SP32 | RHINOVIRUS AS A POTENTIAL TRIGGER OF IDIOPATHIC PNEUMONIA SYNDROME AFTER ALLOGENEIC HEMATOPOIETIC STEM CELL TRANSPLANTATION: A BUTTERFLY EFFECT?

Idiopathic pneumonia syndrome (IPS) is a rare yet life-threatening complication following allogeneic hematopoietic stem cell transplantation (allo-HSCT). Due to its rarity, evidence regarding its risk factors and optimal management is limited. We report two adult cases of IPS in patients with prolonged rhinovirus shedding—detected by nasopharyngeal swab before transplant and as the sole positive finding in bronchoalveolar lavage during the complication. In the first case, a 26-year-old woman underwent HSCT from a matched unrelated donor for severe aplastic anemia. The conditioning regimen included ATG, fludarabine, cyclophosphamide, and total body irradiation, while GvHD prophylaxis comprised post-transplant cyclophosphamide on days +3 and +4 (PTCY), sirolimus, and mycophenolate mofetil (MMF). On day +110, she developed acute respiratory failure. CT scan revealed extensive bilateral pulmonary consolidations, and treatment with high-dose intravenous methylprednisolone alongside three doses of tocilizumab led to rapid clinical improvement, successful extubation, and resolution of the radiographic abnormalities (figure 1). The second case involved a 74-year-old man with very high-risk myelodysplastic syndrome who received HSCT from his haploidentical son. The conditioning regimen included dose-reduced thiotepa, busulfan, and fludarabine, with GvHD prophylaxis consisting of PTCY, sirolimus, and MMF. He developed IPS on day +101. When treatment with corticosteroids and tocilizumab produced only a partial response, the addition of anakinra achieved clinical improvement, enabling successful oxygen weaning. Notably, in both cases, inflammatory markers—such as IL-6 and C-reactive protein—were elevated at the onset of IPS, and rhinovirus remained detectable long after clinical resolution, though without further clinical or radiological sequelae. These findings underscore that even mild, prolonged respiratory viral infections can foster a pro-inflammatory state that may trigger IPS in immunocompromised hosts. The synergistic effect of infections and the lymphodepletion induced by PTCY—which can alter cytokine profiles—might have contributed to IPS development. Moreover, the successful use of anti-cytokine therapies targeting IL-6 and IL-1 suggests a promising new direction for IPS management. Further multicentre studies are warranted to validate these observations and refine therapeutic strategies in the adult HSCT population.