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Patrick Borentain, MD, PhD; Sébastien Renard, MD; Philippe Colson, PharmD, PhD
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FINANCIAL/NONFINANCIAL DISCLOSURES: See earlier cited article for author conflicts of interest.

aHepato-Gastroenterology, Hôpital de la Timone, Marseille, France

bCardiology, CHU Timone, Marseille, France

cIHU Méditerranée Infection, Hôpital de la Timone, Marseille, France

CORRESPONDENCE TO: Patrick Borentain, MD, PhD, Hôpital de la Timone - Hepato-Gastroenterology, 264 Rue St Pierre, Marseille 13385, France


Copyright 2016, American College of Chest Physicians. All Rights Reserved.


Chest. 2016;150(1):258. doi:10.1016/j.chest.2016.05.012
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We would like to thank Savale et al for their interest in our recent article in CHEST. They report three additional cases of newly diagnosed pulmonary arterial hypertension (PAH) occurring during direct-acting antiviral (DAA) therapy for chronic hepatitis C virus (HCV) infection. These observations underline the importance of systematic report of potential cardiopulmonary side effects related to DAA therapy. In their comment, Savale et al also report safety of DAA therapy in previous known patients with PAH. They did not observe any significant hemodynamics worsening after HCV treatment completion compared with pretherapeutic assessment. These data, collected in 13 patients, argue for a good tolerance of DAA therapy in this clinical setting. However, in our experience, we observed one case of PAH worsening occurring during DAA therapy.

A 48-year-old HIV/1a genotype HCV coinfected cirrhotic woman with mild PAH on bosentan therapy received DAA therapy in our institution. Pretherapeutic noninvasive evaluation found World Health Organization (WHO) functional class (FC) II, systolic pulmonary arterial pressure (sPAP) estimated at 50 mm Hg, right ventricle (RV) of normal size, and brain natriuretic peptide level at 73 pg/mL. The patient started a DAA combination (sofosbuvir plus ledipasvir) for 24 weeks. Sixteen weeks after treatment initiation and 8 weeks after HCV suppression, the patient presented with dyspnea worsening (WHO FC III). Noninvasive results were sPAP at 86 mm Hg, with RV enlargement and brain natriuretic peptide level at 275 pg/mL. Despite this worsening, DAA was continued without PAH treatment modification. An early monitoring on DAA therapy revealed a regression of PAH with WHO FC II and sPAP at 50 mm Hg with normal RV size. This regression was confirmed 1 month after DAA cessation.

The present case demonstrates that patients with PAH could experience a transient PAH worsening during DAA therapy. However, as reported here, spontaneous regression could be observed despite DAA continuation. Therefore, in accordance with Savale et al, reported data suggest that DAA therapy remains usually safe in stable patients with PAH, but can be associated with PAH worsening. The long-term impact of DAA-induced HCV eradication in patients with PAH should be assessed.

References

Savale L. .Chaumais M.C. .Montani D. .et al Direct-acting antiviral medications for hepatitis C virus infection and pulmonary arterial hypertension. Chest. 2016;150:256-258 [PubMed]journal
 
Renard S. .Borentain P. .Salaun E. .et al Severe pulmonary arterial hypertension in patients treated for hepatitis C with sofosbuvir. Chest. 2016;149:e69-e73 [PubMed]journal. [CrossRef] [PubMed]
 

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References

Savale L. .Chaumais M.C. .Montani D. .et al Direct-acting antiviral medications for hepatitis C virus infection and pulmonary arterial hypertension. Chest. 2016;150:256-258 [PubMed]journal
 
Renard S. .Borentain P. .Salaun E. .et al Severe pulmonary arterial hypertension in patients treated for hepatitis C with sofosbuvir. Chest. 2016;149:e69-e73 [PubMed]journal. [CrossRef] [PubMed]
 
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