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Pulmonary hypertension associated with veno-occlusive disease in systemic sclerosis: Insight into the mechanism of resistance to vasodilator

フォーマット:
論文
責任表示:
Tada, Hayato ; Konno, Tetsuo ; Aizu, Motohiko ; Yokawa, Junichiro ; Tsubokawa, Toshinari ; Fujii, Hiroshi ; Hayashi, Kenshi ; Uchiyama, Katsuharu ; Matsumura, Masami ; Kawano, Mitsuhiro ; Kawashiri, Masa-aki ; Yamagishi, Masakazu
言語:
英語
出版情報:
Elsevier / Japanese College of Cardiology, 2012-02-01
著者名:
Tada, Hayato
Konno, Tetsuo
Aizu, Motohiko
Yokawa, Junichiro
Tsubokawa, Toshinari
Fujii, Hiroshi
Hayashi, Kenshi
Uchiyama, Katsuharu
Matsumura, Masami
Kawano, Mitsuhiro
Kawashiri, Masa-aki
Yamagishi, Masakazu
続きを見る
掲載情報:
Journal of Cardiology Cases
ISSN:
1878-5409  CiNii Research  Webcat Plus  JAIRO
巻:
5
通号:
1
開始ページ:
e44
終了ページ:
e47
バージョン:
author
概要:
We report a case with pulmonary veno-occlusive disease (PVOD) associated with systemic sclerosis which exhibits strong resistance to pulmonary vasodilator.A 55-year-old female with severe pulmonary hypertension was admitted to our hospital to be introduced to epoprostenol infusion therapy. She was diagnosed as having pulmonary arterial hypertension (PAH) associated with systemic sclerosis at the age of 51. Several aggressive treatments with pulmonary vasodilators, including oral prostaglandin, endothelin receptor antagonists, and phosphodiesterase 5 inhibitors, failed to improve her symptoms. We introduced continuous intravenous epoprostenol therapy from 2. μg/kg/min for her. However, pulmonary edema appeared and worsened in a dose-dependent manner. We made a diagnosis of PVOD clinically at that time. Thereafter, pulmonary edema gradually disappeared consistent with the reduction of the dose of epoprostenol infusion. She died of renal failure and infection 4. months after the introduction of epoprostenol infusion therapy. A histological examination revealed severe stenosis and occlusions of pulmonary veins as well as pulmonary arteries over a wide area. We suggest that prevalence of veno-occlusive type of disease could be one of the major mechanisms of less responsive or even refractory to pulmonary vasodilator therapies in patients with PAH associated with connective tissue disease. © 2011 Japanese College of Cardiology. 続きを見る
URL:
http://hdl.handle.net/2297/30319
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