was completely reversible by discontinuation of dasatinib. This case highlights dasatinib’s ability to cause PAH in patients predisposed to pulmonary vascular disease.<\/p>\n<\/div>\n<\/div>\n
Copyright \u00a9 2019 Canadian Cardiovascular Society. Published by Elsevier Inc. All rights reserved.<\/p>\n\nFull text links<\/h3>\n<\/a><\/div>\n<\/section>\n<\/div>\n<\/td>\n<\/tr>\n\n\n3.<\/div>\n<\/td>\n\n\n\nDasatinib-induced pulmonary arterial hypertension – A rare late complication<\/a><\/h1>\nJ Oncol Pharm Pract.\u00a02019 Apr;25(3):727-730.<\/span>\u00a0doi: 10.1177\/1078155217753740.\u00a0<\/span>Epub 2018 Jan 17.<\/span><\/div>\n\n\n\nAuthors<\/h3>\nUroosa Ibrahim<\/a>\u00a0\u00a01\u00a0<\/sup>,\u00a0<\/span>Amina Saqib<\/a>\u00a0\u00a02\u00a0<\/sup>,\u00a0<\/span>Vidhya Dhar<\/a>\u00a0\u00a03\u00a0<\/sup>,\u00a0<\/span>Marcel Odaimi<\/a>\u00a0\u00a01<\/sup><\/span><\/div>\n<\/div>\n\nAffiliations<\/h3>\n\n- 1<\/sup>\u00a0<\/span>1 Department of Hematology\/Oncology, Staten Island University Hospital, Staten Island, New York, USA.<\/li>\n
- 2<\/sup>\u00a0<\/span>2 Department of Pulmonary\/Critical Care, Staten Island University Hospital, Staten Island, New York, USA.<\/li>\n
- 3<\/sup>\u00a0<\/span>3 Department of Medicine, Staten Island University Hospital, Staten Island, New York, USA.<\/li>\n<\/ul>\n<\/div>\n<\/div>\n<\/div>\n
\n- PMID:\u00a029343154<\/a><\/span><\/li>\n
- DOI:\u00a010.1177\/1078155217753740<\/a><\/span><\/li>\n<\/ul>\n<\/header>\n\n
Abstract<\/h2>\n\nDasatinib is a dual Src\/Abl tyrosine kinase inhibitor approved for frontline and second line treatment of chronic phase chronic myelogenous leukemia. Pulmonary arterial hypertension is defined by an increase in mean pulmonary arterial pressure >25 mmHg at rest. Dasatinib-induced pulmonary hypertension has been reported in less than 1% of patients on chronic dasatinib treatment for chronic myelogenous leukemia. The pulmonary arterial hypertension from dasatinib may be categorized as either group 1 (drug-induced) or group 5 based on various mechanisms that may be involved including the pathogenesis of the disease process of chronic myelogenous leukemia. There have been reports of dasatinib-induced pulmonary arterial hypertension being reversible. We report a case of pulmonary arterial hypertension in a 46-year-old female patient with chronic phase chronic myelogenous leukemia on dasatinib treatment for over 10 years. She had significant improvement in symptoms after discontinuation of dasatinib and initiation of vasodilators. Several clinical questions arise once patients experience significant adverse effects as discussed in our case.<\/p>\n<\/div>\n
Keywords:\u00a0<\/span><\/strong>CML; Chronic myeloid leukemia; dasatinib; pulmonary arterial hypertension; tyrosine kinase inhibitor.<\/p>\n<\/div>\n\nFull text links<\/h3>\n<\/a><\/div>\n<\/section>\n<\/div>\n<\/td>\n<\/tr>\n\n\n4.<\/div>\n<\/td>\n\n\n\n[Reversible dasatinib-related pulmonary arterial hypertension in a CML patient]<\/a><\/h1>\nRinsho Ketsueki.\u00a02016 May;57(5):618-23.<\/span>\u00a0doi: 10.11406\/rinketsu.57.618.<\/span><\/div>\n[Article in Japanese]<\/div>\n\n\n\nAuthors<\/h3>\nJoji Nagasaki<\/a>\u00a0\u00a01\u00a0<\/sup>,\u00a0<\/span>Yasutaka Aoyama<\/a>,\u00a0<\/span>Yuta Nomoto<\/a>,\u00a0<\/span>Kentaro Ido<\/a>,\u00a0<\/span>Hiroyoshi Ichihara<\/a>,\u00a0<\/span>Atsuko Mugitani<\/a><\/span><\/div>\n<\/div>\n\nAffiliation<\/h3>\n\n- 1<\/sup>\u00a0<\/span>Department of Hematology, Seichokai Fuchu Hospital.<\/li>\n<\/ul>\n<\/div>\n<\/div>\n<\/div>\n
