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Øie MR, Helvik AS, Sue-Chu M, Steinsvåg SK, Thorstensen WM. Int J Chron Obstruct Pulmon Dis. 2022;17:2137–2147. Page 2137, Abstract, Patients and Methods section, line 2, the text “in 93 COPD patients” should read “in 90 COPD patients”. The authors have also advised Figure 1 on page 2138 is incorrect. Without RSsNP should be n=44 and With RSsNP should be n=46. The correct Figure 1 is as follows. Figure 1 Flow chart of the study participants and the subjects excluded. Abbreviations: EPOS, European Position Paper on Rhinosinusitis and Nasal Polyps (2012); RSsNP, Rhinosinusitis sin Nasal Polyps.

The validity of the united airway disease concept for rhinosinusitis (RS) and chronic obstructive pulmonary disease (COPD) has been questioned because of methodological limitations in previous studies. In this study we investigated the prevalence of RS without nasal polyps (RSsNP) and the severity of sinonasal symptoms in COPD and a corresponding control group. We also evaluated the diagnostic accuracy of these symptoms for RSsNP in COPD. 90 COPD patients and 93 controls were included in an observational cross-sectional study where globally accepted diagnostic criteria of RS and COPD (EPOS 2012 and GOLD) were incorporated; symptomatic and endoscopic criteria for the diagnosis of RS, and spirometry with reversibility for diagnosis of COPD. RS symptoms were identified by responses to the sinonasal outcome test (SNOT-22), nasal endoscopy identified signs of sinonasal disease and discriminated between RS with and without nasal polyps, and visual analogue scales (VAS) rated the severity of sinonasal symptoms. We found RSsNP in 51% of our COPD patients which is threefold greater than in the control group (p, Rhinosinusitis is associated with COPD and is significantly more prevalent (51%) compared to controls https://bit.ly/2YrIsmm

Background: Olfaction is poorly characterized in COPD. To test the hypothesis that olfaction is reduced in COPD, we assessed olfaction with the “Sniffin’ Sticks” test and a questionnaire addressing olfaction in COPD and a corresponding control group in respect to age and sex. We also explored whether there is an association between COPD, chronic rhinosinusitis without nasal polyps (CRSsNP), and other predefined covariates with olfactory function. Methodology: Olfactory function was assessed by the score for threshold (T), discrimination (D) and identification (I), and the composite TDI score in the “Sniffin’ Sticks” test and by self-reported evaluation of impaired olfaction and of “decreased sense of smell and taste” in the 22-item Sino-Nasal Outcome Test (SNOT-22) in 90 COPD patients and 93 controls. A clinical interview and ENT-examination with nasal endoscopy, skin prick test and spirometry with reversibility were performed. Results: The TDI, D and I scores were significantly lower in the COPD group than in the control group. The T score was not significantly different between the two groups. Hyposmia and anosmia were present in up to 79% of patients with COPD. The prevalence of self-reported impaired olfactory function and for 'decreased sense of smell and taste'; - was more than two-fold greater in the COPD than in the control group. COPD, higher age, male sex and allergy were associated with a lower TDI score, while CRSsNP was not associated with the TDI score. Conclusions: COPD is associated with olfactory dysfunction and the underlying mechanisms for this dysfunction should be elucidated.

Rhinosinusitis without nasal polyps (RSsNP) is prevalent in COPD. Previous studies on its association with health-related quality of life (HRQoL) have limitations, and RSsNP is currently not recognized as a comorbidity. This study investigates HRQoL in COPD including a focus on RSsNP. Generic HRQoL was assessed with the Short Form-36 (SF-36v2) questionnaire and compared between 90 COPD and 93 control subjects and in subgroups with and without RSsNP. The association between RSsNP and COPD versus not and generic HRQoL was assessed by multivariable linear regression with adjustments for age, education, and body mass index (BMI). Disease-specific HRQoL was assessed by Sinonasal outcome test-22 (SNOT-22), St. Georges Respiratory Questionnaire (SGRQ), and COPD Assessment Test (CAT) and compared between COPD with and without RSsNP, and their association to RSsNP was assessed by multivariable linear regression with adjustments for age, BMI, and FEV1% predicted. RSsNP was associated with poorer disease-specific HRQoL, with higher SNOT-22 total score (14.67 points; 95% CI, 7.06–22.28; P < .001) and psychological subscale score (3.24 points; 95% CI, 0.37–6.11; P = .03), SGRQ symptom score (13.08 points; 95% CI, 2.73–23.4; P = .014), and CAT score (4.41 points; 95% CI, 1.15–7.66; P = .009). Generic HRQoL was poorer in COPD patients than in the control subjects. In addition to COPD, concomitant RSsNP was associated with poorer physical functioning, general health, vitality, and physical component summary. RSsNP in COPD is associated with poorer disease-specific HRQoL that is clinically relevant and, as it is amenable for treatment, should be recognized as a comorbidity of COPD.

