Search

Mental health issues such as depression and anxiety are common comorbidities of individuals suffering from chronic obstructive pulmonary disease (COPD), though they are frequently underdiagnosed and consequently undertreated. To that end we sought to identify the impact of co-morbid anxiety and depression in COPD patients and evaluate recent evidence regarding the management of such cases. A Pubmed search was conducted for relevant original articles with emphasis on the past 5 years. The studies we identified indicate that psychiatric comorbidity negatively impacts the prognosis of COPD, as it is associated with reduced adherence to treatment, reduced physical activity and a general reduction in quality of life, in turn leading to more frequent exacerbations and increased severity of exacerbations (which are more likely to require hospitalization), resulting in increased mortality. Despite the evidence showing a high prevalence and exceedingly negative impact of depression and anxiety in patients with COPD, very few clinical trials (for both pharmacological and psychological treatments) with small sample sizes have been conducted in this population. As treatment for co-morbid mental health conditions may reduce mortality, interventions to ensure prompt identification of mental health issues and subsequent initiation of treatment are warranted.

Objective: Osteoporosis is highly prevalent among patients with chronic obstructive pulmonary disease (COPD) and most commonly presents as a vertebral compression fracture (VCF). Our objective was to quantify the effect of osteoporosis and VCFs on the mortality and pulmonary function tests (PFTs), such as forced expiratory volume in 1 second (FEV1) and forced vital capacity (FVC), of patients with COPD. Methods: A PubMed/Medline search was conducted using the search terms “chronic obstructive pulmonary disease”, “osteoporosis” and “vertebral compression fracture”. Meta-analyses were conducted to evaluate the differences in mortality and PFTs between patients with COPD with and without osteoporosis or VCFs, according to PRISMA guidelines. PROSPERO registration: CRD42019120335. Results: Of the 896 abstracts identified, 27 studies describing 7662 patients with COPD of which 1883 (24.6%) had osteoporosis or VCFs, were included. Random effects model analysis demonstrated that patients with COPD and osteoporosis or VCFs had an increased OR for mortality of 2.40 (95% CI: 1.24; 4.64, I2 = 89%, P < 0.01), decreased FEV1/FVC with a mean difference of −4.80% (95% CI: −6.69; −2.90, I2 = 83%, P < 0.01) and decreased FEV1, with a mean difference of −4.91% (95% CI: −6.51; −3.31, I2 = 95%, P < 0.01) and −0.41 L (95% CI: −0.59; −0.24, I2 = 97%, P < 0.01), compared to control subjects. Apart from FEV1 (liters) in subgroup 1 (P = 0.06), all subgroup analyses found significant differences between groups, as did sensitivity analysis of low risk of bias studies. Conclusion: Osteoporosis and VCFs are associated with a significant reduction in survival and pulmonary function among patients with COPD.

The disease burden associated with schizophrenia and bipolar disorder is substantial, with affected individuals having a shorter life expectancy and a high risk of severe physical comorbid conditions. These individuals are more likely to smoke and have a longer smoking history compared to the general population. Furthermore, use of antipsychotic drugs has also been linked to active smoking. Chronic obstructive pulmonary disease (COPD) is a respiratory condition affecting elderly individuals with a long smoking history, so it would be expected that individuals suffering from major mental disorders may exhibit a higher prevalence of COPD compared to the general population. We searched the databases Pubmed and Scopus for observational studies of at least 200 patients including at least one group suffering from schizophrenia or bipolar disorder and a comparison group of individuals at risk of COPD. The initial search, along with the data extraction process and the risk of bias assessment were carried out independently by the two reviewers. Eight studies were included. The risk of bias was substantial as most studies did not adequately address confounding variables. A pooled analysis showed a greater likelihood of suffering from comorbid COPD compared with the general population both for schizophrenic (OR 1.573, 1.439-1.720) and bipolar individuals (OR 1.551, 1.452-1.658). Based on these findings, COPD is more common in individuals suffering from major mental illness compared to the general population. Further research is required to ascertain whether smoking is the only cause and develop strategies for the prevention of COPD in these high-risk groups.