\n- PMID:\u00a027263788<\/a><\/span><\/li>\n
- DOI:\u00a010.11406\/rinketsu.57.618<\/a><\/span><\/li>\n<\/ul>\n<\/header>\n\n
Abstract<\/h2>\n\nA 59-year-old man diagnosed with the chronic phase of chronic myeloid leukemia (CML) in June 2011 was started on dasatinib (100 mg\/day). He had no signs of pleural effusion (PE) or right heart failure before treatment, but symptoms of PE and dyspnea (New York Heart Association class III) appeared in January 2013 and May 2014, respectively. Doppler transthoracic echocardiography and right heart catheterization revealed pulmonary arterial hypertension (PAH) with an estimated pulmonary artery systolic pressure (PASP) of 80 mmHg and estimated mean pulmonary artery pressure of 29 mmHg. Rheumatoid factor, antinuclear antibody, dsDNA antibody, and SCL70 were not elevated, and computed tomography confirmed the absence of a pulmonary embolism. Therefore, dasatinib-related PAH was diagnosed and treatment with this agent was discontinued. The PASP had decreased to 51 and 40 mmHg at one month and one year, respectively, after dasatinib discontinuation. This patient developed PAH while receiving dasatinib administration and only discontinuation of this agent improved his symptoms. The possibility that dasatinib can cause PAH must be considered before administering this agent to patients with CML.<\/p>\n<\/div>\n<\/div>\n\nFull text links<\/h3>\n<\/a><\/div>\n<\/section>\n<\/div>\n<\/td>\n<\/tr>\n\n\n5.<\/div>\n<\/td>\n\n\n\nBeneficial Effects of Imatinib in a Patient with Suspected Pulmonary Veno-Occlusive Disease<\/a><\/h1>\nTohoku J Exp Med.\u00a02019 Feb;247(2):69-73.<\/span>\u00a0doi: 10.1620\/tjem.247.69.<\/span><\/div>\n\n\n\nAuthors<\/h3>\nHaruka Sato<\/a>\u00a0\u00a01\u00a0<\/sup>,\u00a0<\/span>Koichiro Sugimura<\/a>\u00a0\u00a01\u00a0<\/sup>,\u00a0<\/span>Masanobu Miura<\/a>\u00a0\u00a01\u00a0<\/sup>,\u00a0<\/span>Ryo Konno<\/a>\u00a0\u00a01\u00a0<\/sup>,\u00a0<\/span>Katsuya Kozu<\/a>\u00a0\u00a01\u00a0<\/sup>,\u00a0<\/span>Nobuhiro Yaoita<\/a>\u00a0\u00a01\u00a0<\/sup>,\u00a0<\/span>Toru Shimizu<\/a>\u00a0\u00a01\u00a0<\/sup>,\u00a0<\/span>Saori Yamamoto<\/a>\u00a0\u00a01\u00a0<\/sup>,\u00a0<\/span>Tatsuo Aoki<\/a>\u00a0\u00a01\u00a0<\/sup>,\u00a0<\/span>Shunsuke Tatebe<\/a>\u00a0\u00a01\u00a0<\/sup>,\u00a0<\/span>Kimio Satoh<\/a>\u00a0\u00a01\u00a0<\/sup>,\u00a0<\/span>Hiroaki Shimokawa<\/a>\u00a0\u00a01<\/sup><\/span><\/div>\n<\/div>\n\nAffiliation<\/h3>\n\n- 1<\/sup>\u00a0<\/span>Department of Cardiovascular Medicine, Tohoku University Graduate School of Medicine.<\/li>\n<\/ul>\n<\/div>\n<\/div>\n<\/div>\n
\n- PMID:\u00a030700638<\/a><\/span><\/li>\n
- DOI:\u00a010.1620\/tjem.247.69<\/a><\/span><\/li>\n<\/ul>\n
Free article<\/span><\/p>\n<\/header>\n\nAbstract<\/h2>\n\nPulmonary veno-occlusive disease (PVOD) is a rare form of pulmonary hypertension (PH). The prognosis of PVOD patients remains poor, since no effective medical therapy is yet available. Imatinib is a tyrosine kinase inhibitor specific for platelet-derived growth factor receptor and is expected as a treatment option for pulmonary arterial hypertension (PAH). Recently, it has been reported that imatinib improved functional capacity of a patient with PVOD. We here report a patient with suspected PVOD who has been successfully treated with imatinib and is alive for 6 years after diagnosis. A 57-year-old woman was admitted to a hospital for severe dyspnea. Echocardiography suggested