Anna Agnese Stanziola

Humming-induced release of nasal nitric oxide for assessment of sinus obstruction in allergic rhinitis: pilot study

Background  Humming greatly increases nasal nitric oxide (NO) in healthy people by causing a rapid washout of NO from the sinuses. This increase is abolished in patients with complete sinus ostial obstruction.

Treating severe allergic asthma with anti-IgE monoclonal antibody (omalizumab): a review.

Increased asthma severity is not only associated with enhanced recurrent hospitalization and mortality but also with higher social costs.Several cases of asthma are atopic in nature, with the trigger for acute asthma attacks and chronic worsening of inflammation being allergens inducing an immune, IgE mediated response.Anti-inflammatory treatments are effective for most of asthma patients, but there are subjects whose disease is incompletely controlled by inhaled or systemic corticosteroids and these patients account for about 50% of the healthcare costs of asthma.Omalizumab is a biological engineered, humanized recombinant monoclonal anti-IgE antibody developed for the treatment of allergic diseases and with clear efficacy in adolescent and adult patients with severe allergic asthma. The anti-IgE antibody inhibits IgE functions blocking free serum IgE and inhibiting their binding to cellular receptors. By reducing serum IgE levels and IgE receptor expression on inflammatory cells in the context of allergic cascade, omalizumab has demonstrated to be a very useful treatment of atopic asthma, improving quality of life of patients with severe persistent allergic asthma that is inadequately controlled by currently available asthma medications. Several trials have demonstrated that this therapy is well tolerated and significantly improves symptoms and disease control, reducing asthma exacerbations and the need to use high dosage of inhaled corticosteroids.

Climate Change and Air Pollution: Effects on Respiratory Allergy

A body of evidence suggests that major changes involving the atmosphere and the climate, including global warming induced by anthropogenic factors, have impact on the biosphere and human environment. Studies on the effects of climate change on respiratory allergy are still lacking and current knowledge is provided by epidemiological and experimental studies on the relationship between allergic respiratory diseases, asthma and environmental factors, such as meteorological variables, airborne allergens, and air pollution. Urbanization with its high levels of vehicle emissions, and a westernized lifestyle are linked to the rising frequency of respiratory allergic diseases and bronchial asthma observed over recent decades in most industrialized countries. However, it is not easy to evaluate the impact of climate changes and air pollution on the prevalence of asthma in the general population and on the timing of asthma exacerbations, although the global rise in asthma prevalence and severity could also be an effect of air pollution and climate change. Since airborne allergens and air pollutants are frequently increased contemporaneously in the atmosphere, an enhanced IgE-mediated response to aeroallergens and enhanced airway inflammation could account for the increasing frequency of respiratory allergy and asthma in atopic subjects in the last 5 decades. Pollen allergy is frequently used to study the relationship between air pollution and respiratory allergic diseases, such as rhinitis and bronchial asthma. Epidemiologic studies have demonstrated that urbanization, high levels of vehicle emissions, and westernized lifestyle are correlated with an increased frequency of respiratory allergy prevalently in people who live in urban areas in comparison with people living in rural areas. Climatic factors (temperature, wind speed, humidity, thunderstorms, etc.) can affect both components (biological and chemical) of this interaction.

Climate change and air pollution: Effects on pollen allergy and other allergic respiratory diseases

SummaryThe observational evidence indicates that recent regional changes in climate, particularly temperature increases, have already affected a diverse set of physical and biological systems in many parts of the world. Allergens patterns are also changing in response to climate change and air pollution can modify the allergenic potential of pollen grains especially in the presence of specific weather conditions.Although genetic factors are important in the development of asthma and allergic diseases, their rising trend can be explained only by changes occurring in the environment and urban air pollution by motor vehicles has been indicated as one of the major risk factors responsible for this increase.Despite some differences in the air pollution profile and decreasing trends of some key air pollutants, air quality is an important concern for public health in the cities throughout the world.Due to climate change, air pollution patterns are changing in several urbanized areas of the world with a significant effect on respiratory health. The underlying mechanisms of all these interactions are not well known yet. The consequences on health vary from decreases in lung function to allergic diseases, new onset of diseases, and exacerbation of chronic respiratory diseases. In addition, it is important to recall that an individual’s response to pollution exposure depends on the source and components of air pollution, as well as meteorological conditions. Indeed, some air pollution-related incidents with asthma aggravation do not depend only on the increased production of air pollution, but rather on atmospheric factors that favor the accumulation of air pollutants at ground level.Associations between thunderstorms and asthma morbidity of pollinosis-affected people have also been identified in multiple locations around the world (Fig.1). Cite this as D’Amato G, Bergmann KC, Cecchi L, Annesi-Maesano I, Sanduzzi A, Liccardi G, Vitale C, Stanziola A, D’Amato M. Climate change and air pollution — Effects on pollen allergy and other allergic respiratory diseases. Allergo J Int 2014; 23: 17–23 DOI 10.1007/s40629-014-0003-7 A factor clouding the problem is that laboratory evaluations do not reflect what happens during natural exposition.Considering these aspects, governments worldwide, international organizations, and cooperations such as the World Health Organization (WHO) and the European Health Policy of the European Union (EU) are facing a growing problem of the respiratory effects induced by gaseous and particulate pollutants arising from motor vehicle emissions.

