Asthma-chronic obstructive pulmonary disease overlap: Results from a national-multicenter study.

Introduction: Patients with asthma-chronic obstructive pulmonary disease (COPD) overlap (ACO) have a greater disease burden than those with COPD or asthma alone. In this study, it was aimed to determine the prevalence, risk factors, and clinical features of ACO because there are limited national data in Türkiye. Materials and Methods: The study was conducted in a cross-sectional design in nine tertiary-care hospitals. The patients followed with a diagnosis of asthma or COPD for at least one year were enrolled in the study. The frequency of ACO and the characteristics of the patients were evaluated in the asthma and COPD groups. Result: The study included 408 subjects (F/M= 205/203, mean age= 56.24 ± 11.85 years). The overall prevalence of ACO in both groups was 20.8% (n= 85). The frequency was higher in the COPD group than in the asthma group (n= 55; 33.3% vs. n= 22; 9.8%), respectively (p= 0.001). Patients with ACO had similarities to patients with COPD in terms of advanced age, sex, smoking, exposure to biomass during childhood, being born in rural areas, and radiologic features. Characteristics such as a history of childhood asthma and allergic rhinitis, presence of chronic sinusitis, NSAID hypersensitivity, atopy, and high eosinophil counts were similar to those of patients with asthma (p<0.001). The annual decline in FEV1 was more prominent in the ACO group (mean= -250 mL) than in the asthma (mean change= -60 mL) and COPD (mean change= -230 mL) groups (p= 0.003). Conclusions: This study showed that ACO was common among patients with asthma and COPD in tertiary care clinics in our country. ACO should be considered in patients with asthma and COPD who exhibit the abovementioned symptoms.

Comparison of 300 mg versus 600 mg daily maintenance doses of aspirin treatment after desensitization in N-ERD: A three-year multicentre experience.

Background: Aspirin treatment after desensitization (ATAD) is effective in preventing nasal polyps recurrence as well as respiratory symptoms in patients with nonsteroidal anti-inflammatory drug (NSAID)-exacerbated respiratory diseases (N-ERD). However, there is no consensus on effective daily maintenance doses in ATAD. Therefore, we aimed to compare the effects of two different maintenance doses of aspirin on clinical outcomes for 1-3 years of ATAD. Methods: This was a retrospective, multicenter study that involved four tertiary centers. The maintenance doses of daily aspirin were 300 mg in one center and 600 mg in the remaining three. The data of patients who were on ATAD for 1-3 years were included. Study outcomes (nasal surgeries, sinusitis, asthma attacks, hospitalization, oral corticosteroid use, and medication uses) were assessed in a standardized way and recorded from case files. Results: The study initially included 125 subjects, 38 and 87 were receiving 300 and 600 mg daily aspirin for ATAD, respectively. Number of nasal polyp surgeries decreased after 1 -3 years compared with before ATAD in both groups (group 1, baseline: 0.44 ± 0.07 versus first year: 0.08 ± 0.05; p < 0.001 and baseline: 0.44 ± 0.07 versus 3rd year: 0.01 ± 0.01; p < 0.001; and group 2, baseline 0.42 ± 0.03 versus first year: 0.02 ± 0.02; p < 0.001 and baseline: 0.42 ± 0.03 versus 3rd year: 0.07 ± 0.03; p < 0.001). Conclusion: Given the comparable effects of 300 mg and 600 mg aspirin daily as maintenance treatment of ATAD on both asthma and sinonasal outcomes in N-ERD, our results suggest using 300 mg of aspirin daily in ATAD owing to its better safety profile.

What happens to basophils and tryptase, LXA4 and CysLTs during aspirin desensitization?

INTRODUCTION: Aspirin desensitization (AD) is an effective treatment in patients with non-steroidal anti-inflammatory drugs (NSAID)-exacerbated respiratory disease (NERD) by providing inhibitory effect on symptoms and polyp recurrence. However, limited data is available on how AD works. We aimed to study comprehensively the mechanisms underlying AD by examining basophil activation (CD203c upregulation), mediator-releases of tryptase, CysLT, and LXA4, and LTB4 receptor expression for the first 3 months of AD. METHODS: The study was conducted in patients with NERD who underwent AD (group 1: n = 23), patients with NERD who received no desensitization (group 2: n = 22), and healthy volunteers (group 3, n = 13). All participants provided blood samples for flow cytometry studies (CD203c and LTB4 receptor), and mediator releases (CysLT, LXA4, and tryptase) for the relevant time points determined. RESULTS: All baseline parameters of CD203c and LTB4 receptor expressions, tryptase, CysLT, and LXA4 releases were similar in each group (p > 0.05). In group 1, CD203c started to be upregulated at the time of reactions during AD, and continued to be high for 3 months when compared to controls. All other study parameters were comparable with baseline and at the other time points in each group (p > 0.05). CONCLUSION: Although basophils are active during the first 3 months of AD, no releases of CysLT, tryptase or LXA4 exist. Therefore, our results suggest that despite active basophils, inhibition of mediators can at least partly explain underlying the mechanism in the first three months of AD.

