Kartagener syndrome (KS) is a rare autosomal recessive motile ciliopathy and a well-recognized subtype of primary ciliary dyskinesia, classically defined by the triad of situs inversus totalis, chronic sinusitis, and bronchiectasis, with frequent accompanying infertility. Because of its non-specific clinical manifestations overlapping with common respiratory disorders and limited availability of gold-standard diagnostic tools in primary care settings, KS is frequently misdiagnosed or diagnosed late. This study retrospectively analyzed the clinical data, diagnostic trajectories, and treatment outcomes of three adult patients with clinically diagnosed complete KS admitted to our institution between May 2021 and December 2022. All patients presented with long-standing recurrent cough and expectoration; two presented with hemoptysis and one with type II respiratory failure. Initial misdiagnoses included bronchiectasis, non-tuberculous mycobacterial infection, and chronic obstructive pulmonary disease. Clinical diagnosis of complete KS was established based on the classic triad on imaging combined with core clinical features, as confirmatory genetic or ultrastructural testing was not available. Pathogen testing detected Acinetobacter baumannii in one patient, while another patient had a coinfection of Pseudomonas aeruginosa and Enterobacter cloacae. One more patient received empirical antimicrobial therapy because their family declined bronchoscopy. After individualized treatment, clinical improvement was observed in all patients, with symptom resolution, normalized inflammatory markers, and stable disease during 6-12 months of follow-up. These findings underscore that the combined features of "situs inversus totalis + bronchiectasis + chronic sinusitis + childlessness/infertility (when formally confirmed)" are key diagnostic clues for KS in primary care. Primary care clinicians should strengthen awareness of this rare entity and use a multisystem diagnostic approach to prevent misdiagnosis and underdiagnosis. Prompt targeted antimicrobial therapy and sustained comprehensive long-term management were associated with favorable clinical outcomes in this small case series.

Allergic rhinitis (AR) and chronic rhinosinusitis (CRS) in their non-polypous (CRS without nasal polyps - CRSsNP) and polypous (CRS with nasal polyps - CRSwNP) main phenotypes are chronic inflammatory diseases of the nasal mucosa and/or paranasal sinuses with a whole series of unknowns regarding etiology, pathogenesis, clinical manifestations, and therapeutic modalities. Although intranasal and oral antihistamines and intranasal corticosteroids are the main drugs in AR therapy, emerging evidence on the effects of herbal and biological drugs may add a new dimension to the treatment of these patients. CRS is a far more heterogeneous disease with numerous clinical phenotypes that require completely different approaches. In addition to endoscopic sinus surgery (ESS), which remains the mainstay of treatment, intranasal and systemic corticosteroids, macrolide antibiotics, and tetracyclines, as well as nasal irrigation with saline solutions, are the main modalities, especially in the period after surgical treatment. Recently, there has been increasing evidence for the beneficial effects of herbal medicines and biological therapy. However, to assess how well conservative treatment of AR and CRS keeps chronic inflammation under control, numerical parameters derived from cytological findings, biochemical analysis of nasal secretions by enzyme-linked immunoassay (ELISA), flow cytometry, and pathohistological and immunohistochemical analyses of tissue samples are necessary. This narrative review of the literature was done through a critical approach, which included our long-term experience in researching the effects of various drugs, as well as the results of other authors. The results of numerous studies have shown that the application of these drugs can significantly change the profile of inflammatory mediators (cytokines, chemokines, enzymes, growth factors) and thus direct the course of inflammation to a less intense form. Nevertheless, in spite of everything, the control of AR and CRS is still not at a satisfactory level, which directs us towards finding new modalities of conservative therapy, especially in the field of application of biological drugs and plant extracts.

Chronic rhinosinusitis (CRS) frequently co-occurs with depressive disorders. TCF4 aberrant expression is strongly linked to CRS with depression-like behaviors (CRSDB), highlighting the urgent need for TCF4-targeted drugs to treat this complex comorbidity. This study validated the reproducibility and stability of the previously developed mouse model of CRSDB by assessing nasal and hippocampal histopathology via H&E, PAS, and Nissl staining. ELISA determined inflammatory cytokine levels. TCF4's role was explored through lentivirus-mediated in vivo and in vitro microglial knockdown. TLR4/NF-κB pathway regulation by TCF4 was confirmed via immunofluorescence, Western Blot, and RT-qPCR. Metformin's therapeutic effect was tested, with its TCF4 targeting verified by molecular docking and in vitro experiments. The study comprehensively links TCF4 to neuroinflammation in CRSDB, highlighting metformin's potential as a therapeutic agent. The CRSDB model exhibited excellent reproducibility and time-dependent exacerbation of depression-like behaviors, cognitive deficits, and concurrent nasal and hippocampal inflammation. Mechanistically, CRSDB induced TCF4 upregulation, which activated the TLR4/NF-κB signaling pathway, leading to microglial activation and neuroinflammation. Knockdown of TCF4 significantly alleviated behavioral impairments, suppressed microglial activation, and mitigated peripheral inflammation. Furthermore, We identified TCF4 as a direct target of metformin, through which it inhibits the TLR4/NF-κB pathway and subsequent microglial activation. TCF4 has been confirmed as a key regulatory mediator of CRSDB, and it has been demonstrated that metformin exerts its antidepressant effect by specifically targeting TCF4 in microglia to inhibit the TLR4/NF-κB axis.

