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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.

Background Obstructive Sleep Apnea (OSA) is an independent risk factor for cardiovascular disease and has been linked to the development of atherosclerosis. However, the underlying role of metabolic derangements in the development of atherosclerosis in OSA patients is not well-defined yet. Objective The aim of this study was to test whether patients with newly diagnosed OSA have an increased probability to develop carotid atherosclerosis as compared to healthy individuals. Methods A total of 40 subjects without a previous history of cardiovascular disease that underwent full night polysomnography were included in the study. Subjects with an apnea/hypopnea index (AHI) ≥15/h) were classified as moderate/severe OSA. Ultrasound was used to measure the carotid mean intima media thickness (cIMT) and the presence of atheromatic plaques on both carotid arteries of the subjects. Results All participants were well matched and had a similar cardiovascular risk profile (Framingham risk factors). Moderate to severe OSA was diagnosed in 21 subjects. The two groups had similar measurements of cIMT (0.66±0.17 vs 0.75±0.20 p= 0.33) and presence of atheromatic plaque (50% vs 45%, p=1.00). Conclusion Our study suggests that in patients with a similar cardiovascular risk profile and without history of cardiovascular disease, the severity of newly diagnosed OSA is not correlated to carotid atherosclerosis.

Introduction: Obstructive Sleep Apnoea Syndrome (OSA) is a highly prevalent sleep disorder characterized by recurrent airflow obstruction. OSA leads to chronic intermittent hypoxia and sleep fragmentation; thus provoking multiple metabolic derangements. The relationship between obesity resistance in patients with OSA is rather complex. Aim of the study: Our study attempted to reveal a connection between excessive daytime sleepiness (EDS) in OSA and insulin resistance by the means of homeostatic assessment of b-cell function (HOMA-IR). Materials and methods: We studied a population of 19 OSA patients with EDS, 19 OSA patients without EDS and 20 healthy non-OSA individuals closely matched. Both patients and controls had undergone full night polysomnography. All blood samples were obtained at 6PM in the morning after the night study and were used for the measurement of insulin. Daytime sleepiness was assessed and quantified by the Epworth Sleepiness Scale (ESS). Excessive daytime sleepiness is defined as ESS score>10. Results: There were no significant differences in HOMA-IR index values between the two groups of patients suffering from OSA who had EDS and those who did not have EDS (5.50±2.49 vs. 2.94±0.73 p=0.349). Conclusions: Our study shows that in patients with OSA the excessive daytime sleepiness is not a discriminative characteristic of those who have already developed insulin resistance. Therefore, daytime symptoms in patients with a diagnosis of OSA do not help in the identification of those at risk of metabolic syndrome.

Background: Obstructive Sleep Apnea (OSA) has been associated with both subclinical and accelerated atherosclerosis; however, it remains unknown whether this association is unique or is mediated by the higher burden of co-existing cardio-metabolic disorders frequently seen in patients with OSA. Objective: To prospectively examine whether patients with newly diagnosed moderate/severe OSA carry a higher burden of carotid atherosclerosis as compared to healthy, well matched for all standard Framingham risk factors patients. Methods: A total of 40 subjects without clinically diagnosed cardiovascular disease referred for polysomnography test were included in the study. Subjects with apnea/hypopnea index (AHI) ≥15/h) were classified as moderate/severe OSA. Subclinical changes in carotid atherosclerosis were assessed using mean intima media thickness (cIMT) and presence of atheromatic plaques on both carotid arteries. Measurement was performed using B-mode ultrasonogram. Results: Moderate to severe OSA was diagnosed in 21 subjects. While patients with OSA had a higher BMI compared to healthy subjects, both groups were well matched and of similar cardiovascular risk profile. No significant differences were detected in terms of C-reactive protein levels. The two groups had similar cIMT (0.66±0.17 vs. 0.75±0.20 p=0.33) and presence of atheromatic plaque (50% vs. 45%, p=1.00). Conclusion: Our study suggests that among patients with similar cardiovascular risk profile and free of overt CVD, the severity of newly diagnosed OSA was not correlated with increased inflammation or subclinical carotid atherosclerosis.