NMR Metabolomic Analysis of Exhaled Breath Condensate of Asthmatic Patients at Two Different Temperatures

Exhaled breath condensate (EBC) collection is a noninvasive method to investigate lung diseases. EBC is usually collected with commercial/custom-made condensers, but the optimal condensing temperature is often unknown. As such, the physical and chemical properties of exhaled metabolites should be considered when setting the temperature, therefore requiring validation and standardization of the collecting procedure. EBC is frequently used in nuclear magnetic resonance (NMR)-based metabolomics, which unambiguously recognizes different pulmonary pathological states. Here we applied NMR-based metabolomics to asthmatic and healthy EBC samples collected with two commercial condensers operating at -27.3 and -4.8 °C. Thirty-five mild asthmatic patients and 35 healthy subjects were included in the study, while blind validation was obtained from 20 asthmatic and 20 healthy different subjects not included in the primary analysis. We initially analyzed the samples separately and assessed the within-day, between-day, and technical repeatabilities. Next, samples were interchanged, and, finally, all samples were analyzed together, disregarding the condensing temperature. Partial least-squares discriminant analysis of NMR spectra correctly classified samples, without any influence from the temperature. Input variables were either integral bucket areas (spectral bucketing) or metabolite concentrations (targeted profiling). We always obtained strong regression models (95%), with high average-quality parameters for spectral profiling (R(2) = 0.84 and Q(2) = 0.78) and targeted profiling (R(2) = 0.91 and Q(2) = 0.87). In particular, although targeted profiling clustering is better than spectral profiling, all models reproduced the relative metabolite variations responsible for class differentiation. This warrants that cross comparisons are reliable and that NMR-based metabolomics could attenuate some specific problems linked to standardization of EBC collection.

Serum soluble ST2 and interleukin-33 levels in patients with pulmonary arterial hypertension

arterial hypertension Guido Carlomagno , Giancarlo Messalli , Rosa Marina Melillo , Anna Agnese Stanziola , Carla Visciano , Valentina Mercurio , Massimo Imbriaco , Stefano Ghio , Matteo Sofia , Domenico Bonaduce , Serafino Fazio a,⁎ a Department of Clinical Medicine, Cardiovascular and Immunological Sciences, Federico II University — Naples, Italy b Department of Biomorphological and Functional Sciences, Federico II University — Naples, Italy c Department of Cellular and Molecular Biology and Pathology “L. Califano”, Federico II University — Naples, Italy d Department of Respiratory Diseases, Federico II University — Naples, Italy e Department of Cardiology, Fondazione IRCCS Policlinico S. Matteo, Pavia, Italy

Exhaled nitric oxide monitoring in COPD using a portable analyzer.

BACKGROUND The exhaled nitric oxide (FeNO) is a non-invasive marker of airway inflammation in asthma. A very recent statement has suggested FeNO as potential outcome in chronic obstructive pulmonary disease (COPD). Recently, a new hand-held FeNO analyzer (NIOX MINO) has been developed. PATIENTS AND METHODS We have evaluated the NIOX MINO in COPD patients and monitored FeNO levels during 1-year assessment in the outpatient setting. Short-term variability in FeNO was compared using a NIOX MINO and a stationary chemiluminescence analyzer (NOA, Sensormedics) in healthy volunteers and COPD patients on two consecutive months. Long-term FeNO variability was assessed on a cohort of 70 COPD outpatients measuring FeNO for 1 year. The intra-individual FeNO coefficient of variation (eNOCoV) was taken as index FeNO long-term variability. RESULTS In COPD there were no significant differences between NIOX MINO and NOA FeNO values recorded at baseline and 1 month later. Ninety five percent limits of agreement between NIOX MINO and NOA were-2.7 and 1.9ppb with significant reliability (r=0.96, p<0.0001). Mean FeNO at baseline was 15.0+/-9.5ppb. Over the 1-year period the overall mean FeNO was 15.5+/-10.1ppb. The long-term eNOCoV was 33.9+/-16.4% (range 8.1-83.1%), and it was significantly associated with exacerbation rate (r=0.57, p<0.0001). CONCLUSION FeNO electrochemical hand-held analyzer is feasible in COPD showing good agreement with stationary chemiluminescence analyzer. COPD patients exhibit a wide range of FeNO levels and a high variability of FeNO over time, which was positively associated with the number of exacerbations.