Aspirin desensitization following endoscopic sinus surgery is effective in patients with nonsteroidal antiinflammatory drug exacerbated respiratory disease.

INTRODUCTION: Aspirin desensitization (AD) is effective in relieving asthma and sinonasal outcomes in patients with non-steroidal anti-inflammatory drug (NSAID)-exacerbated respiratory disease (N-ERD). So far, only a limited number of studies evaluated the effect of AD prospectively in a controlled manner in N-ERD. It is also a current approach to recommend endoscopic sinus surgery (ESS) before AD. This study aimed to prospectively document the clinical effects of AD for 1 year in patients with N-ERD who underwent ESS in the presence of a control group. METHODS: The study included patients with N-ERD who underwent AD (group 1, n = 22) and patients with N-ERD in whom desensitization was indicated but was not performed (group 2, n = 21). All patients had ESS before enrollment in the study. Asthma and rhinosinusitis outcomes were assessed at baseline and after 1 year. RESULTS: The study included a total of 43 subjects (F/M:28/15, mean age: 44.7 ± 2.8 years). Fewer patients had nasal polyp recurrency in group 1 (5/22, 22.7%) than in group 2 (11/21, 52.3%) at the end of the first year (p = 0.035). Smell-test scores were preserved only in group 1 after 1 year. There were significant decreases in the use of both asthma and nasal medications only in group 1. CONCLUSION: Our results strongly support the use of AD for the improvement of both nasal and asthmatic outcomes in patients with N-ERD for 1 year. We also recommend patients undergo ESS before AD. Further controlled studies are necessary to evaluate whether this effect lasts longer.

Smoking attitudes of the patients with allergic rhinitis: a comparison with asthma and chronic obstructive pulmonary disease. Are there differences when only upper airways are involved?

INTRODUCTION: Despite the well documented relationship between lower airway diseases and smoking, there are limited data about smoking and allergic rhinitis (AR). In this study, we aimed to document the smoking behaviour and environmental tobacco smoke (ETS) exposure of the patients with AR in comparison with patients with asthma, chronic obstructive pulmonary diseases (COPD) and healthy controls (HC). MATERIALS AND METHODS: Demographics and disease characteristics were recorded from case files whereas smoking history, childhood and current exposures to ETS, as well as the smoking behaviors were investigated by a self reported questionnaire. RESULT: A total of 937 subjects comprising patients with AR (n= 252), asthma (n= 249), COPD (n= 188) and HCs (n= 248) were enrolled in the study. The rates of active smokers were 35% (HCs), 26% (COPD), 21% (AR), and 11% (asthma). Exposure to ETS while with friends was significantly higher among HCs and AR groups (p< 0.0001). The rate of willingness to quit smoking is high in AR patients (73%) but they did not determined about date of quiting. CONCLUSIONS: Our results showed that a significant number of patients with AR actively smoke and neither the patients with AR nor the people in their surroundings were sufficiently aware of the health hazards of smoking with AR. It seems necessary to inform patients with about the health effects of smoking on all respiratory tract diseases.

[Acute exacerbation in COPD and asthma]. / KOAH ve astimda atak.

Chronic obstructive pulmonary disease (COPD) and asthma are airway diseases with acute exacerbations. Natural course of both disease are affected by exacerbations. COPD exacerbations may be caused by infections and other causes; indoor and outdoor pollution, cardiovascular diseases, asthma-COPD overlap syndrome, COPD- obstructive sleep apnea syndrome, pulmonary embolism, gastro-oesophageal reflux, anxiety-depression, pulmonary hypertension. Exposure to triggering factors, viral infections, treatment insufficiency may cause asthma exacerbations. Smoking cessations, prevention of infections, long-acting anticholinergics, long-acting 2 agonists, inhaled corticosteroids, phosphodiesterase-4 inhibitors, mucolytics, prophilactic antibiotics can be effective on the prevention of COPD exacerbations. Asthma exacerbations may be decreased by the avoidance of allergens, viral infections, occupational exposures, airpollution, treatment of comorbid diseases. Effective treatment of asthma is required to prevent asthma exacerbations. Inhaled steroids and combined treatments are the most effective preventive therapy for exacerbations. Patient education and cooperation is an element of the preventive measures for asthma attacks. Compliance to therapy, inhalation techniques, written asthma plans are required. The essential of COPD and asthma exacerbation treatment is bronchodilator therapy. Steroids are also implemented to the therapy, targeting the inflammation. Specific treatments of the cause (infection, airpollution, pulmonary embolism etc.) should be administered.