Pituitary neuroendocrine tumours (PitNETs) commonly present with symptoms related to mass effect or hormonal dysfunction, including headache, visual disturbances, and endocrine abnormalities. However, atypical presentations without neurological or hormonal "red flag" symptoms may delay diagnosis, particularly in primary care settings where benign upper respiratory conditions are more frequently encountered. We report the case of a 56-year-old postmenopausal woman who presented with a five-month history of persistent postnasal drip, chronic non-productive cough and a sensation of nasal congestion characterised by fullness in the nasal and retro-orbital region. Despite conservative medical management, persistent symptoms prompted a computed tomography (CT) of the brain and paranasal sinuses, which unexpectedly revealed a sellar mass extending into the left sphenoid sinus. Subsequent magnetic resonance imaging (MRI) confirmed a 3.4cm pituitary macroadenoma with left cavernous and sphenoid sinus invasion, left internal carotid artery encasement, optic nerve involvement, and imaging features of pituitary apoplexy. Hormonal evaluation showed hyperprolactinaemia, and histopathology following endoscopic endonasal resection confirmed a lactotroph PitNET. This case highlights the importance of diagnostic reassessment in patients with persistent symptoms and demonstrates that clinically significant PitNETs can masquerade behind common benign upper respiratory conditions.

Chronic rhinosinusitis with nasal polyps (CRSwNP) is a heterogeneous inflammatory disease in which type 2 inflammation, epithelial dysfunction, and tissue remodeling determine severity, recurrence, and treatment response. Although molecular biomarkers have clarified disease endotypes, their routine use remains limited by cost, availability, and invasiveness. Nasal cytology offers a simple, repeatable, and minimally invasive method to assess-at the mucosal surface-both epithelial morphology and the dominant inflammatory infiltrate, whether neutrophilic, eosinophilic, mast cell, or mixed. Clinical-Cytological Grading (CCG) integrates the dominant cytological pattern with selected comorbidities, including asthma, allergy, and NSAID-exacerbated respiratory disease (N-ERD), into a weighted clinical-cytological framework. In the founding cohort, the highest relapse association was observed when mixed eosinophil-mast cell inflammation coexisted with asthma and N-ERD. This review discusses the rationale, clinical relevance, and translational applications of CCG in CRSwNP, addressing eosinophilic and mixed mast cell-eosinophilic inflammation, epithelial morphology, disease recurrence, difficult-to-treat phenotypes, biologic monitoring, and the operative dialogue between nasal cytology and histopathology. By linking cytological findings with selected clinical comorbidities, CCG may support biologically informed patient characterization and may prompt targeted mast cell assessment in tissue. However, its prognostic accuracy, incremental clinical value, and role in therapeutic decision-making require independent external validation.

A boy in middle childhood presented with a 1-month history of intermittent discharge from sinus openings on the posterior aspect of the left forearm. Examination revealed two small draining sinus tracts with mild surrounding erythema and induration but no systemic features. Routine blood investigations, plain radiographs and ultrasonography were unremarkable. The draining sinuses and local inflammatory changes were considered consistent with a localised chronic infection; surgical exploration was therefore undertaken and a 9 cm wooden fragment was identified within the posterior extensor muscle plane. The fragment was removed intact and the sinus tracts were excised. The boy recovered uneventfully, regained full elbow, wrist and finger motion and had no recurrence at the 1-year follow-up. This case demonstrates that radiolucent organic foreign bodies may remain occult on routine investigations and that material-specific imaging knowledge, anatomical localisation and persistent clinical suspicion are essential.

Eosinophilic chronic rhinosinusitis (CRS), characterized by prominent eosinophil infiltration, has the highest postoperative recurrence rate among CRS subtypes. Given the critical role of eotaxins in CRS pathogenesis, this study aimed to identify eotaxins associated with eosinophilic CRS and evaluate their correlation with surgical outcomes. Transcriptomic data from GSE36830 revealed 125 differentially expressed genes (49 up-regulated, 76 down-regulated) in CRSwNP compared to CRSsNP, with significant enrichment of eosinophil and dendritic cell infiltration pathways. Functional analysis identified chemotaxis and cell migration as key dysregulated processes in CRSwNP. Among eotaxins, CCL26 and CCL13 emerged as hub molecules from the intersection of these dysregulated pathways. In a clinical cohort of 115 CRS patients, preoperative serum CCL26 and CCL13 levels were significantly elevated in CRSwNP compared to CRSsNP (P<0.001). ROC analysis demonstrated strong diagnostic power for nasal polyps (CCL26: AUC=0.895; CCL13: AUC=0.830). Higher preoperative CCL26 levels predicted poorer symptom improvement post-surgery (standardized β=-0.564, P<0.001). In conclusion, preoperative serum CCL26 serves as both a diagnostic biomarker for CRSwNP and a prognostic indicator for surgical outcomes, with elevated levels associated with reduced symptom improvement.