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.

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

Asthma is a chronic heterogeneous inflammatory disease of the respiratory system in which numerous cytokines play a significant role. Among them TNF-α (tumour necrosis factor α), a proinflammatory cytokine, has a predominant role in orchestrating airway inflammation and affecting treatment outcome. In this review we attempt to summarize the involvement of TNF-α in the pathogenesis of asthma, illustrate variations of TNF-α gene that potentially influence asthma phenotype and highlight promising therapies by blocking the production of TNF-α or inhibiting its action. A cytokine specific target therapy seems to be very promising since agents that block TNF-α slow disease progression, suppress inflammation and in some cases induce remission of chronic inflammation.

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.

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.

The aim of this work was to study whether social factors are risk factors for obstructive sleep apnea (OSA). A second objective was to investigate gender differences in relation to referral to a sleep laboratory for sleep-related breathing symptoms.A retrospective cross-sectional study was conducted in the referral sleep disorders laboratory in the tertiary University Hospital in Patras in southwest Greece. A sample of 362 subjects originated from this geographic region was screened for social characteristics, i.e., marital status, occupation, and education.The apnea hypopnea index (AHI) was approximately three times as high in men as in women (p0.05). Snoring was reported to be a symptom by 76.6% of males and 75% of females. Excessive daytime sleepiness (EDS) was reported by 25.5% of males and 15% of females. Arousals during sleep were reported by 5.7% of men and 10% of women. The ratio of subjects with concomitant disorders or symptoms did not differ between sexes (p0.05). The influence of age, body mass index (BMI), gender, smoking, and social characteristics on AHI was examined by multinomial logistic regression. The following factors remained independent risk factors for the presence of moderate to severe OSA (i.e., AHI15/h compared with AHI5): (1) Gender: the odds ratio (OR) of males to females was 6.23 (CI = 1.89-20.5). (2) Obesity: the OR of subjects with BMI30.5 kg/m(2) in comparison to those with lower BMI was 3.83 (CI = 1.86-7.86). (3) Marital status: The OR of married subjects to singles was 2.30 (CI = 1.01-5.32). (4) Occupational status: The OR of subjects outside the work force was 3.85 (CI = 1.16-12.74) and that of the self-employed was 1.70 (CI = 0.70-4.10) compared to a reference group of clerks/employees.In our study factors associated with the presence of sleep apnea include gender (men), obesity, marriage, and self-employment or being outside the work force.

Introduction: Obstructive Sleep Apnoea Syndrome (OSAS) is a sleep disorder characterized by recurrent airflow obstruction. OSAS is an established independent factor of cardiovascular risk and is supposed to lead to the development of arterial hypertension; however the underlying mechanisms still remain unclear. The aims of our study was to measure serum levels of aldosterone and renin in OSAS patients and compare them to matched healthy subjects in order to investigate the results of chronic intermittent hypoxia and autonomous system activation on the renin-angiotensin-aldosterone system. Materials and methods: We studied a population of 19 OSAS patients and 20 healthy non-OSAS individuals closely matched regarding their age, gender and Body Mass Index (BMI). Both patients and controls had undergone full polysomnography. It is known that aldosterone levels follow a diurnal variation, therefore blood samples for the measurement of renin and aldosterone were obtained at 6 AM, in a supine position. Serum aldosterone and direct renin concentration were measured by radioimmunoassay. Results: There were no significant differences in serum aldosterone levels between the two studied groups of OSAS patients without arterial hypertension and the healthy subjects group (140,6pg/ml ± 25,2 vs 133,2pg/ml ± 18,5 with p=0,223). Similar were the results for the renin levels (25,0 ± 6,9 vs 24,9 ± 4,4 with p=0,360). Conclusions: Our study shows that patients with OSAS, but without existing hypertension have aldosterone and renin levels similar to healthy subjects. According to our findings a direct connection between OSAS and the development of arterial hypertension may not be established via sympathetic system activation.

