Gemcitabine-Induced Pulmonary Toxicity: A Case Report of Pulmonary Veno-Occlusive Disease

Author:

Turco Célia123,Jary Marine13,Kim Stefano1,Moltenis Mélanie4,Degano Bruno5,Manzoni Philippe6,Nguyen Thierry1,Genet Bruno7,Rabier Marie-Blanche Valnet4,Heyd Bruno2,Borg Christophe13

Affiliation:

1. Department of Medical Oncology, University Hospital of Besançon, Besançon, France.

2. Department of Digestive Surgery and Liver Transplantation, University Hospital of Besançon, Besançon, France.

3. INSERM, Unit 1098, University of Franche-Comté, Besançon, France.

4. Regional center of Pharmacovigilance, University Hospital of Besançon, Besançon, France.

5. Functional Explorations, University Hospital of Besançon, Besançon, France.

6. Radiology and Interventional Pain Management Unit, University Hospital of Besançon, Besançon, France.

7. Department of Cardiology, University Hospital of Besançon, Besançon, France.

Abstract

Introduction Gemcitabine is a chemotherapeutic agent frequently used by for the treatment of several malignancies both in the adjuvant and metastatic setting. Although myelosuppression is the most adverse event of this therapy, gemcitabine might induce severe pulmonary toxicities. We describe a case of pulmonary veno-occlusive disease (PVOD) related to gemcitabine. Case Presentation The patient was an 83-year-old man with a metastatic pancreatic cancer who was treated by gemcitabine as first-line therapy. He was in good health and received no other chemotherapy. A dose of 1000 mg/m2 of gemcitabine was administered over a 30-minute intravenous infusion on days 1, 8, and 15 of a 28-day cycle. After a period of 6 months, a complete response was observed. Nevertheless, the patient developed a severe dyspnea, with arterial hypoxemia and very low lung diffusion for carbon monoxide. A CT scan showed diffuse ground glass opacities with septal lines, bilateral pleural effusion, and lymph node enlargement. On echocardiography, there was a suspicion of pulmonary hypertension with elevated systolic pulmonary artery pressure and normal left ventricular pressures. Right heart catheterization confirmed pulmonary hypertension and normal pulmonary artery occlusion pressure. Diagnosis of PVOD was made, and a gemcitabine-induced toxicity was suspected. A symptomatic treatment was started. At last follow-up, patient was in functional class I with near-normal of CT scan, arterial blood gases, and echocardiography. A gemcitabine-induced PVOD is the more likely diagnosis.

Publisher

SAGE Publications

Subject

Oncology

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