Pulmonary artery hypertension during interferon-α therapy for chronic myelogenous leukemia

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...

Full description

Saved in:
Bibliographic Details
Main Authors: Frühauf, Stefan (Author) , Steiger, S. (Author) , Topaly, Julian (Author) , Ho, Anthony Dick (Author)
Format: Article (Journal)
Language:English
Published: 31 March 2001
In: Annals of hematology
Year: 2001, Volume: 80, Issue: 5, Pages: 308-310
ISSN:1432-0584
DOI:10.1007/s002770100298
Online Access:Verlag, lizenzpflichtig, Volltext: https://doi.org/10.1007/s002770100298
Get full text
Author Notes:S. Fruehauf, S. Steiger, J. Topaly, A. Ho
Description
Summary: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.
Item Description:Gesehen am 21.12.2021
Physical Description:Online Resource
ISSN:1432-0584
DOI:10.1007/s002770100298