Background: The effect of pulmonary pathology on peak nasal inspiratory flow (PNIF) remains largely unknown. We investigated an association between a diagnosis of asthma and of lung function on PNIF when adjusted for possible confounders. Further, we investigated the perception of nasal obstruction in asthmatics compared to healthy controls when adjusted for PNIF. Methodology: Eighty-seven asthmatics and 92 non-asthmatic controls underwent PNIF (categorized into groups of high, medium and low), acoustic rhinometry (AR) and spirometry, and we assessed symptoms of nasal obstruction on visual analogue scales (VAS) in three categories. Results: PNIF was significantly associated with asthma and forced expiratory volume in the first second (FEV1) (% predicted). Other factors associated with PNIF were the degree of nasal obstruction measured both subjectively on a VAS and objectively with AR, age and disease status. Asthma patients were 19 times more likely to be in a higher VAS category compared to non-asth- matic controls independent of PNIF group. Conclusion: Special care has to be taken when interpreting PNIF values in patients with asthma or reduced FEV1 (% predicted). The sensation of nasal obstruction in asthmatics is different from controls despite being in the same PNIF group.

In sarcoidosis, increased Th17 cell fractions have been reported in bronchoalveolar lavage fluid, and elevated numbers of Th17 cells producing IFN-γhave been observed in peripheral blood. The balance between Th1, Th17, and FoxP3+CD4+T cell subsets in sarcoidosis remains unclear. Bronchoalveolar lavage fluid cells, from 30 patients with sarcoidosis, 18 patients with other diffuse parenchymal lung diseases, and 15 healthy controls, were investigated with flow cytometry for intracellular expression of FoxP3. In a subset of the patients, expression of the cytokines IL17A and IFN-γwas investigated. The fractions of FoxP3+CD4+T cells and Th17 cells were both lower in sarcoidosis compared to controls (P=0.017andP=0.011, resp.). The proportion of Th17 cells positive for IFN-γwas greater in sarcoidosis than controls (median 72.4% versus 31%,P=0.0005) and increased with radiologic stage (N=23,rho=0.45, andP=0.03). IFN-γ+Th17 cells were highly correlated with Th1 cells (N=23,rho=0.64, andP=0.001), and the ratio of IFN-γ+Th17/FoxP3+CD4+T cells was prominently increased in sarcoidosis. IFN-γ+Th17 cells may represent a pathogenic subset of Th17 cells, yet their expression of IFN-γcould be a consequence of a Th1-polarized cytokine milieu. Our results indicate a possible immune cell imbalance in sarcoidosis.

The clinical diagnosis of pulmonary sarcoidosis is based on the presence of noncaseating granulomas in an appropriate clinical setting with either bilateral hilar adenopathy and/or parenchymal infiltrates. Lymphocytosis with an increased CD4/CD8 T cell ratio in bronchoalveolar lavage fluid is supportive. We evaluated the diagnostic accuracy of a predictive binary logistic regression model in sarcoidosis based on sex, age, and bronchoalveolar lavage fluid cell profile with and without the inclusion of HLA-DR(+) CD8(+) T cells and natural killer T-cell fractions.A retrospective analysis of differential cell counts and lymphocyte phenotypes by flow cytometry in bronchoalveolar lavage was performed in 183 patients investigated for possible diffuse parenchymal lung disease. A logistic regression model with age, sex, lymphocyte fraction, eosinophils, and CD4/CD8 ratio in bronchoalveolar lavage fluid (basic model) was compared with a final model, which also included fractions of HLA-DR(+) CD8(+) T cells and natural killer T cells. Diagnostic accuracy of the two models was assessed by receiver operating characteristic (ROC) curves.The area under the ROC curve for the basic and final model was 0.898 [95 % confidence interval (CI) 0.852-0.945] and 0.937 (95 % CI 0.902-0.972), respectively, p = 0.008.Assessment of HLA-DR(+) CD8(+) T cell and natural killer T-cell fractions may improve diagnostic accuracy and further strengthen the importance of bronchoalveolar lavage in the diagnostic workup of sarcoidosis.