COPD: adherence to therapy

Adherence to medical therapies is a growing issue, so much so that the World Health Organization defined it as “a new pharmacological problem”. The main factors affecting compliance are: frequency of administration, rapid onset of action, role of device. The most severe consequence of non-adherence is the increased risk of poor clinical outcome, associated with worsening of the quality of life and increase in health-care expenditure. It appears crucial to identify those COPD patients who are “poorly or not at all compliant with their treatment”. In order to evaluate adherence to the medical therapy, several methods were proposed, the most effective of which turned out to be self-reports, i.e. simple, brief questionnaires (e.g. Morisky test). To increase the likelihood of quickly identifying non-compliant patients, it may be useful to administer a simple questionnaire to naïve subjects (for example, in the waiting room before an examination) including six specific items allowing to identify the patient’s key characteristics. Depending on the answers, patients who do not comply with their pharmacological treatment may be classified as belonging to 6 phenotypes. For patients who are already under treatment it might be useful to administer another short questionnaire during follow up examination. Once the risk of non-compliance is identified, four possible types of measures can be taken: prescription-related, educational, behavioral and complex combined measures (combination of two or more actions).Therefore, while it is clear that adherence in COPD is a critical issue, it is also obvious that raising awareness on the disease and improving cooperation among specialists, general practitioners, health-care professionals, and patients is the starting point at which this evolution should immediately begin. Each medication is able to foster good compliance with the therapy, and consequently to maximize the efficacy, by virtue of its specific inhaler and its own active ingredient.

Venous thromboembolism and lung cancer: a review.

Venous thromboembolism (VTE) is a common complication of malignancies and epidemiological studies suggest that lung cancer belonged to the group of malignancies with the highest incidence rates of VTE. Risk factors for VTE in lung cancer patients are adenocarcinoma, NSCLC in comparison with SCLC, advanced disease, pneumonectomy, chemotherapy including antiangiogenic therapy. Other risk factors are pretreatment platelet counts and increased release of TF-positive microparticles. Elevated D-dimer levels do not necessarily indicate an increased risk of VTE but have been shown to be predictive for a worse clinical outcome in lung cancer patients. Mechanisms responsible for the increase in venous thrombosis in patients with lung cancer are not understood.Currently no biomarker is recognized as a predictor for VTE in lung cancer patients.Although several clinical trials have reported the efficacy of antithrombotic prophylaxis in patients with lung cancer who are receiving chemotherapy, further trials are needed to assess the clinical benefit since these patients are at an increased risk of developing a thromboembolism.

Sildenafil in severe pulmonary hypertension associated with chronic obstructive pulmonary disease: A randomized controlled multicenter clinical trial

BACKGROUND Pulmonary hypertension (PH) is a well-known independent prognostic factor in chronic obstructive pulmonary disease (COPD) and a sufficient criterion for lung transplant candidacy. Limited data are currently available on the hemodynamic and clinical effect of phosphodiesterase 5 inhibitors in patients with severe PH associated with COPD. This study assessed the effect of sildenafil on pulmonary hemodynamics and gas exchange in severe PH associated with COPD. METHODS After screening, this multicenter, randomized, placebo-controlled double-blind trial randomized patients to receive 20 mg sildenafil or placebo 3 times a day (ratio 2:1) for 16 weeks. The primary end point was the reduction in pulmonary vascular resistance. Secondary end points included BODE (body mass index, airflow obstruction, dyspnea, and exercise capacity) index, 6-minute walk test, and quality of life questionnaire. Changes in the partial pressure of arterial oxygen were evaluated as a safety parameter. RESULTS The final population included 28 patients, 18 in the sildenafil group and 10 in the placebo group. At 16 week, patients treated with sildenafil had a decrease in pulmonary vascular resistance (mean difference with placebo -1.4 WU; 95% confidence interval, ≤ -0.05; p = 0.04). Sildenafil also improved the BODE index, diffusion capacity of the lung for carbon monoxide percentage, and quality of life. Change from baseline in the partial pressure of arterial oxygen was not significantly different between the sildenafil and placebo groups. CONCLUSIONS This pilot study found that treatment with sildenafil reduced pulmonary vascular resistance and improved the BODE index and quality of life, without a significant effect on gas exchange.