EARLY HYPOXEMIA WITH DIFFUSE GROUND-GLASS OPACITIES AFTER ALLOGENEIC HEMATOPOIETIC STEM CELL TRANSPLANTATION: DIAGNOSTIC CHALLENGE BETWEEN NONINFECTIOUS PNEUMONITIS AND OPPORTUNISTIC INFECTION
- 1Rede Materdei Saúde, Belo Horizonte, MG, Brazil
Abstract
Introduction: Early pulmonary complications after allogeneic hematopoietic stem cell transplantation (HSCT) are diagnostically challenging because opportunistic infection, inflammatory toxicity, diffuse alveolar injury, and noninfectious syndromes may overlap. Idiopathic pneumonia syndrome is a diagnosis of exclusion, defined by diffuse lung injury, hypoxemia, and absence of a predominant infectious, cardiogenic, or fluid-overload cause. Case report: A 25-year-old woman with B-cell acute lymphoblastic leukemia underwent allogeneic haploidentical HSCT, after conditioning with fludarabine, melphalan, and total body irradiation. She received a peripheral blood stem cell graft containing 5.24 × 10⁶ CD34+ cells/kg. Around day +27, she developed cough, tachypnea, and new-onset hypoxemia. Chest computed tomography showed extensive bilateral confluent centrilobular ground-glass opacities with mild septal thickening, without pleural effusion or pneumothorax, and with a small pericardial effusion. An extensive infectious workup was performed. The molecular respiratory viral panel was negative for adenovirus, bocavirus, seasonal coronaviruses, SARS-CoV-2, enterovirus, metapneumovirus, rhinovirus, influenza A/B, parainfluenza, respiratory syncytial virus, Mycoplasma pneumoniae, and Bordetella spp. She was receiving acyclovir and letermovir prophylaxis, plus therapeutic-dose trimethoprim-sulfamethoxazole and levofloxacin for Stenotrophomonas maltophilia. CMV monitoring showed transient low-level positivity, subsequently below the lower limit of detection. She also received meropenem, liposomal amphotericin B, vancomycin, and polymyxin B, in the context of previous catheter-related bloodstream infection by Enterococcus faecium and S. maltophilia. Bronchoalveolar lavage bacterial culture was negative. BAL galactomannan index was 1.048, borderline and slightly above the positivity cutoff; however, the clinical-radiological pattern did not support a predominant invasive fungal disease, although antifungal coverage was maintained as a precaution. She required intensive care and sedation, with progressive hypoxemia and worsening PaO₂/FiO₂ ratio, consistent with severe acute respiratory distress syndrome, requiring lung-protective ventilation and prone positioning, with partial improvement after the maneuver. Discussion: This case illustrates the complexity of classifying acute hypoxemia with diffuse pulmonary infiltrates early after HSCT. Timing, new hypoxemia, bilateral ground-glass pattern, negative extended viral panel, and absence of findings strongly suggestive of invasive fungal disease favored post-transplant noninfectious pneumonitis within the spectrum of idiopathic pneumonia syndrome. Borderline BAL galactomannan positivity required caution, since opportunistic infection and inflammatory lung injury may coexist. Management integrated ventilatory support, broad-spectrum antimicrobials, systemic antifungal therapy, exclusion of cardiogenic or fluid-overload causes, and early consideration of a noninfectious pulmonary complication. Conclusion: In allogeneic HSCT recipients, early hypoxemia with diffuse ground-glass opacities requires broad investigation and integrated management. Noninfectious pneumonitis/idiopathic pneumonia syndrome should be considered when the initial infectious workup is inconclusive and the clinical-radiological pattern does not support a predominant infectious etiology.