SummaryEndothelin-1 (ET-1) has been implicated in the pathogenesis of Chronic Obstructive Pulmonary Disease (COPD) for establishing an inflammatory loop in the respiratory mucosa that could become independent from the initial irritant factor. Common causes of COPD exacerbations are associated with elevated ET-1 sputum concentrations. Genetic variants of the ET-1 gene, that lead to elevated ET-1 peptide levels, have not been investigated in COPD.We performed a case control, genetic study to assess possible associations of two polymorphisms of the ET-1 gene, an adenine insertion (+134 insA/delA) and a guanine to thymine transversion (G198T) with the COPD phenotype and disease severity.The genotypes of 209 subjects, 107 COPD smokers (patients) and 102 non-COPD smokers (controls) were examined. Statistical analysis revealed that the 3A/4A and 4A/4A genotypes were more common (P

Clear decrements in lung function have been reported in patients with diabetes over the past two decades, and many reports have suggested plausible pathophysiological mechanisms. However, there are no reports of functional limitations of activities of daily living ascribable to pulmonary disease in patients with diabetes. This review attempts to summarize the available information from the present literature, to describe the nature of the lung dysfunction in diabetes and the emerging clinical implications of such dysfunction.

This report describes a female patient with bronchiectasis, presented to our department with recurrent hemoptysis. Bronchoscopy revealed nothing else but blood arising from the upper lobe bronchus. High resolution computing tomography of the lung (HRCT) revealed bronchiectasis of the upper lobe. A right upper lobectomy was performed. Behind bronchiectasis multiple nodular lesions, 5-10 mm were observed. Histological and immunohistochemical examination revealed findings consistent with peripheral typical bronchial carcinoids.

Tuberculosis (TB) caused by the human pathogen Mycobacterium tuberculosis, is the leading cause of morbidity and mortality caused by infectious agents worldwide. Recently, there has been an ongoing concern about the clarification of the role of specific human genes and their polymorphisms involved in TB infection. In the vast majority of individuals, innate immune pathways and Thelper 1 (Th1) cell mediated immunity are activated resulting in the lysis of the bacterium. Firstly, PTPN22 R620W polymorphism is involved in the response to cases of infection. The Arg753Gln polymorphism in TLR-2 leads to a weaker response against the M. tuberculosis. The gene of the vitamin D receptor (VDR) has a few polymorphisms (BsmI, ApaI, Taq1, FokI) whose mixed genotypes alter the immune response. Solute carrier family 11 member (SLC11A1) is a proton/divalent cation antiporter that is more familiar by its former name NRAMP1 (natural resistance associated macrophage protein 1) and can affect M. tuberculosis growth. Polymorphisms of cytokines such as IL-10, IL-6, IFN-g, TNF-a, TGF-b1 can affect the immune response in various ways. Finally, a major role is played by M. tuberculosis antigens and the Ras-associated small GTP-ase 33A. As far as we know this is the first review that collates all these polymorphisms in order to give a comprehensive image of the field, which is currently evolving.

Background: Endothelin-1 (ET-1) has been implicated in the pathogenesis of asthma and chronic obstructive pulmonary disease (COPD). The ET-1 levels are elevated during exacerbations of asthma and COPD in bronchoalveolar lavage, serum, and sputum and fails with treatment of the exacerbations. Hypoxemia stimulates ET-1 secretion. Objective: The aim of this study was to examine the serum ET-1 levels in stable asthmatic and COPD patients. Materials and methods: We examined 48 COPD and 26 asthmatic patients and 34 normal subjects. We collected arterial samples to measure baseline ET-1 levels in all patients and in the control group, during the day. All the patients underwent formal polysomnography (EEG, ECG, airflow, respiratory muscle movement, oximeter) to detect the presence of nocturnal, nonapneic, and oxyhemoglobin desaturation. Twelve of the COPD patients and six of the asthmatic patients were disqualified because of inadequate sleep or sleep apnea syndrome. Nineteen of the COPD patients desaturated below a baseline sleep saturation of 90% for 5min or more, reaching a nadir saturation of at least 85%. We collected arterial samples to measure ET-1 levels, 5min after the first period of desaturation in each of the 19 desaturators COPD patients. None of the 20 asthmatic patients exhibited oxyhemoglobin desaturation during sleep. Results: Baseline arterial ET-1 levels during the day were significantly higher in “desaturators” COPD patients (2.08±0.28pg/ml) compared to “non-desaturators” COPD patients (1.38±0.16pg/ml) (P

