Chest Infections: Fellow Case Report Slide: Chest Infections II |

A Troubling Trifecta: Pulmonary Alveolar Proteinosis and Pneumocystis Pneumonia in Acute Myeloid Leukemia FREE TO VIEW

Priya Patel, MD; Robert Lee, MD; Manju Pillai, MD; Diane Stover, MD
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Memorial Sloan-Kettering Cancer Center, New York, NY

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

Chest. 2016;150(4_S):138A. doi:10.1016/j.chest.2016.08.147
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SESSION TITLE: Fellow Case Report Slide: Chest Infections II

SESSION TYPE: Affiliate Case Report Slide

PRESENTED ON: Tuesday, October 25, 2016 at 07:30 AM - 08:30 AM

INTRODUCTION: This case highlights a unique and rare combination of diseases affecting the lungs and causing hypoxemia.

CASE PRESENTATION: 68 year-old male with acute myeloid leukemia presents with dypsnea, hypoxemia and fevers after completion of experimental chemotherapy which included cytarabine. Physical examination revealed new oxygen requirement, decreased breath sounds from mid to lower left lung field with dullness to percussion. Further workup showed pancytopenia, LDH 368, BNP 90. Imaging revealed a left pleural effusion, bilateral ground glass opacities, and infiltrates. A left sided chest tube and bronchoscopy with bronchoalveolar lavage were completed. Microbiologic examination of bronchoalveolar fluid revealed positive pneumocystis pneumonia PCR, beta-d-glucan level >500, and cytology revealing histiocytes and abundant granular proteinaceous material, positive by periodic acid-Schiff staining.

DISCUSSION: There are a number of interesting points this case elucidates. The first is that pulmonary alveolar proteinosis (PAP) can be due to many causes, including primary and congenital causes. Secondary causes of PAP include infections (in this case PCP) and hematological malignancies (in this case AML). A second point our case shows is of PCP being a rare but serious cause of pulmonary infection in AML. Given the wide array of drug therapy from corticosteroids to chemotherapy agents, one should not exclude T cell dysfunction in the neutropenic host. Third, the combination of these diseases may be an indicator of poor clinical outcomes. Raising the question if the simultaneous presence of these entities are determinants in the development of acute respiratory distress and whether they should be routinely considered and tested in our practice.

CONCLUSIONS: Diagnosis: Acquired pulmonary alveolar proteinosis secondary to pneumocystis pneumonia infection

Reference #1: Nhieu J, Vojtek A, Bernaudin J, et al. Pulmonary alveolar proteinosis associated with pneumocystis carinii: Ultrastructural identification in bronchoalvelar lavage in AIDS and immunocompromised non-AIDS patients. Chest 1990;98: 801-05.

Reference #2: Chaulagain C, Pilichowska M, Brinckerhoff L, et al. Secondary pulmonary alveolar proteinosis in hematologic malignancies. Hematol Oncol Stem Cell Ther 2014;7(4):127-135.

Reference #3: Pagano L, Fianchi L, Mele L, et al. Pneumocystis carinii pneumonia in patients with malignant hematological diseases: 10 years’ experience of infection in GIMEMA centers. Brit J of Hematology, 2002; 117:379-386

DISCLOSURE: The following authors have nothing to disclose: Priya Patel, Robert Lee, Manju Pillai, Diane Stover

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