There are several types of fungal sinusitis. The classification depends on the degree of invasion of the sinuses. The overarching categories are non-invasive and invasive fungal sinusitis. There are three subtypes of non-invasive fungal sinusitis (FS): Fungal ball (FB), saprophytic fungal sinusitis (SFS), and allergic fungal rhinosinusitis (AFRS). Similarly, there are three subtypes of invasive fungal sinusitis (IFS): acute invasive rhinosinusitis (AIRS), chronic invasive rhinosinusitis (CIRS), and granulomatous invasive sinusitis (GIFS). To accurately diagnose fungal sinusitis, a physician must take into account several variables, including patient history and clinical presentation, imaging, endoscopic biopsy with histopathology, and lab work. For this activity and to ease following the material, we classify the infections into allergic fungal sinusitis, fungal ball, invasive fungal sinusitis, and granulomatous sinusitis.  The other categorization of fungal sinusitis has its basis on the immune-competence profile of patients. The broad understanding is that immunocompromised patients are the primary victims of fungal sinusitis. The non-invasive fungal sinusitis tends to primarily occur in immunocompetent individuals as opposed to invasive sinusitis's which is more prevalent in immunodeficiency. Invasive fungal sinusitis could be fatal in that the infection could spread into the intracerebral space; this correlates with an increase in mortality and morbidity of victims. Immunocompromised patients should take special precautions and should be aggressively treated should there be any suspicion of fungal sinusitis.

The nasal mucosa functions as a highly specialized barrier that integrates epithelial, stromal, neuronal, and immune signals to maintain homeostasis and mount rapid responses to environmental challenges. Among its resident immune populations, innate lymphoid cells-particularly type 2 ILCs (ILC2s)-play a pivotal role in orchestrating type 2 inflammation driven by epithelial-derived alarmins such as IL-25, IL-33, and TSLP. Upon activation, ILC2s release IL-5 and IL-13, promoting eosinophilic inflammation, goblet cell hyperplasia, mucus hypersecretion, and tissue remodeling, all central features of chronic rhinosinusitis with nasal polyps (CRSwNP) and severe allergic rhinitis. Recent advances have revealed substantial ILC plasticity, the presence of nasal-resident ILC progenitors, and the influence of metabolic and neuroimmune cues in shaping ILC activation and persistence. Dupilumab, a monoclonal antibody targeting IL-4Rα, has emerged as a highly effective therapy, providing unique mechanistic insight into the epithelial-ILC axis. By blocking IL-4/IL-13 signaling, dupilumab dampens ILC2 effector functions, reduces IL-5/IL-13 output, restores epithelial barrier integrity, interrupts alarmin-driven amplification loops, and rebalances innate and adaptive immune networks. Clinical and translational studies indicate that baseline ILC2 phenotypes-particularly inflammatory ILC2 subsets-may predict treatment responsiveness, positioning ILC profiling as a promising biomarker strategy. This review synthesizes current knowledge of ILC classification, plasticity, progenitor biology, and epithelial-ILC communication in the nasal mucosa, while integrating emerging evidence on dupilumab-mediated immunomodulation. Collectively, these insights highlight ILCs as central drivers of type 2 inflammation and key targets for precision immunomodulation, offering a framework for personalized treatment approaches in CRSwNP and allergic rhinitis.

BACKGROUND Actinomycosis is an uncommon bacterial infection caused by the commensal organism Actinomyces spp., which can become pathogenic upon tissue injury or disruption of the mucosal barrier. While primarily recognized for its cervicofacial and abdominopelvic presentations, actinomycosis can also involve the gallbladder and potentially the pancreas, posing diagnostic and therapeutic challenges due to its ability to mimic other conditions. CASE REPORT We present the case of a 26-year-old woman with a history of recurrent acute pancreatitis and cholecystitis, followed by the development of thrombotic microangiopathy. An atypical hemolytic-uremic syndrome panel revealed gene mutations previously associated with the onset of this condition. Computed tomography, endoscopic ultrasound, and abdominal ultrasound revealed focal enlargement of secondary ducts in the head of the pancreas. While no gallbladder wall thickening was observed, imaging demonstrated a substantial amount of heterogeneous, predominantly hypoechoic and amorphous content within the gallbladder, suggestive of biliary sludge. The patient subsequently underwent cholecystectomy, and histopathological examination of the gallbladder specimen confirmed the presence of Actinomyces spp., observed as sulfur granules and Gram-stained bacilli, as well as varying degrees of mucosal hyperplasia, transmural fibrosis, xanthomatous histiocytes, and Rokitansky-Aschoff sinuses. CONCLUSIONS Following the procedure and appropriate antimicrobial therapy, the patient experienced resolution of the infection, improvement in overall health status, and no new episodes of pancreatitis during the following year. We propose that underlying CFHR3 and CFI gene mutations and initial systemic inflammation precipitated the thrombotic microangiopathy-atypical hemolytic uremic syndrome, and facilitated Actinomyces colonization of the compromised gallbladder, ultimately leading to chronic gallbladder disease and recurrence.