Endothelins are a family of peptide mediators that have a number of biological properties, including the ability to act as bronchoconstrictors and vasoconstrictors of isolated airways and vessels. Endothelin-1 (ET-1) is the more potent peptide compared with the other two peptides of the family. To examine a possible involvement of ET- 1 in the pathogenesis of asthma, we measured arterial ET-1 levels in 11 patients with atopic asthma during attack and during remission, and in 11 healthy control subjects. We also performed fiberoptic bonchoscopy and bronchoalveolar lavage (BAL) to measure ET-1 levels in the 11 asthmatic patients during remission, and in the 11 healthy control subjects. ET-1 concentrations in arterial blood and in BAL were measured by a radioimmunoassay method. Arterial ET-1 levels were very significantly higher in asthma attack (3.67 +/- 0.51 pg ml(-1)) and in asthma remission (2.65 +/- 10.62 pg ml(-1)) compared with those of the healthy controls (1.37 +/- 0.14 pg ml(-1)) (P < 0.001). Arterial ET-1 levels were also very significantly higher during asthma attack compared with those in asthma remission (P < 0.001). BAL ET-1 levels were significantly higher in asthma remission (0.73 +/- 0.53 pmol g(-1)) compared with those of the healthy controls (0.16 +/- 0.02 pmol g(-1)) (P < 0.05). No correlation was observed between arterial and BAL ET-1 levels, PaO2 and peak expiratory flow rate (PEFR). These data are consistent with the hypothesis that ET-1 contributes to the pathophysiology of asthma. However, it is likely that the true importance of this vasoconstrictor peptide will only be revealed by pharmacological studies with specific receptor antagonists.

Gene therapy uses a variety of techniques as the introduction of a normal allele of a gene in cases where the cell does not express the gene or in other cases where the gene is underexpressed. In order to achieve effective gene therapy for a specific gene in a certain type of cells a lot of work is needed. More specifically the following steps are essential: 1. Isolation of target gene, 2. Development of a specific gene vector, 3. Specification of the target cell, 4. Definition of route of administration, and 5. Identification of other potential uses of the gene.

Respiratory disease is common and amenable to early detection and management in the primary care setting. Spirometric and phlethysmographic evaluation of ventilatory function plays a critical role in the diagnosis, differentiation and management of respiratory illness such as asthma, chronic obstructive pulmonary disease and restrictive disorders.Study subjects consisted of 58 workers in the production of bread and 45 salesclerks of bread from the same bakeries. The lung function of employees was checked using a spirometry and body phlethysmography, calculating the indexes Forced expiratory volume 1 sec (FEV1), forced vital capacity (FVC), FEV1/FVC ratio, residual volume (RV), total lung capacity (TLC), and RV/TLC ratio. The percentage of the obstructive and the restrictive impairment both in the bread producers and sellers was also searched as well as the percentage of response in the bronchodilation.Bread producers recorded significantly lower mean lung functions compared with salesclerks, for FEV1, FVC and FEV1/FVC ratio, when observed values were expressed as percentages of predicted normal values. Furthermore the percentage of obstructive impairment among the bread producers was 12.6%, while a percentage of 20.68% of them presented a response in bronchodilation (while the percentage in salesclerks was 6.6% respectively). The percentage of restrictive impairment was similar in both groups (12.6% for bread producers and 11.1% for salesclerks).The study concluded that bread producers in traditional bakeries in Greece are at increased risk of developing airway obstruction compared with salesclerks of bread from the same bakeries. A different degree of smoking status and of wheat flour dust exposure may explain this difference. Technical preventive measures such as well ventilated work areas and appropriate respiratory protective devices should be adopted.

The purpose of this review article is to prove the damage that alcohol causes to the respiratory system. We will make a brief review of alcohols history in the course of the centuries till nowadays. The problem of addiction to alcohol (alcoholism) will be examined for several countries. Alcohol’s metabolism is another topic to be discussed parallel to its pharmacological action. In addition, alcohol’s impact on the respiratory system varies from damaging the mucociliary system to the regulation of breathing and from the sleep apnea syndrome to diffusion disorders. “Alcoholic lung disease” constitutes a syndrome despite the fact that the damage of the lung due to concurrent smoking and drug use is often indistinguishable.