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BibTeX
@article{anastacio2026early,
title = {{EARLY HYPOXEMIA WITH DIFFUSE GROUND-GLASS OPACITIES AFTER ALLOGENEIC HEMATOPOIETIC STEM CELL TRANSPLANTATION: DIAGNOSTIC CHALLENGE BETWEEN NONINFECTIOUS PNEUMONITIS AND OPPORTUNISTIC INFECTION}},
author = {Lucas De Barros ANASTACIO and Cássia Caetano de Oliveira MIRANDA and Anderson Martins PEREIRA and Wellington Morais de AZEVEDO},
journal = {Hematology, Transfusion and Cell Therapy},
year = {2026},
month = oct,
doi = {10.1016/j.htct.2026.106859},
url = {https://doi.org/10.1016/j.htct.2026.106859},
note = {CC BY},
}
RIS
TY - JOUR
TI - EARLY HYPOXEMIA WITH DIFFUSE GROUND-GLASS OPACITIES AFTER ALLOGENEIC HEMATOPOIETIC STEM CELL TRANSPLANTATION: DIAGNOSTIC CHALLENGE BETWEEN NONINFECTIOUS PNEUMONITIS AND OPPORTUNISTIC INFECTION
AU - Lucas De Barros ANASTACIO
AU - Cássia Caetano de Oliveira MIRANDA
AU - Anderson Martins PEREIRA
AU - Wellington Morais de AZEVEDO
PY - 2026
DA - 2026/10/23
JO - Hematology, Transfusion and Cell Therapy
DO - 10.1016/j.htct.2026.106859
UR - https://doi.org/10.1016/j.htct.2026.106859
AB - Introduction: Early pulmonary complications after allogeneic hematopoietic stem cell transplantation (HSCT) are diagnostically challenging because opportunistic infection, inflammatory toxicity, diffuse alveolar injury, and noninfectious syndromes may overlap. Idiopathic pneumonia syndrome is a diagnosis of exclusion, defined by diffuse lung injury, hypoxemia, and absence of a predominant infectious, cardiogenic, or fluid-overload cause. Case report: A 25-year-old woman with B-cell acute lymphoblastic leukemia underwent allogeneic haploidentical HSCT, after conditioning with fludarabine, melphalan, and total body irradiation. She received a peripheral blood stem cell graft containing 5.24 × 10⁶ CD34+ cells/kg. Around day +27, she developed cough, tachypnea, and new-onset hypoxemia. Chest computed tomography showed extensive bilateral confluent centrilobular ground-glass opacities with mild septal thickening, without pleural effusion or pneumothorax, and with a small pericardial effusion. An extensive infectious workup was performed. The molecular respiratory viral panel was negative for adenovirus, bocavirus, seasonal coronaviruses, SARS-CoV-2, enterovirus, metapneumovirus, rhinovirus, influenza A/B, parainfluenza, respiratory syncytial virus, Mycoplasma pneumoniae, and Bordetella spp. She was receiving acyclovir and letermovir prophylaxis, plus therapeutic-dose trimethoprim-sulfamethoxazole and levofloxacin for Stenotrophomonas maltophilia. CMV monitoring showed transient low-level positivity, subsequently below the lower limit of detection. She also received meropenem, liposomal amphotericin B, vancomycin, and polymyxin B, in the context of previous catheter-related bloodstream infection by Enterococcus faecium and S. maltophilia. Bronchoalveolar lavage bacterial culture was negative. BAL galactomannan index was 1.048, borderline and slightly above the positivity cutoff; however, the clinical-radiological pattern did not support a predominant invasive fungal disease, although antifungal coverage was maintained as a precaution. She required intensive care and sedation, with progressive hypoxemia and worsening PaO₂/FiO₂ ratio, consistent with severe acute respiratory distress syndrome, requiring lung-protective ventilation and prone positioning, with partial improvement after the maneuver. Discussion: This case illustrates the complexity of classifying acute hypoxemia with diffuse pulmonary infiltrates early after HSCT. Timing, new hypoxemia, bilateral ground-glass pattern, negative extended viral panel, and absence of findings strongly suggestive of invasive fungal disease favored post-transplant noninfectious pneumonitis within the spectrum of idiopathic pneumonia syndrome. Borderline BAL galactomannan positivity required caution, since opportunistic infection and inflammatory lung injury may coexist. Management integrated ventilatory support, broad-spectrum antimicrobials, systemic antifungal therapy, exclusion of cardiogenic or fluid-overload causes, and early consideration of a noninfectious pulmonary complication. Conclusion: In allogeneic HSCT recipients, early hypoxemia with diffuse ground-glass opacities requires broad investigation and integrated management. Noninfectious pneumonitis/idiopathic pneumonia syndrome should be considered when the initial infectious workup is inconclusive and the clinical-radiological pattern does not support a predominant infectious etiology.
SN - 2531-1379
SN - 2531-1387
ER -