Objective: To investigate the clinicopathological characteristics of granulomatosis with polyangiitis (GPA) involving the nasal cavity and paranasal sinuses. Methods: Twenty-two cases of GPA involving the nasal cavity and paranasal sinuses, diagnosed at the Eye, Ear, Nose and Throat Hospital of Fudan University from June 2018 to January 2025, were retrospectively reviewed. Clinical data, pathological features, treatment, and clinical outcomes were analyzed. Relevant literature was also reviewed to summarize diagnostic and differential diagnostic points. Results: Among the 22 patients, 13 were male and 9 were female, with median age of 43.5 (31.0, 55.0) years, ranging 14-73 years. Local sinonasal symptoms were present in 95.5% (21/22) of the cases, while 63.6% (14/22) of the cases involved adjacent regions, and 9.1% (2/22) had fever. Excluding one case with unknown systemic involvement, 17 cases were localized GPA, while 4 were systemic GPA. All cases showed mixed acute and chronic inflammatory cell infiltration. Granuloma formation was observed in 86.4% (19/22) of the cases, including 14 cases of necrotizing granulomas and 5 cases of non-necrotizing granulomas. Vasculitis involving small vessels was seen in 95.5% (21/22) of the cases. Necrosis was identified in 68.2% (15/22) of the cases, comprising geographic necrosis (8 cases) and focal necrosis (7 cases). Fibrous tissue hyperplasia was present in 40.9% (9/22) of the cases. Among the 17 cases with localized GPA, vasculitis was observed in 16 cases (16/17). Granuloma formation was identified in 14 cases (14/17), of which 11 had necrotizing granulomas and 3 had non-necrotizing granulomas. All 4 systemic GPA cases exhibited small-vessel vasculitis, with 2 cases of necrotizing and 2 cases of non-necrotizing granulomas. Seven cases had previously undergone biopsy at other institutions but were not correctly diagnosed. The initial diagnoses included sinusitis (5 cases), tuberculosis (1 case), and low-grade mesenchymal tumor (1 case). Anti-neutrophil cytoplasmic antibodies (ANCA) were tested in 18 cases. Seventeen cases (17/18) were positive for anti-proteinase 3 antibodies (PR3-ANCA). Among them, 15 were also positive for cytoplasmic ANCA (c-ANCA), 2 were positive for PR3-ANCA but negative for c-ANCA, and 1 was positive for anti-myeloperoxidase antibodies (MPO-ANCA) and perinuclear ANCA (p-ANCA). Detailed treatment information was available for 17 cases. The therapeutic regimen was primarily based on glucocorticoids, supplemented with rituximab or cyclophosphamide in some cases. The median follow-up was 38 months, with 2 deaths identified by the end of the follow-up. The 1-year and 3-year overall survival rates were 94% and 84%, respectively. Conclusions: Sinonasal GPA primarily occurs in young and middleaged adults, typically presenting with nonspecific clinical symptoms. Its characteristic pathological findings include necrotizing granulomas and vasculitis. However, in most cases, only small biopsy specimens are available for histopathological evaluation, making it challenging to identify all diagnostic features microscopically. Therefore, a definitive diagnosis should be made by comprehensively evaluating clinical manifestations, radiological findings, histopathological characteristics, and serological testing.

Background and Clinical Significance: Granulomatosis with polyangiitis (GPA), an immune-mediated systemic small-vessel vasculitis affecting the upper/lower respiratory tracts and kidneys, frequently presents with non-specific nasal symptoms that lead to misdiagnosis. Case Presentation: We report a case of a 55-year-old female with GPA complicated by Bartter syndrome. She presented with one month of left nasal congestion, rhinorrhea, epistaxis, and headache. Initial diagnosis was acute sinusitis. Computed tomography (CT) revealed left maxillary and ethmoid sinus inflammation with bone destruction, while metagenomic next-generation sequencing (mNGS) suggested conventional bacterial infection. Postoperative pathology demonstrated chronic mucosal inflammation with lymphoid tissue hyperplasia. GPA was ultimately diagnosed based on PR3-ANCA seropositivity and chest CT findings of cavitary pulmonary nodules. Postoperatively, severe hypokalemia and hypomagnesemia secondary to Bartter syndrome emerged. Following electrolyte correction, induction therapy with glucocorticoids and cyclophosphamide was initiated. Conclusions: This case underscores that GPA's head and neck manifestations are frequently misdiagnosed as infections or malignancies. Early diagnosis requires vigilance for GPA 'red flags', such as refractory nasal symptoms to conventional therapy (e.g., bloody rhinorrhea), characteristic CT findings (e.g., sinus opacification without ostiomeatal complex obstruction), and nasal endoscopy findings (e.g., ulcers/crusting). Otolaryngologists play a pivotal role in recognizing early disease onset and initiating timely treatment.

A 66-year-old male with a history of chronic epistaxis and sinusitis presented with a non-healing ulcer on the right nasolabial region persisting for 7 months. While denying additional symptoms, he admitted to recreational cocaine smoking. Examination revealed an ulcerated plaque with raised, pink-edged borders extending from the right nasal rim to the upper lip. A thorough diagnostic workup was unremarkable, although wound cultures identified growth of Pseudomonas aeruginosa and Staphylococcus aureus. Despite a year-long trial of antibiotics, the ulcer remained resistant to treatment. Biopsy findings included pseudoepitheliomatous hyperplasia with a dense dermal plasmocytic infiltrate and scattered eosinophils. A 6-week course of oral steroids achieved rapid and significant clinical improvement, though the lesion recurred following steroid tapering below 5 mg daily.