Background The aim of this study was to evaluate the significance of albumin in bronchial washing fluid (BWF) and its relationship to three tumor markers (CEA, CA 19–9 and NSE). Methods Serum and BWF samples were collected in a group of 60 patients. Albumin and tumor markers in the BWF and serum of three groups: a control group (CG), a chronic bronchitis group (CBG) and a lung cancer group (CaG), were analyzed in a prospective cross-sectional study. The diagnostic yields of the tests in each environment (serum and BWF) were evaluated by using as cutoff points the values of the corresponding 90th percentile of CG and CBG taken together. Results A significant difference in albumin level (pConclusion Measurement of albumin levels in BWF could be a useful additional diagnostic tool to differentiate malignant from non-malignant lung diseases. Moreover, the combined measurement of CEA in serum and albumin in BWF could be of aid in the follow-up of lung cancer patients.

Pregnancy is associated with significant alterations in respiratory function. Changes during pregnancy include reduced functional residual capacity (FRC) and residual volume (RV), increased alveolar-arterial difference for oxygen (A-αPO 2 ) and in the supine position, reduced cardiac output. In conjunction with sleep-related apneas or hypopneas, these could lead to maternal oxygen desaturation during sleep. Because of the conflicting data from sleep studies in late pregnancy, we performed complete polysomnography on 11 pregnant women at 36 weeks of gestation and again postpartum. We also measured the PaO 2 , every 2h. The frequency of apneas and hypopneas was significantly lower during pregnancy compared with that on the postpartum control night. PaO 2 levels in the supine position, during sleep, were also significantly lower during pregnancy compared to the postpartum period. No correlation was observed between PaO 2 levels and apneas or hypopneas or percent of REM sleep.

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

Marathon racing is a strenuous exercise that has a profound effect on many laboratory parameters. Participants in marathon races may require abstinence of exercise and the performance of laboratory assays several days after the event. The aim of this study was to evaluate the possible changes in blood cell count and biochemical parameters observed in participants in a marathon 3 days before and 3 days after and before and immediately after a cardiopulmonary exercise test. Incremental cycle ergometry up to maximal capacity was performed in 7 marathon runners, 3 days before and 3 days after the race. The % peak oxygen consumption (peak %VO(2)) achieved was statistically significantly lower after than before the race ( p = 0.02). No statistically significant differences were observed in cardiac frequency ( p = 0.148) or blood cell count ( p = 0.501). Also, the concentration of sodium, potassium, calcium, magnesium, lactate dehydrogenase (LDH), phosphocreatine kinase (CPK) and glucose, measured before and immediately after the pulmonary exercise test, did not differ significantly ( p < 0.5). A significant percentage of the laboratory results were outside the standard reference rates. According to our data, exercise performance, as expressed by peak %VO(2), continued to be decreased in marathon runners 3 days after the race. The blood cell count and biochemical parameters did not differ significantly but many marathon runners were outside the standard reference rates. Unfortunately, only 7 subjects were available for this study. Further studies with larger samples and with samples obtained at multiple times during and after exercise are needed to clarify the effects of long-distance running.

Objective: The aim of this study was to determine prognostic factors for outcome in patients with lower respiratory tract infections (LRTI). LRTI are an heterogeneous group of disorders, including acute bronchitis, pneumonia, superinfection of chronic bronchitis and influenza. Methodology: A total of 616 patients with LRTI were retrospectively reviewed with regard to epidemiological, clinical, laboratory and radiographical data. Prognostic analysis included a univariate as well as a multivariate approach, in order to identify parameters associated with death. Results: The parameters found to be significantly different between survivors and non-survivors in the univariate analysis, were respiratory rate, Pao2, heart rate, systolic and diastolic blood pressure, platelet count, urea, creatinine, previous admission to the hospital in the last year and cavitations visible on the chest radiograph. Conclusions: LRTI remain a widespread problem and have a significant impact on primary healthcare resources. The great variability seen in rates of hospital admission and lengths of stay in part reflects uncertainty among physicians in assessing the severity of the illness. According to our data, Pao2 and heart rate were most closely associated with patient death and are readily defined and available at presentation.