the presence of PH, because tricuspid regurgitation pressure gradient was elevated. The patient was then transferred to our hospital by an ambulance ahead of schedule due to fever and worsening dyspnea. Because the patient had no left heart disease, we diagnosed that she had PAH associated with severe right heart failure. We immediately started treatment with nitric oxide (NO) for her severe hypoxia; however, it caused pulmonary edema. We suspected PVOD from CT characteristics and pulmonary edema after PAH-targeted vasodilator therapy, and then started oral imatinib treatment. In response to imatinib, her pulmonary edema gradually improved. Since then, the patient has been alive for 6 years with imatinib and pulmonary vasodilators. At present, lung transplantation is the only effective therapy for PVOD with limited availability. We therefore propose that imatinib may be a treatment option for PVOD and a bridge to lung transplantation.<\/p>\n<\/div>\n
Keywords:\u00a0<\/span><\/strong>imatinib; pulmonary arterial hypertension; pulmonary hypertension; pulmonary veno-occlusive disease; transplantation.<\/p>\n<\/div>\n\n
- \n
- PMID:\u00a031590985<\/a><\/span><\/li>\n
- DOI:\u00a010.1016\/j.cjca.2019.08.002<\/a><\/span><\/li>\n<\/ul>\n<\/header>\n
\nAbstract<\/h2>\n
\nA 73-year-old woman with chronic myeloid leukemia developed severe pulmonary arterial hypertension (PAH) and pleural effusions after treatment with dasatinib. During workup, partial anomalous pulmonary venous connection and a sinus venosus atrial septal defect were found; these anomalies may have predisposed her to developing this rare and life-threatening condition. Fortunately, her PAH was completely reversible by discontinuation of dasatinib. This case highlights dasatinib’s ability to cause PAH in patients predisposed to pulmonary vascular disease.<\/p>\n<\/div>\n<\/div>\n
Copyright \u00a9 2019 Canadian Cardiovascular Society. Published by Elsevier Inc. All rights reserved.<\/p>\n
\n Full text links<\/h3>\n
<\/a><\/div>\n<\/section>\n<\/div>\n<\/td>\n<\/tr>\n\n \n 3.<\/div>\n<\/td>\n\n \n\n Dasatinib-induced pulmonary arterial hypertension – A rare late complication<\/a><\/h1>\n
J Oncol Pharm Pract.\u00a02019 Apr;25(3):727-730.<\/span>\u00a0doi: 10.1177\/1078155217753740.\u00a0<\/span>Epub 2018 Jan 17.<\/span><\/div>\n\n\n\nAuthors<\/h3>\n
Uroosa Ibrahim<\/a>\u00a0\u00a01\u00a0<\/sup>,\u00a0<\/span>Amina Saqib<\/a>\u00a0\u00a02\u00a0<\/sup>,\u00a0<\/span>Vidhya Dhar<\/a>\u00a0\u00a03\u00a0<\/sup>,\u00a0<\/span>Marcel Odaimi<\/a>\u00a0\u00a01<\/sup><\/span><\/div>\n<\/div>\n\nAffiliations<\/h3>\n
- \n
- 1<\/sup>\u00a0<\/span>1 Department of Hematology\/Oncology, Staten Island University Hospital, Staten Island, New York, USA.<\/li>\n
- 2<\/sup>\u00a0<\/span>2 Department of Pulmonary\/Critical Care, Staten Island University Hospital, Staten Island, New York, USA.<\/li>\n
- 3<\/sup>\u00a0<\/span>3 Department of Medicine, Staten Island University Hospital, Staten Island, New York, USA.<\/li>\n<\/ul>\n<\/div>\n<\/div>\n<\/div>\n
- \n
- PMID:\u00a029343154<\/a><\/span><\/li>\n
- DOI:\u00a010.1177\/1078155217753740<\/a><\/span><\/li>\n<\/ul>\n<\/header>\n
\nAbstract<\/h2>\n
