Surfactant proteins A, B, C and D in the human nasal airway: associated with mucosal glands and ciliated epithelium but absent in fluid-phase secretions and mucus.

AIMS: To investigate the presence of surfactant protein (SP) A, B, C and D in nasal airways and to determine whether the proteins exert their main functions in nasal secretions or in the deeper layers of the nasal mucosa. METHODS: Volunteers were recruited from the Department of ENT Head and Neck Surgery, Odense University Hospital, Denmark. The study included 39 subjects. Nasal mucosal biopsies were analyzed by immunohistochemistry, and bronchoalveolar and nasal lavages, nasal brush biopsies and nasal mucus were analyzed for SP-A, -B, -C and -D by SDS-PAGE and Western blotting. The presence of SP-A and SP-D in the first three samplings were also analyzed by enzyme-linked immunosorbent assay. RESULTS: In nasal mucosal biopsies, SP-A, -B, -C and -D were all demonstrated in the serous acini of the submucosal glands and in the surface epithelium. SP-D was detected in nasal brush biopsies, whereas the other SPs were absent. Moreover, SP-A, -B, -C and -D were absent in nasal lavage and mucus. CONCLUSION: SP-A, -B, -C and -D exert their protective effect in the ductal epithelium of the submucosal glands rather than in nasal secretions and mucus. Further studies are required to clarify the functions of these proteins in nasal secretory pathways for understanding upper airway diseases.

Vocal cord paralysis as primary and secondary results of malignancy. A prospective descriptive study.

OBJECTIVE: Vocal cord paralysis (VCP) may be caused by a primary malignancy and associated immune cross-reactivity. We aimed to illuminate underlying causes of VCP and to assess if onconeural antibodies occur in association to VCP as an early predictor of cancer. METHODS: A prospective study was performed in patients with newly diagnosed VCP from 2014 to 2016. All patients underwent fiberoptic laryngoscopy, ultrasound of the neck and computed tomography (CT) of the neck and thorax. Patients with idiopathic VCP underwent neurological examination, positron emission tomography/CT, and serum analysis for onconeural antibodies. All patients were offered a one-year clinical follow-up. RESULTS: In total 53 patients fulfilled the inclusion criteria. Left VCP occurred in 37 (70%), right in 15 (28%), and bilateral in one patient (2%). The cause of VCP was cancer in 27 (51%) patients, of those 15 (56%) had VCP as the primary symptom, including all cases with laryngeal and esophageal cancer. Median time interval between VCP and cancer was 7 days (range 1-30). In 12 (23%) VCP was a secondary symptom. Lung cancer was the most common etiology, 14 of 27 (52%), 12 patients (86%) with non-small cell lung cancer. Idiopathic VCP was diagnosed in 18 (34%) patients, of those nine patients had a neurological examination and were screened for well-known onconeural antibodies, which were not detected. Reactions against Purkinje cell nuclei were seen in three patients, none showed symptoms or signs of cancer at follow-up. CONCLUSIONS: The causes of VCP were described. VCP was frequently the primary symptom, and also occurred as a secondary symptom of cancer. Exclusion of malignancy is important in patients with VCP. LEVEL OF EVIDENCE: 1b.

Complement defects in patients with chronic rhinosinusitis.

The complement system is an important part of our immune system, and complement defects lead generally to increased susceptibility to infections and autoimmune diseases. We have studied the role of complement activity in relation with chronic rhinosinusitis (CRS), and more specifically studied whether complement defects collectively predispose individuals for CRS or affect CRS severity. The participants comprised 87 CRS patients randomly selected from the general population, and a control group of 150 healthy blood donors. The CRS patients were diagnosed according to the European Position Paper on Rhinosinusitis and nasal Polyps criteria, and severity was evaluated by the Sino-nasal Outcome Test-22. Serum samples were analysed by ELISA for activity of the respective pathways of complement, and subsequently for serum levels of relevant components. We found that the frequency of complement defects was significantly higher among CRS patients than among healthy control subjects. A majority of Mannan-binding lectin deficient CRS patients was observed. The presence of complement defects had no influence on the severity of subjective symptoms. Our studies show that defects in the complement system collectively may play an immunological role related to the development of CRS. However, an association between severity of symptoms and presence of complement defects could not be demonstrated.