Pulmonary artery hypertension during interferon-α therapy for chronic myelogenous leukemia
Clicks: 206
ID: 120104
1970
Article Quality & Performance Metrics
Overall Quality
Not rated
Combines reader engagement with the AI quality analysis. This
article has not been analysed, so there is no overall score —
reader engagement is measured and shown alongside.
Reader Engagement
Steady Performance
30.0
/100
206 views
41 readers
AI Quality Assessment
Not analyzed
Readership in this journal
SteadyRanked #45 of 85 articles by views in Annals of hematology
Most read
Least read
Bar heights use a square-root scale.
Mint this article as an NFT
Not yet mintedCreate a permanent, verifiable on-chain record of this article on the Scimatic Network. The NFT is held in your Journament account, and you can withdraw it to your own wallet at any time.
5
SUSD
one-off · no wallet required
Abstract
In the conventionally treated group of patients with chronic myelogenous leukemia (CML) the prognosis has been significantly improved by interferon-α (IFN-α). Several side effects in association with IFN-α treatment have been reported. Here we present the first case of a CML patient with reversible pulmonary artery hypertension (PAH) during IFN-α therapy. The patient received IFN-α-2b (up to 10 million U/day) for 6 months until he started to complain of dyspnea on exertion and an afebrile non-productive cough. An echocardiography and right heart catheterization showed signs of right heart failure with PAH (80 mmHg). A reduced carbon monoxide diffusion capacity and partial respiratory insufficiency were noted. Inflammatory markers were not elevated and pulmonary infiltrates could not be detected. Respiratory infections, thromboembolic causes or autoimmune diseases were carefully ruled out. IFN-α was suspected as causative agent, because experimental investigations in sheep showed that IFN-α can stimulate the thromboxane cascade which resulted in transient PAH. A reduced pulmonary diffusion capacity had been observed secondary to PAH. After discontinuation of IFN-α, our patient's clinical status improved rapidly. After 6 months the pulmonary artery pressure had returned to near normal values (35 mmHg) and the pulmonary diffusion capacity was normal. It took one year until the electrocardiogram reverted to the pre-IFN-α pattern. PAH should be included in the differential diagnosis of patients treated with IFN-α who complain of exertional dyspnea in the absence of inflammatory signs.
| Reference Key |
fruehauf1970annalspulmonary
Use this key to autocite in the manuscript while using
SciMatic Manuscript Manager or Thesis Manager
|
|---|---|
| Authors | S. Fruehauf;S. Steiger;J. Topaly;A. Ho;S. Fruehauf;S. Steiger;J. Topaly;A. Ho; |
| Journal | Annals of hematology |
| Year | 1970 |
| DOI |
doi:10.1007/s002770100298
|
| URL | |
| Keywords |
Citations
No citations found. To add a citation, contact the admin at info@scimatic.org
Comments
No comments yet. Be the first to comment on this article.