What does this research mean for the field?

Filgrastim administration can precipitate acute respiratory distress syndrome (ARDS) during neutrophil recovery, particularly in immunocompromised patients with preexisting pulmonary infections. Novelty: ClaimNovelty.CONFIRMATORY. Consensus alignment: ConsensusAlignment.NEUTRAL.

What question did this study set out to answer?

This case examines acute respiratory distress syndrome induced by filgrastim in a patient with advanced HIV/AIDS and pneumonia.

May 20, 2026

C48-43 Filgrastim-Induced Acute Respiratory Distress Syndrome in a Patient With Advanced Acquired Immunodeficiency Syndrome and Pseudomonas Pneumonia

Key Points

This case examines acute respiratory distress syndrome induced by filgrastim in a patient with advanced HIV/AIDS and pneumonia.
A 61-year-old male with untreated HIV/AIDS and serious symptoms received filgrastim after developing neutropenia.
Patient was managed with antibiotics, corticosteroids, and lung-protective ventilation following ARDS onset after filgrastim administration.
WBC count increased from 0.3 to > 11 × 109/L within 48 hours of filgrastim administration.
Patient developed worsening oxygenation and new bilateral lung infiltrates consistent with ARDS.
He successfully extubated on hospital day 10 after lung-protective ventilation and other supportive measures.

Abstract

Abstract Introduction Granulocyte colony-stimulating factor (G-CSF, filgrastim) is commonly used to reverse neutropenia in immunocompromised hosts. While typically well tolerated, rare cases of acute respiratory distress syndrome (ARDS) have been reported during neutrophil recovery, likely due to exaggerated inflammatory responses in previously injured lungs. Case Presentation A 61-year-old man with untreated HIV/AIDS (CD4 count 2-3 cells/µL), polysubstance use, and chronic HCV presented with fever (104 °F), cough, encephalopathy, and hypoxemic respiratory failure after being found unresponsive. Chest CT revealed multifocal pneumonia; broad-spectrum antibiotics and high-dose TMP-SMX with corticosteroids were initiated for presumed Pneumocystis jirovecii pneumonia. Endotracheal aspirate cultures later grew Pseudomonas aeruginosa. He developed severe neutropenia (WBC 0.3 × 109/L) and received filgrastim. Within 48 hours, his WBC abruptly increased to 11 × 109/L, followed by worsening oxygenation, rising ventilatory pressures, and new diffuse bilateral infiltrates consistent with ARDS by Berlin criteria. Cardiac function was preserved. No new infection was identified. He was managed with lung-protective ventilation, corticosteroids, conservative fluids, and vasopressors for septic shock. Over the following week, his oxygenation and hemodynamics improved, allowing extubation on hospital day 10. Discussion Filgrastim-induced ARDS is rare but recognized, particularly in patients with pulmonary infection. The mechanism involves neutrophil sequestration and activation within the lung microvasculature, triggering capillary leak and alveolar damage. In this patient, the tight temporal relationship between G-CSF administration, leukocytosis, and rapid respiratory decline supports drug-related lung injury rather than infection progression. Conclusion Clinicians should recognize filgrastim as a potential precipitant of ARDS, especially in immunocompromised or septic patients with preexisting lung injury. Judicious use and close monitoring during neutrophil recovery may mitigate risk. This abstract is funded by: None

Ask AI

Mark Helpful

Bookmark

Relay