[Asthma-COPD overlap syndrome]. / Astim-KOAH overlap Sendromu.

Asthma and chronic obstructive pulmonary disease (COPD) are common lung diseases characterized by chronic airway inflammation and airway obstruction. Among patient with COPD and asthma; there is a group of patients with an overlap between clinical, functional characteristics and airway inflammation patterns, named "Asthma-COPD Overlap Syndrome" (ACOS). ACOS is a syndrome characterized by reversible but persistant airflow limitation (postbronchodilator FEV1/FVC < 70%) which has some features of both asthma and COPD. ACOS should be suspected in a patient > 40 years, with smoking history, previous asthma diagnosis or history of childhood asthma who has persistant airflow limitation and reversible ariway obstruction (defined by an increase of > %12 of FEV1 pred or increase of FEV1 > 200 mL after inhalation of 400 mcg salbutamol or 1000 mcg terbutaline). The prevalence for ACOS has been reported 11-55% in different case series to date and increases by age and is more frequent in females in different age groups. Patients with ACOS are younger than COPD patients and older than asthma patients. Frequent and severe exacerbations and related hospitalization and emergency room visits are common in ACOS and this causes an impaired quality of life. Current recommendations of guidelines for pharmacologic treatment of ACOS have been composed of a combination with optimal COPD and asthma treatment. Future therapeutic approaches should be based on endotypes. Clinical phenotype and underlying endotype driven clinical studies may be the base of ACOS guidelines.

Churg-Strauss syndrome: a new endotype of severe asthma? Results of 14 Turkish patients.

INTRODUCTION: Churg-Strauss syndrome (CSS) is a rare multisystem vasculitis. Considering the variation of autoimmune diseases in different races, it is of interest to determine whether any outstanding features exist for Turkish patients with CSS. OBJECTIVE: The aim of this study was to evaluate the clinical and serological features of the disease, the treatment, and long-term follow-up details, and to investigate possible etiological factors of Turkish CSS patients. METHODS: The study included 14 patients who were diagnosed with CSS, and followed by our department between 2004 and 2012. Possible etiological factors, initial symptoms, clinical presentations, treatment, as well as outcomes were documented. The study was approved by the local ethics. RESULTS: All patients fulfilled the American College of Rheumatology criteria. Initial symptoms were worsening asthma (n = 14; 100%) and skin lesions (n = 6; 43%). All patients had a diagnosis of asthma and nasal polyps, whereas 57.1% had aspirin hypersensitivity at the time of diagnosis. The lungs (100%) and skin (43%) were most commonly involved. Peripheral eosinophilia dominated on initial presentations of all patients. Initial treatments included oral methyl prednisolone in all cases, whereas cyclophosphamide and azathioprine were used in three cases. Relapses were detected in five cases. None of the cases were able to stop the oral corticosteroid treatment. No fatalities were observed. CONCLUSION: We herein describe a new severe asthma endotype in connection with CSS. We suggest that physicians who deal with uncontrolled severe asthma cases should consider CSS in the presence of nasal polyps, aspirin hypersensitivity, and especially peripheral blood eosinophilia over 10%.

Direct medical cost of asthma in Ankara, Turkey.

BACKGROUND: There has been no documented data regarding the cost of asthma in our country. OBJECTIVE: In this 1-year prospective study, we aimed to determine the annual cost of asthma in Ankara, Turkey. METHODS: Direct medical cost analysis was performed in 118 patients. RESULTS: Mean annual direct medical costs of asthma were USD 1,465.7 +/- 111.8 per capita. Medication cost comprised the majority (81%) of the total direct cost. Mean direct medical costs according to the stage of disease were USD 172.5 +/- 51.7, 860.7 +/- 70.2, 1,671.6 +/- 141.8 and 3,491.9 +/- 417.6 for stage 1 (n = 4), 2 (n = 54), 3 (n = 46) and 4 (n = 14) patients, respectively. CONCLUSIONS: In this first study to document the cost of asthma for our region, direct cost of asthma was found to be increased with the severity of the illness. Considering the fact that medication cost comprises the major fraction of the direct cost, cost-effectiveness trials to determine the effective treatment with optimal cost for different asthma stages should be the next step.