Exhaled nitric oxide measurement in patients affected by nasal polyposis.

OBJECTIVES: Nitric oxide (NO) is produced in the respiratory tract with a major contribution coming from paranasal sinuses and the nose. The pathophysiological role of NO in the airways has been debated. The aims of this study were to measure fraction of exhaled NO (FENO), a validated marker of airway inflammation, in patients affected by nasal polyposis with and without asthma; to assess the importance of FENO measurement in detecting subclinical involvement of lower airways in patients with clinical rhinosinusal symptoms; and to clarify the impact of endoscopic surgical removal of polyps on airway inflammation. SETTING: The study was conducted at the O.R.L. Clinic and Clinical Pharmacology Unit, University Hospital Agostino Gemelli, Rome, Italy. STUDY DESIGN: Prospective study. SUBJECTS AND METHODS: Concentrations of FENO were measured with the NIOX system (Aerocrine, Stockholm, Sweden) by using a single-breath online method, according to the American Thoracic Society guidelines. RESULTS: Compared with those in healthy subjects (15 [11-19] ppb, n = 15; P < .0001), FENO values were elevated in patients with nasal polyposis (41 [21-77] ppb, n = 43). There was no significant difference in FENO concentrations between asthmatic and nonasthmatic patients with nasal polyposis (P = .73). Concentrations of FENO in patients with nasal polyposis were decreased after surgery (64.2 [30.0-132.7] ppb vs 56.0 [26.4-73.8] ppb, respectively; P = .03). CONCLUSION: The fraction of exhaled NO is elevated in the inflammatory process involving both the rhinosinusal district and lower airways, supporting the one-airway disease hypothesis.

Olfactory dysfunction in Parkinsonism caused by PINK1 mutations.

Hyposmia is a common nonmotor feature of Parkinson's disease (PD) and has been variably detected in monogenic Parkinsonisms. To assess olfactory dysfunction in PINK1-related Parkinsonism, we evaluated olfactory detection threshold, odor discrimination, and odor identification in five groups of subjects: sporadic PD (n = 19), PINK1 homozygous (n = 7), and heterozygous (n = 6) parkinsonian patients, asymptomatic PINK1 heterozygous carriers (n = 12), and Italian healthy subjects (n = 67). All affected subjects and all healthy heterozygotes but one resulted hyposmic, with most patients in the range of functional anosmia or severe hyposmia. Detection threshold was more preserved and discrimination more impaired in patients with PINK1 mutations than in PD cases. Alterations of detection and discrimination were observed also in PINK1 asymptomatic heterozygotes. On the contrary, odor identification appeared to be mostly related to the disease status, as it was impaired in nearly all patients (including PD and PINK1 cases) and preserved in healthy heterozygotes. Our data indicate that olfactory dysfunction is common in PINK1 Parkinsonism and consists typically in defective odor identification and discrimination. A milder olfactory deficit, mostly involving discrimination, can be found in asymptomatic heterozygotes, possibly indicating an underlying preclinical neurodegenerative process.