Inflammation is supposed to play a great role in the pathogenesis of the most common diseases of the respiratory system. In Chronic Obstructive Pulmonary Disease (COPD), which is a major cause of morbidity and mortality all around the world, smoking mainly causes the initiation of the inflammatory process that leads to an impaired respiratory function. Moreover, in bronchial asthma there are numerous proinflammatory mediators that are responsible for the onset and the progression of the disease. Finally, pulmonary infections and especially tuberculosis result in the orchestration of an inflammatory process that targets the causative agent in order to protect the host. L. M. O. Caram et al. have evaluated the levels of vitamin A in the serum and sputum and attempted to correlate it with known inflammatory markers, such as tumor necrosis factor alpha (TNF-α), interleukin- (IL-) 6, IL-8, and C-reactive protein (CRP) in 50 COPD patients and 50 individuals without COPD. The authors concluded that serum concentration of vitamin A is negatively associated with the presence of COPD and that it is positively associated with smoking status. Although COPD patients exhibited increased inflammation, these inflammatory markers were not associated with serum retinol concentrations. The manuscript of W. Zhang et al. tested the effect of a novel γ-secretase inhibitor to promote Th17 cell differentiation in a mouse model of allergic asthma. Their findings suggest that the inhibitor directly regulates Th17 responses in the mouse model of allergic asthma that they used, making it potentially efficacious. In their study, R. Rajajendram et al. tried a synthetic chalcone analogue in a murine model of asthma. Their results demonstrate a potential role of the substance in asthma, as the treatment with it inhibited eosinophilia, goblet cell hyperplasia, peripheral blood total IgE, and airway hyperresponsiveness in ovalbumin-sensitized and challenged mice. However, the tested nonsteroid potentially anti-inflammatory substance is far away from clinical use. In the manuscript entitled “Binding of CXCL8/IL-8 to Mycobacterium tuberculosis Modulates the Innate Immune Response,” A. Krupa et al. illustrate the role of IL-8 in the pathogenesis of tuberculosis (TB). The authors investigated the contribution of IL-8 in the inflammatory processes that are typically elicited in patients with TB. Their findings show that IL-8 seems to be the major chemokine responsible for recruiting T lymphocytes (CD3+, CD4+, and CD8+ T cells) and plays important role in the innate immunity against Mycobacterium tuberculosis. Last but not least, the study of R. Baumann et al. investigated the IgA and IgG responses to mycobacterial protein antigens in subjects with latent tuberculosis, active tuberculosis, and healthy individuals. In their conclusions they present a new biomarker for the diagnosis of active pulmonary tuberculosis.

Background: Nonapneic, oxyhemoglobin desaturation associated with sleep has been described in patients with chronic obstructive pulmonary disease (COPD). Hypoxemia stimulates endothelin-1 (ET-1) secretion. Once released, ET-1 can act locally to elicit sustained pulmonary artery vasoconstriction, bronchoconstriction and activation of alveolar macrophages. Objective: The aim of this study was to examine a possible correlation between ET-1 levels and nocturnal, nonapneic, oxyhemoglobin desaturation during sleep, in patients with COPD. Methods: We examined 48 COPD patients with formal polysomnography (EEG, ECG, airflow, respiratory muscle movement, oximeter) to detect the presence of nocturnal, nonapneic, oxyhemoglobin desaturation. Twelve of them were disqualified because of inadequate sleep or sleep apnea syndrome. Nineteen of them desaturated below a baseline sleep saturation of 90% for 5 min or more, reaching a nadir saturation of at least 85%. We collected arterial samples to measure ET-1 levels, after 5 min of the first period of desaturation, in each of the 19 patients. We also collected arterial samples in the morning, before the study, to measure baseline ET-1 levels in all patients. Results: Baseline arterial ET-1 levels during the day were very significantly higher in ‘desaturator’ COPD patients (2.058 ± 0.252 pg/ml) compared to ‘non-desaturator’ COPD patients (1.382 ± 0.159 pg/ml; p < 0.001). Also in ‘desaturator’ COPD patients ET-1, levels during the night were significantly higher (4.297 ± 1.107 pg/ml) compared to those during the day (p ≤ 0.001) and a significant negative correlation was observed between ET-1 levels and degree of desaturation (p < 0.0001, r = 0.9305). Conclusions: According to our study we can conclude that (1) ET-1 levels are significantly higher in ‘desaturator’ COPD patients both during the day and during the night, and (2) ET-1 levels correlate negatively significant with the degree of the oxyhemoglobin desaturation. These findings are consistent with the hypothesis that ET-1 plays a very important role in the pathophysiological manifestations of COPD patients.