Summary Background The Unified Airways hypothesis suggests an involvement of the upper airways in asthma. Critical parameters of the nasal airway can be quantified objectively with acoustic rhinometry (AR) and peak nasal inspiratory flow (PNIF). Objective We aimed to investigate nasal airway patency in asthmatics compared to non-asthmatic controls. Nasal volume, cross sectional area and flow were measured using acoustic rhinometry (AR) and peak nasal inspiratory flow (PNIF) in 87 asthmatics and 93 non-asthmatic controls before and after decongestion with xylometazoline. Nasal congestion index (NCI) was calculated, and allergy status was assessed by skin prick test or specific IgE. Results We found significantly smaller minimum cross sectional area and nasal cavity volume in asthmatics than controls, and the cross sectional area is at its minimum at 2–3 cm from the nasal orifice in both groups. AR and PNIF measurements are not different in allergic and non allergic subjects in either group. The effect of xylometazoline is not significantly different between the 2 groups with regard to AR, but there is a significant improvement in PNIF for the asthmatics when assessed by the NCI. Conclusion The present study demonstrates a significantly smaller nasal airway when assessed by minimum cross sectional area and nasal cavity volume in asthmatics than controls, and these findings apply to asthmatics and controls irrespective of allergy status.

A higher prevalence of airway hyperresponsiveness, airway remodeling, and asthma has been identified among athletes who compete and train in environmental conditions of cold dry air and/or high air pollution. Repeated long-duration exposure to cold/dry air at high minute ventilation rates can cause airway damage. Competition or training at venues close to busy roadways, or in indoor ice arenas or chlorinated swimming pools, harbors a risk for acute and chronic airway disorders from high pollutant exposure. This article discusses the effects of these harsh environments on the airways, and summarizes potential mechanisms and prevalence of airway disorders in elite athletes.

BOLGER, C., E. TUFVESSON, M. SUE-CHU, G. DEVEREUX, J. G. AYRES, L. BJERMER, and P. KIPPELEN. Hyperpnea-Induced Bronchoconstriction and Urinary CC16 Levels in Athletes. Med. Sci. Sports Exerc., Vol. 43, No. 7, pp. 1207-1213, 2011. Purpose: Exercise-induced bronchoconstriction (EIB) is a common condition in both individuals with asthma and otherwise healthy elite athletes. Although excessive water loss by peripheral airways during hyperpnea is regarded as the initial trigger for EIB, the cascade of events that follows remains unclear. Our goal was to establish whether transient disruption of the airway epithelial barrier occurs after a short period of hyperpnea of dry air in athletes with EIB. Methods: Urinary concentration of the pneumoprotein Clara cell (CC16) was used as an assumed biomarker of lung epithelial cell damage or dysfunction. Samples were collected at baseline and for 90 min after an 8-min eucapnic voluntary hyperpnea (EVH) test in 50 female individuals (28 athletes and 22 untrained). Results: Nineteen subjects (10 athletes) demonstrated a sustained bronchoconstriction after EVH (mean +/- SE forced expiratory volume in the first second (FEV1) fall from baseline = 23.4% +/- 2.6%). The remaining subjects had a negative challenge result with an FEV1 fall of 5.9% +/- 0.6%. An increase (P 0.05). Conclusions: Urinary levels of CC16 are increased after EVH in all individuals (trained and untrained, with and without EIB) suggestive of dehydration-induced perturbation of the distal respiratory epithelium during episodes of hyperventilation. (Less)