\nDasatinib is a dual Src\/Abl tyrosine kinase inhibitor approved for frontline and second line treatment of chronic phase chronic myelogenous leukemia. Pulmonary arterial hypertension is defined by an increase in mean pulmonary arterial pressure >25 mmHg at rest. Dasatinib-induced pulmonary hypertension has been reported in less than 1% of patients on chronic dasatinib treatment for chronic myelogenous leukemia. The pulmonary arterial hypertension from dasatinib may be categorized as either group 1 (drug-induced) or group 5 based on various mechanisms that may be involved including the pathogenesis of the disease process of chronic myelogenous leukemia. There have been reports of dasatinib-induced pulmonary arterial hypertension being reversible. We report a case of pulmonary arterial hypertension in a 46-year-old female patient with chronic phase chronic myelogenous leukemia on dasatinib treatment for over 10 years. She had significant improvement in symptoms after discontinuation of dasatinib and initiation of vasodilators. Several clinical questions arise once patients experience significant adverse effects as discussed in our case.<\/p>\n<\/div>\n
Keywords:\u00a0<\/span><\/strong>CML; Chronic myeloid leukemia; dasatinib; pulmonary arterial hypertension; tyrosine kinase inhibitor.<\/p>\n<\/div>\n
\n Full text links<\/h3>\n
<\/a><\/div>\n<\/section>\n<\/div>\n<\/td>\n<\/tr>\n\n \n 4.<\/div>\n<\/td>\n\n \n\n [Reversible dasatinib-related pulmonary arterial hypertension in a CML patient]<\/a><\/h1>\n
Rinsho Ketsueki.\u00a02016 May;57(5):618-23.<\/span>\u00a0doi: 10.11406\/rinketsu.57.618.<\/span><\/div>\n[Article in Japanese]<\/div>\n\n\n\nAuthors<\/h3>\n
Joji Nagasaki<\/a>\u00a0\u00a01\u00a0<\/sup>,\u00a0<\/span>Yasutaka Aoyama<\/a>,\u00a0<\/span>Yuta Nomoto<\/a>,\u00a0<\/span>Kentaro Ido<\/a>,\u00a0<\/span>Hiroyoshi Ichihara<\/a>,\u00a0<\/span>Atsuko Mugitani<\/a><\/span><\/div>\n<\/div>\n\nAffiliation<\/h3>\n
- \n
- 1<\/sup>\u00a0<\/span>Department of Hematology, Seichokai Fuchu Hospital.<\/li>\n<\/ul>\n<\/div>\n<\/div>\n<\/div>\n
- \n
- PMID:\u00a027263788<\/a><\/span><\/li>\n
- DOI:\u00a010.11406\/rinketsu.57.618<\/a><\/span><\/li>\n<\/ul>\n<\/header>\n
\nAbstract<\/h2>\n
\nA 59-year-old man diagnosed with the chronic phase of chronic myeloid leukemia (CML) in June 2011 was started on dasatinib (100 mg\/day). He had no signs of pleural effusion (PE) or right heart failure before treatment, but symptoms of PE and dyspnea (New York Heart Association class III) appeared in January 2013 and May 2014, respectively. Doppler transthoracic echocardiography and right heart catheterization revealed pulmonary arterial hypertension (PAH) with an estimated pulmonary artery systolic pressure (PASP) of 80 mmHg and estimated mean pulmonary artery pressure of 29 mmHg. Rheumatoid factor, antinuclear antibody, dsDNA antibody, and SCL70 were not elevated, and computed tomography confirmed the absence of a pulmonary embolism. Therefore, dasatinib-related PAH was diagnosed and treatment with this agent was discontinued. The PASP had decreased to 51 and 40 mmHg at one month and one year, respectively, after dasatinib discontinuation. This patient developed PAH while receiving dasatinib administration and only discontinuation of this agent improved his symptoms. The possibility that dasatinib can cause PAH must be considered before administering this agent to patients with CML.<\/p>\n<\/div>\n<\/div>\n
\n Full text links<\/h3>\n
<\/a><\/div>\n<\/section>\n<\/div>\n<\/td>\n<\/tr>\n\n \n 5.<\/div>\n<\/td>\n\n \n\n Beneficial Effects of Imatinib in a Patient with Suspected Pulmonary Veno-Occlusive Disease<\/a><\/h1>\n
Tohoku J Exp Med.\u00a02019 Feb;247(2):69-73.<\/span>\u00a0doi: 10.1620\/tjem.247.69.<\/span><\/div>\n\n\n\nAuthors<\/h3>\n