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.

This article deals with the Learning Patterns (LPs)' generation, a major aspect of Feed-Forward Artificial Neural Networks (FANNs)' learning process. Currently, more work is done to understand the mechanisms and improve the speed, learning accuracy, and implementation features of FANNs' teaching algorithms, though little is done towards the development of enhanced techniques that would extract experts' knowledge (from examples, rules, etc.) and obtain standardised LPs that would improve this learning process. A new approach in generating LPs is thereby introduced, that is used to train a new Medical Decision Support System (MDSS) based on FANNs, and its performance is analysed and compared with previous methods. It can handle incomplete data archives, individually boost any particular dataum special characteristics, and its application induces the FANNs to show better convergent facets. The efficiency of the resulting MDSS was thoroughly tested by pulmonologists and haematologists using medical data archives of a regional hospital.

Pulmonary alveolar microlithiasis is a rare disease characterized by widespread intra-alveolar calcification of both lungs that is asymptomatic in the early stages. The disease typically follows a protracted course, and death can occur in 5 to 41 years after the initial diagnosis. Rheumatic fever is a multisystemic inflammatory disease that afflicts the child and juvenile population, and it is still very common in developing countries. Valve failure is the condition most linked to increased morbidity and mortality rates in this population and is the most severe complication of rheumatic fever, with consequent onset of chronic heart valve disease. We present a case of a female patient with a potential diagnosis of pulmonary alveolar microlithiasis with concurrent rheumatic valvular disease.

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.

The article presents a novel modular medical decision support system, called Georgia, that has been evaluated in the Regional Hospital in Patras, for general use in the field of pulmonary diseases. Georgia can suggest potential diseases and recommend treatment for the disease to the physician. It is the first system by which a whole category of distressed body organs' diseases can be identified and treated by a decision support system. It is based on the application of artificial neural networks that have been taught and tested by means of the experience of medical doctors and clinical data, resulting in accurate recognition of the disease in 88-95% of the cases that have been evaluated. A user friendly expert-to-machine interface is integrated into this system to assure its usability by medical doctors.

This article reviews studies of upper airway muscles in humans, observed in patients with obstructive sleep apnea syndrome (OSAS). These studies include neuromuscular abnormalities of the upper airway muscles, along with changes of the upper airway lumen which is narrower in patients with OSAS than normal subjects. Several approaches have been made in the imaging of the upper airway using X-ray, CT, and MRI in order to characterize the severity of OSAS. Up to date results on histopathology of the muscles across with nervous lesions, are also reviewed.