Aseptic (avascular) necrosis of the femoral head in adults has been associated with a variety of disease entities. It is also recognized as a potential complication of systemic corticosteroid therapy. Inhaled corticosteroids are the first line anti-inflammatory agents for the long term treatment of asthma. However, long term treatment of asthma with inhaled corticosteroids has been accompanied by concern about both systemic and topical side effects. The most worrying potential systemic effects are adrenal insufficiency, growth suppression, glaucoma and osteoporosis. Fluticasone proprionate may be prescribed at higher doses to relieve respiratory symptoms in the belief that it generates fewer side effects than other inhaled steroids. Studies have shown that fluticasone is safer than beclomethasone or budesonide, with limited oral absorption and extensive hepatic first pass metabolism leading to a lower systemic bioavailability. However growth retardation and asymptomatic adrenal suppression in children receiving high-dose fluticasone have been reported. We report a rare case of avascular osteonecrosis of the femoral head associated with the use of long term inhaled fluticasone propionate along with the intranasal application of triamcinolone acetonide.

Asthma and chronic obstructive pulmonary disease (COPD) are complex genetic diseases that cause considerable morbidity and mortality worldwide. Genetic variability interacting with environmental and ethnic factors is presumed to cause tobacco smoke susceptibility and to influence asthma severity. A disintegrin and metalloproteinase 33 (ADAM33) and matrix metalloproteinase-9 (MMP9) appear to have important roles in asthma and COPD pathogenesis. ADAM33 and MMP9 genetic alterations could possibly contribute to the establishment and progression of these multifactorial diseases, although their association with the clinical phenotypes has not yet been elucidated. However, the occurrence of these alterations does not always result in clear disease, implying that either they are an epiphenomenon or they are in proximity to the true causative alteration. This review summarises the most recent literature dealing with the genetic variations of metalloproteinases and outlines their potential pathogenetic outcome.

Endometriosis is a common cause of chronic pelvic pain and infertility affecting women of reproductive age, but the disease in rare conditions may be extragenital so may be present with a variety of symptoms. This is a report of an unusual case of pelvic endometriosis that presented with a recurrent hemothorax.

Background Working on shifts, especially on a night shift, influences the endogenous sleep regulation system leading to diminished sleep time and increased somnolence. We attempted to evaluate the impact of shifts on sleepiness and correlate the sleepiness score to the experience in a shift schedule. Materials and methods This cross-sectional study consists of 42 male and 2 female workers involved in a tunnel construction. They underwent spirometry, pulse oximetry and were asked to complete the Epworth Sleepiness Scale questionnaire. Results Statistical analysis revealed that workers of lower Epworth had a mean age of 43.6 years, compared to the mean age of 36.4 years of workers with higher Epworth. Furthermore, workers of lower Epworth were characterized by a mean number of shift years equal to 14.8, while those of higher Epworth possessed a mean number of shift years equal to 8. The shift schedule did not reveal any statistically significant correlation. Conclusions Workers employed for a longer time had diminished sleepiness. However, there is no relationship between night shifts and sleepiness, possibly because of exposure to artificial lighting in the construction site.

Summary Purpose : The purpose of this study was to examine exercise tolerance in patients with COPD from measurements of resting pulmonary function parameters. Methods : A total of 57 COPD patients were administered the pulmonary function test (PFT) and cardiopulmonary exercise test. The results were analyzed and essentially linear relationships emerged when each subject's V O 2 peak was plotted against his individual PFT parameters. Those significant contributors were then introduced in a stepwise multiple regression analysis to determine the best predictor of the V O 2 peak. Results : Stepwise multiple regressions in variables revealed that peak oxygen consumption ( V O 2 peak) was predicted best by the following equation: V O 2 peak=(maximum voluntary ventilation×0.024)+(forced mid-expiratory flow×0.47)+(body surface area×0.988)−0.913 ( r = 0.90 ; r 2 = 0.81 SE=0.29L/min). Conclusion : We conclude that exercise capacity was predicted from measurements of resting pulmonary function parameters with excellent accuracy in the COPD patient.