Interferon-α-2b
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Reactions 1232 - 13 Dec 2008 S Interferon-α-2b Nonreversible pulmonary arterial hypertension: case report A 40-year-old woman developed nonreversible pulmonary arterial hypertension (PAH) during long-term adjuvant treatment with interferon-α-2b for melanoma. The woman started receiving interferon-α-2b [dosage not stated] and, 30 months later, she reported that she had increasing dyspnoea on exertion, a nonproductive cough, malaise and lower-leg oedema. Sinus tachycardia and right axis deviation were shown on electrocardiography. A chest x- ray revealed right-sided pleural effusion and signs of right ventricular dilatation. Abdominal sonography showed ascites. Findings on transthoracic echocardiography were PAH with a calculated systolic pulmonary artery pressure (PAP syst) of 80mm Hg, right ventricular dilatation and hypertrophy, reduced right ventricular ejection fraction (40%), grade II-III tricuspid insufficiency with morphologically normal valves, pericardial effusion without signs of tamponade and hypokinetic right ventricle. She had slightly increased liver enzyme and d-dimer levels. A diagnostic right heart catheter showed a PAP mean of 56mm Hg (PAP syst 87mm Hg), an impaired cardiac index, increased total peripheral resistance (3-fold) and a pulmonary vascular resistance (PVR) of 1.128 dyn × sec/cm 5 . Testing of pulmonary vasoreactivity with sildenafil revealed a reduction in her PAP mean from 56mm Hg to 26mm Hg. The woman received sildenafil and, after 1 month, there was an improvement in her tricuspid insufficiency to grade I-II. After 6 months, she had reduced right ventricular dilatation and hypertrophy. Sildenafil was stopped, but her mean PAP promptly increased to 57mm Hg. There was higher PVR reduction with vardenafil compared with sildenafil, so she was switched to vardenafil. She resumed working 24 months after PAH onset. After stopping vardenafil for 2 days, her PAP syst increased by about 40mm Hg; it decreased 120 minutes after vardenafil administration. Vardenafil treatment is still necessary. At last follow-up, she only complained of dyspnoea with heavy exercise, and her PAP and PVR were 50mm Hg and 1.5 WU, respectively. Author comment: "If [interferon] alpha treated patients develop respiratory symptoms, PAH should be considered in the differential diagnosis." Panda A, et al. Nonreversible interferon-alpha-induced pulmonary arterial hypertension requiring continuous vasodilator therapy. 2008 Annual Meeting of the American College of Chest Physicians : abstr. 16001S, 27 Oct 2008. - USA 801133448 1 Reactions 13 Dec 2008 No. 1232 0114-9954/10/1232-0001/$14.95 Adis © 2010 Springer International Publishing AG. All rights reserved
Transcript of Interferon-α-2b
Reactions 1232 - 13 Dec 2008
SInterferon-α-2b
Nonreversible pulmonary arterial hypertension:case report
A 40-year-old woman developed nonreversible pulmonaryarterial hypertension (PAH) during long-term adjuvanttreatment with interferon-α-2b for melanoma.
The woman started receiving interferon-α-2b [dosage notstated] and, 30 months later, she reported that she hadincreasing dyspnoea on exertion, a nonproductive cough,malaise and lower-leg oedema. Sinus tachycardia and rightaxis deviation were shown on electrocardiography. A chest x-ray revealed right-sided pleural effusion and signs of rightventricular dilatation. Abdominal sonography showed ascites.Findings on transthoracic echocardiography were PAH with acalculated systolic pulmonary artery pressure (PAP syst) of80mm Hg, right ventricular dilatation and hypertrophy,reduced right ventricular ejection fraction (40%), grade II-IIItricuspid insufficiency with morphologically normal valves,pericardial effusion without signs of tamponade andhypokinetic right ventricle. She had slightly increased liverenzyme and d-dimer levels. A diagnostic right heart cathetershowed a PAP mean of 56mm Hg (PAP syst 87mm Hg), animpaired cardiac index, increased total peripheral resistance(3-fold) and a pulmonary vascular resistance (PVR) of1.128 dyn × sec/cm5. Testing of pulmonary vasoreactivity withsildenafil revealed a reduction in her PAP mean from 56mm Hgto 26mm Hg.
The woman received sildenafil and, after 1 month, there wasan improvement in her tricuspid insufficiency to grade I-II.After 6 months, she had reduced right ventricular dilatationand hypertrophy. Sildenafil was stopped, but her mean PAPpromptly increased to 57mm Hg. There was higher PVRreduction with vardenafil compared with sildenafil, so she wasswitched to vardenafil. She resumed working 24 months afterPAH onset. After stopping vardenafil for 2 days, her PAP systincreased by about 40mm Hg; it decreased 120 minutes aftervardenafil administration. Vardenafil treatment is stillnecessary. At last follow-up, she only complained of dyspnoeawith heavy exercise, and her PAP and PVR were 50mm Hg and1.5 WU, respectively.
Author comment: "If [interferon] alpha treated patientsdevelop respiratory symptoms, PAH should be considered inthe differential diagnosis."Panda A, et al. Nonreversible interferon-alpha-induced pulmonary arterialhypertension requiring continuous vasodilator therapy. 2008 Annual Meeting of theAmerican College of Chest Physicians : abstr. 16001S, 27 Oct 2008. -USA 801133448
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Reactions 13 Dec 2008 No. 12320114-9954/10/1232-0001/$14.95 Adis © 2010 Springer International Publishing AG. All rights reserved