Obstructive Sleep Apnea Syndrome (OSAS) is a recognized risk factor for cardiovascular disorders and in some cases is complicated with Pulmonary Arterial Hypertension (PAH), as the endothelium is affected. Recent studies provide strong evidence for endothelial dysfunction in obstructive sleep apnea. The resultant vasoconstriction, abnormal cell proliferation and hyper-coagulability may lead to the initiation or progression of atherosclerotic cardiovascular and cerebrovascular disorders, which are frequently encountered in OSA patients. While the currently available therapies for OSAS, such as Continuous Positive Airway Pressure therapy (CPAP therapy), improve endothelial dysfunction, they are not well-tolerated by patients. CPAP therapy can reduce nocturnal hypoxemias and decrease noradrenaline circulating levels, but does not affect ET-1 plasma levels. Potent and selective Endothelin-1 receptor antagonists have been developed and have shown promising results in the treatment of cardiovascular diseases such as pulmonary arterial hypertension, acute and chronic heart failure, hypertension, renal failure, and atherosclerosis. However, results are often contrasting and complicated because of the tissue-specific vasoconstrictor actions of Endothelin-B receptors and the fact that endothelin is an autocrine and paracrine factor whose activity is difficult to measure in vivo.

New drugs and new approaches of the treatment of chronic obstructive pulmonary disease (COPD) are needed. Despite recent advances in medical therapeutics, treatment of patients with COPD remains largely symptomatic. Although inhaled corticosteroids are currently the drug of choice for anti-inflammatory therapy, the inflammatory process in COPD is essentially steroid resistant. By now, COPD has been increasingly recognized as an inflammatory disease characterized by sputum neutrophilia and, in some cases, eosinophilia. Moreover other cell types thought to play the predominant role in COPD, are cytotoxic T lymphocytes (CD8+ T) cells and machrophages. Leukotriene B4, (LTB 4), a neutrophil and T cell chemoattractant which is produced by machrophages, neurophils and epithelial cells, is a potent inflammatory mediator. Also cysteinyl leukotrienes (LTC4, LTD4 and LTE4) are known to induce mucus secretion, inflammatory cell infiltration, increase vascular permeability and tissue edema, damage ciliary clirens, and cause severe bronchoconstriction. These are derivatives of arachidonic acid, metabolized via 5-lypoxygenase (5-LO) pathway. There are several sites along this pathway that antileukotriene agents exert their action and at the end-organ receptors. They are classified into two major categories: receptor antagonists and synthesis inhibitors. Beneficial effects on therapy of patients with COPD have already derived from studies, while they seem well tolerated. More studies are underway.

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.

Pulmonary Arterial Hypertension (PAH) is defined by a persistent elevation in pulmonary artery pressure with normal left-sided pressures. It is characterized by increased pulmonary vascular resistance due to increased vascular tone and structural remodeling of pulmonary vessels. PAH is a quite rare condition, thus considering the rarity, subtle presentation, and diagnostic dilemma commonly posed by this disease, underdiagnosis and underreporting are probably widespread. In order to reach a diagnosis the use of echocardiography, right-heart catheterization and the six-minute walk test is essential. As far as therapy is concerned, the patient should be supported by oxygen, diuretics, anticoagulants, digoxin and suggest life-style changes. After diagnosing the condition ca-blockers should be administered to those who respond positively in acute vasodilation test. Other agents used, target the endothelin pathway (ET-1 blockers such as bosentan), the NO pathway (sildenafil, inhaled NO, L-arginine) and the prostacyclin pathway (prostacyclin analogues). In some cases surgical treatment is essential (atrial septestomy, pulmonary endarterectomy, lung and heart transplantation). Finally, future therapies include administration of VIP and SSRIs. The goals of evaluating pulmonary hypertension are detection, definition of severity and the nature of the hemodynamic lesion and its consequences, diagnosis of causal or associated conditions, and determination of optimal therapy.

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.

The aim of this work was to study whether chronic obstructive pulmonary disease (COPD) subjects exhibited periodic limb movement (PLMs) during sleep. A retrospective case control study was conducted in the referral sleep disorders laboratory in the University of Patras in southwest Greece. A sample of 23 COPD subjects was compared with 14 severe obstructive sleep apnea (OSA) subjects and 18 periodic limb movement disorder (PLMD) subjects. The PLM Index (PLMI) and PLMs Arousal Index (PLMAI) in COPD subjects differ (p