Background Methacholine hyperresponsiveness is prevalent in elite athletes. Comparative studies have hitherto been limited to methacholine, eucapnic voluntary hyperpnoea and exercise. This study investigated airway responsiveness to these stimuli as well as to adenosine 5′-monophosphate (AMP) and mannitol, in 58 cross-country ski athletes. Methods Exhaled nitric oxide concentration (F E NO), spirometry and bronchial challenge in random order with methacholine, AMP and mannitol were consecutively performed on three study days in the autumn. Specifi c IgE to eight aeroallergens and a self-completed questionnaire about respiratory symptoms, allergy and asthmatic medication were also performed on day 1. Eucapnic voluntary hyperventilation (EVH) and fi eld exercise tests were randomly performed in 33 of the skiers on two study days in the following winter. Results Of 25 (43%) skiers with airway hyperresponsiveness (AHR), 23, fi ve and three skiers were hyperresponsive to methacholine, AMP and mannitol, respectively. Methacholine hyperresponsiveness was more prevalent in subjects without asthma-like symptoms. The F E NO was not signifi cantly different in skiers with and without methacholine hyperresponsiveness. Four of 14 skiers with and four of 19 skiers without methacholine hyperresponsiveness were hyperresponsive to EVH or exercise challenge. AHR to any stimulus was present in 16 asymptomatic and nine symptomatic skiers. Asthma-like symptoms were not correlated with AHR to any stimulus. Conclusions Methacholine hyperresponsiveness is more common in asymptomatic skiers and is a poor predictor of hyperresponsiveness to mannitol and hyperpnoea. The low prevalence of hyperresponsiveness to indirect stimuli may suggest differences in the pathogenesis of methacholine hyperresponsiveness in elite skiers and non-athletes.

Educational aims To define necessary conditions for a successful exercise challenge. To provide operational procedures for performing an exercise challenge in the laboratory or the field for the identification of exercise-induced bronchoconstriction. To compare positive and negative attributes of each challenge. To provide spirometric cut-off criteria for positive challenge tests. Summary Exercise challenge tests are often used for identification of exercise-induced bronchoconstriction (EIB). Optimal test conditions are: absolute humidity of

The aim of this double-blind, placebo-controlled, cross-over study was to investigate possible improvement in physical performance at an ambient temperature of -15 degrees C by an inhaled dose of 50 micrograms salmeterol in 8 highly trained nonasthmatic cross-country skiers. FEV1 was measured before, during and after the treadmill exercise protocol, which consisted of a warm-up run, runs of 10 min at 90% and 5 min at 80% VO2max, followed by a timed run to exhaustion. Despite a significant improvement in FEV1, salmeterol did not have a beneficial effect on heart rate, blood lactate concentration, respiratory exchange ratio, oxygen uptake or minute ventilation during the exercise protocol. Running time to exhaustion was not significantly different from placebo. This lack of enhancement of exercise performance in healthy endurance athletes further supports the recent approval of salmeterol for prophylactic use by asthmatic athletes during training and competition.

Purpose Protocadherin-15 (PCDH15) is one of the five genes currently identified as being mutated in Usher 1 syndrome and defines Usher syndrome type 1F (USH1F). When PCDH15 was systematically analyzed for mutations in a cohort of USH1 patients, a number of deletions were found. Here we characterize these deletions as to extent, position, and breakpoints. Methods Microsatellite and single nucleotide polymorphism (SNP) analyses, used in a preliminary survey of an Usher cohort of 31 patients, revealed large deletions in three patients. These deletions were further characterized by semiquantitative PCR assays to narrow down the breakpoints. Results The analysis of the three large deletions revealed that all six breakpoints are different. The breakpoint junction was identified in one patient and the four other breakpoints were mapped to 4 kb. There were no specific distinguishing features of the isolated breakpoints. Conclusions A complete screen of PCDH15 should include a search for large deletions. Failure to screen for gross genomic rearrangements is likely to significantly lower the mutation detection rate. A likely explanation for the high rate of such deletions is the unusual gene structure. PCDH15 gene spans nearly 1 Mb for a corresponding open reading frame (ORF) of 7,021 bp. The intron sizes of PCDH15 are up to 150 kb, and the first three exons of the gene cover 0.42 Mb. The genomic structure of any gene should be taken into consideration when designing a mutation screening strategy.