Calcified materials in an opacified maxillary sinus often suggest fungal sinusitis, particularly aspergillosis. However, odontogenic maxillary sinusitis may rarely be associated with a bone-like calcified mass, creating diagnostic difficulty. We report a case of chronic odontogenic maxillary sinusitis with sequestrum-like bone formation that mimicked fungal sinusitis. An 88-year-old man was referred for mobility and occlusal pain of the maxillary left first molar. He had no nasal obstruction, rhinorrhea, headache, facial pain, or history of maxillary sinus surgery. Intraoral examination showed marked periodontal destruction, root exposure, tooth mobility, and percussion and occlusal pain. A hard structure was palpable through the periodontal pocket. Panoramic radiography showed increased opacity of the left maxillary sinus and a well-defined, horseshoe-shaped, bone-like radiopaque mass near the root apex. Computed tomography revealed a capsular calcified structure adjacent to the root apex within soft tissue occupying the left maxillary sinus, with extension toward the ethmoid sinus and thickening of the sinus wall. Fungal maxillary sinusitis was considered in the radiographic differential diagnosis. Under local anesthesia, extraction of the affected tooth, removal of the calcified mass, and maxillary sinus fenestration were performed. The mass, identified through the extraction socket, was not adherent to the tooth and was easily separated from the surrounding tissue. No fungal organisms, including Aspergillus species, were identified on histopathological examination. The excised specimen was a hard bone-like mass measuring approximately 20 × 15 mm. Histopathological examination revealed a sequestrum with areas suggestive of pre-existing lamellar bone and newly formed, incompletely mineralized bone. At one-year follow-up, maxillary sinus mucosal thickening had improved. This case illustrates that odontogenic maxillary sinusitis may be associated with a bone-like calcified mass and may radiographically mimic fungal sinusitis. When surgical treatment is clinically indicated, histopathological examination of the removed lesion can help establish a definitive diagnosis.

The nasal microbiome serves as a pivotal regulator of immune homeostasis in the upper airway. Under physiological conditions, it maintains immune equilibrium through mechanisms such as reinforcing the epithelial barrier and modulating innate and adaptive immune responses. Microbial dysbiosis, however, is recognized as a key trigger in the pathogenesis of chronic rhinosinusitis （CRS） and allergic rhinitis （AR）. This review summarizes how the nasal microbiome regulates immune homeostasis by influencing epithelial barrier function and immune responses in both health and disease states, with a focus on CRS and AR. It focuses on the characteristics of microbial dysbiosis and immunopathological mechanisms in CRS and AR, and provides perspectives on microbiome-based diagnostic biomarkers and microecological interventional therapeutic strategies.

Granulomatosis with polyangiitis (GPA) and eosinophilic granulomatosis with polyangiitis (EGPA) are recognized subtypes of antineutrophil cytoplasmic antibody (ANCA)-associated vasculitis (AAV). Their clinical boundaries, however, may be more dynamic than assumed. We describe 2 patients illustrating sequential phenotype transitions with prominent respiratory involvement. The first patient was initially diagnosed with GPA, presenting with neuropathy, purpura, epistaxis, renal disease, and myeloperoxidase (MPO)-ANCA positivity. Six years later, she developed asthma, marked eosinophilia, and eosinophilic myocarditis, consistent with evolution toward EGPA despite stable ANCA serology. The second patient was first classified as EGPA based on eosinophilic asthma, chronic rhinosinusitis with nasal polyps, and MPO-ANCA with borderline proteinase 3 (PR3)-ANCA. After SARS-CoV-2 infection, he developed GPA-like disease with strongly positive PR3-ANCA and destructive airway involvement, including tracheobronchomalacia requiring tracheostomy and stenting. These cases highlight that recognizing this dynamic nature is essential for the timely reassessment of disease classification, prognosis, and therapeutic approach in AAV.

Facial erysipelas is an uncommon but potentially serious manifestation of rhinosinusitis, as involvement of the facial "danger triangle" carries the risk of orbital and intracranial complications. Saline nasal irrigation devices are widely recommended as nonprescription, over-the-counter adjunctive therapy for the symptomatic management of sinonasal disease and are generally considered safe. We report the case of a 60-year-old man who developed rapidly progressive centrofacial erysipelas after one week of using a commercially available pressurized seawater nasal irrigation device for an acute exacerbation of chronic rhinosinusitis. To our knowledge, this is the first reported temporal association between the use of a pressurized nasal irrigation device (PNID) and facial erysipelas. Although causality cannot be inferred from a single case, several biologically plausible mechanisms warrant consideration. This report highlights facial erysipelas as a rare cutaneous manifestation of complicated rhinosinusitis and underscores the importance of obtaining a detailed history of PNID use. Further studies are needed to clarify whether this observed association is causal or incidental and to better define the safety of PNIDs in patients with suspected bacterial rhinosinusitis.