Haruka Sato<\/a>\u00a0\u00a01\u00a0<\/sup>,\u00a0<\/span>Koichiro Sugimura<\/a>\u00a0\u00a01\u00a0<\/sup>,\u00a0<\/span>Masanobu Miura<\/a>\u00a0\u00a01\u00a0<\/sup>,\u00a0<\/span>Ryo Konno<\/a>\u00a0\u00a01\u00a0<\/sup>,\u00a0<\/span>Katsuya Kozu<\/a>\u00a0\u00a01\u00a0<\/sup>,\u00a0<\/span>Nobuhiro Yaoita<\/a>\u00a0\u00a01\u00a0<\/sup>,\u00a0<\/span>Toru Shimizu<\/a>\u00a0\u00a01\u00a0<\/sup>,\u00a0<\/span>Saori Yamamoto<\/a>\u00a0\u00a01\u00a0<\/sup>,\u00a0<\/span>Tatsuo Aoki<\/a>\u00a0\u00a01\u00a0<\/sup>,\u00a0<\/span>Shunsuke Tatebe<\/a>\u00a0\u00a01\u00a0<\/sup>,\u00a0<\/span>Kimio Satoh<\/a>\u00a0\u00a01\u00a0<\/sup>,\u00a0<\/span>Hiroaki Shimokawa<\/a>\u00a0\u00a01<\/sup><\/span><\/div>\n<\/div>\n\nAffiliation<\/h3>\n
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- 1<\/sup>\u00a0<\/span>Department of Cardiovascular Medicine, Tohoku University Graduate School of Medicine.<\/li>\n<\/ul>\n<\/div>\n<\/div>\n<\/div>\n
- \n
- PMID:\u00a030700638<\/a><\/span><\/li>\n
- DOI:\u00a010.1620\/tjem.247.69<\/a><\/span><\/li>\n<\/ul>\n
Free article<\/span><\/p>\n<\/header>\n
\nAbstract<\/h2>\n
\nPulmonary veno-occlusive disease (PVOD) is a rare form of pulmonary hypertension (PH). The prognosis of PVOD patients remains poor, since no effective medical therapy is yet available. Imatinib is a tyrosine kinase inhibitor specific for platelet-derived growth factor receptor and is expected as a treatment option for pulmonary arterial hypertension (PAH). Recently, it has been reported that imatinib improved functional capacity of a patient with PVOD. We here report a patient with suspected PVOD who has been successfully treated with imatinib and is alive for 6 years after diagnosis. A 57-year-old woman was admitted to a hospital for severe dyspnea. Echocardiography suggested the presence of PH, because tricuspid regurgitation pressure gradient was elevated. The patient was then transferred to our hospital by an ambulance ahead of schedule due to fever and worsening dyspnea. Because the patient had no left heart disease, we diagnosed that she had PAH associated with severe right heart failure. We immediately started treatment with nitric oxide (NO) for her severe hypoxia; however, it caused pulmonary edema. We suspected PVOD from CT characteristics and pulmonary edema after PAH-targeted vasodilator therapy, and then started oral imatinib treatment. In response to imatinib, her pulmonary edema gradually improved. Since then, the patient has been alive for 6 years with imatinib and pulmonary vasodilators. At present, lung transplantation is the only effective therapy for PVOD with limited availability. We therefore propose that imatinib may be a treatment option for PVOD and a bridge to lung transplantation.<\/p>\n<\/div>\n
Keywords:\u00a0<\/span><\/strong>imatinib; pulmonary arterial hypertension; pulmonary hypertension; pulmonary veno-occlusive disease; transplantation.<\/p>\n<\/div>\n
\n - DOI:\u00a010.1620\/tjem.247.69<\/a><\/span><\/li>\n<\/ul>\n
- PMID:\u00a030700638<\/a><\/span><\/li>\n
- DOI:\u00a010.11406\/rinketsu.57.618<\/a><\/span><\/li>\n<\/ul>\n<\/header>\n
- PMID:\u00a027263788<\/a><\/span><\/li>\n
- DOI:\u00a010.1177\/1078155217753740<\/a><\/span><\/li>\n<\/ul>\n<\/header>\n
- 2<\/sup>\u00a0<\/span>2 Department of Pulmonary\/Critical Care, Staten Island University Hospital, Staten Island, New York, USA.<\/li>\n
- DOI:\u00a010.1016\/j.cjca.2019.08.002<\/a><\/span><\/li>\n<\/ul>\n<\/header>\n
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