RESUMO
Invasive fungal rhinosinusitis (IFRS) typically affects immunocompromised patients. The coronavirus disease 2019 (COVID-19) pandemic may be associated with rare opportunistic fungal infections, probably as a result of immune dysregulation. The COVID-19 infection is characterized by low levels of CD4+T and CD8+T cells which could increase the risk of co-infections from Mucor or Aspergillus species. An invasive fungal infection should be suspected in patients who have recently recovered from COVID-19 pneumonia and present with acute destructive rhinosinusitis. There are few cases of IFRS reported in Europe during the pandemic of COVID-19. We describe the case of a 67-year-old patient with diabetes who received corticosteroids during the treatment for COVID-19 infection and was readmitted a few days later for radiologically and clinically suggested IFRS. Aspergillus niger was identified, and the patient received pharmacological and surgical treatment.
RESUMO
BACKGROUND: Topical glucocorticosteroids are the first line therapy for airway inflammation. Modern compounds with higher efficacy have been developed, but head-to-head comparison studies are sparse. OBJECTIVE: To compare the activity of two intranasal glucocorticoids, fluticasone furoate (FF) and mometasone furoate (MF) with respect to the inhibition of T helper (Th)1, Th2 and Th17 cytokine release in airway mucosa. METHODS: We used an ex-vivo human nasal mucosal tissue model and employed pre- and post- Staphylococcus aureus enterotoxin B (SEB)-challenge incubations with various time intervals and drug concentrations to mimic typical clinical situations of preventive or therapeutic use. RESULTS: At a fixed concentration of 10-10 M, FF had significantly higher suppressive effects on interferon (IFN)-γ, interleukin (IL)-2 and IL-17 release, but not IL-5 or tumor necrosis factor (TNF)-α, vs. MF. While the maximal suppressive activity was maintained when FF was added before or after tissue stimulation, the cytokine suppression capacity of MF appeared to be compromised when SEB-induced cell activation preceded the addition of the drug. In a pre-challenge incubation setting with removal of excess drug concentrations, MF approached inhibition of IL-5 and TNF-α after 6 and 24 hours while FF maximally blocked the release of these cytokines right after pre-incubation. Furthermore, FF suppressed a wider range of T helper cytokines compared to MF. CONCLUSION: The study demonstrates the potential of our human mucosal model and shows marked differences in the ability to suppress the release of various cytokines in pre- and post-challenge settings between FF and MF mimicking typical clinical situations of preventive or therapeutic use.