Glutathione S-transferases (GSTs) constitute a super family of dimeric phase II metabolic enzymes that catalyze the conjugation of reduced glutathione with various electrophilic compounds and reactive oxygen species (ROS). Failure to detoxify ROS, as a sequel of altered GST genotype is able to aggravate the inflammatory cascade, promote bronchoconstrictor mechanisms, activate asthma-like symptomatology, and hamper lung development. Intriguingly, the same GST genotype can aggravate or improve physiological traits and maturation of respiratory system, from gestation to late adulthood. This article attempts to unravel the complex interaction of GST's genetic variations with "inner" and "outer", polymorphic and erratic, human environment (tobacco smoke, urban pollution, workplaces, and in utero status). Considering that these variations are very frequent among ethnicities and that GSTs play a part in respiratory system formation and maturation, they appear to be of great interest for the clinician and the researcher in this field.

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.

It is known that only 10-20% of smokers develop COPD, implying that apart from environmental features, additional factors such as genetic variability contribute to smoke susceptibility. This proposal is in compatibility with the "Dutch Hypothesis", formulated in the early 60's. Alpha-1-antitrypsin gene was implicated in the pathogenesis of COPD, especially the homozygous state of z allele. Since then many other genes have stepped forward as possible contributors to COPD development. In the present review we attempt to summarize the majority of these, including the genes of matrix metalloproteinases and their inhibitors, elastin, serpine2, tumor necrosis factor - a, transforming growth factor beta, a variety of interleukins and their receptors and antagonists, high affinity IgE receptor , human calcium-activated chloride channel 1, heme oxygenase, vascular endothelial growth factor, microsomal epoxide hydrolase, glutathione S-transferase, cytochrome P45O, superoxide dismutase, vitamin D binding protein, beta2-adrenergic receptor, Toll like receptor, human B defensins, mucins, cystic fibrosis transmembrane regulator, surfactant protein and Nuclear Factor E2 Related Factor 2.

We present a case of an obese young man who developed ischemic hepatitis, severe coagulopathy, acute renal failure, and encephalopathy. Heart failure and hypovolemia were absent. Oxygen arterial saturation was very low, between 77% and 99% during the day, with no history of respiratory failure. A diagnosis of obstructive sleep apnea was made clinically and confirmed by performing formal polysomnography. The polysomnographic study showed multiple episodes of apneas and hypopneas with severe oxygen desaturation. The patient was treated with continuous positive airway pressure through a nose mask and clinical manifestations related to profound nocturnal desaturation were ameliorated. He was discharged 32 days after admission with normal results of laboratory tests. This case report is presented to support the hypothesis that hypoxic hepatitis was directly related to severe arterial hypoxemia.

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.

Chronic obstructive pulmonary disease (COPD) is a major cause of morbidity and mortality all around the world. It has been identified as the fourth leading cause, which will rise globally to the third place, before the end of 2020. It is estimated that more than 12 million adults suffer from COPD in the USA and 24 million patients have an impaired lung function, which may lead to the development of COPD. Tobacco smoke is the predominant but not the only environmental risk factor for COPD. COPD is a burden for health providing systems as the estimated direct and indirect costs are constantly raising. Chronic obstructive pulmonary disease, namely, pulmonary emphysema and chronic bronchitis, is a chronic inflammatory response of the airways to noxious particles or gases, with resulting pathological and pathophysiological changes in the lung. The main pathophysiological aspects of the disease are airflow obstruction and hyperinflation, which are discussed by D. Papandrinopoulou et al. The mechanical properties of the respiratory system and its component parts are studied by determining the corresponding volume-pressure (V-P) relationships. The consequences of the inflammatory response on the lung structure and function are depicted on the volume-pressure relationships. Expiratory flow limitation is well discussed by Tantucci. When expiratory flow is maximal during tidal breathing and cannot be increased unless operative lung volumes move towards total lung capacity, tidal expiratory flow limitation (EFL) is said to occur. In any circumstances, EFL predisposes to pulmonary dynamic hyperinflation and its unfavorable effects such as increased elastic work of breathing, inspiratory muscles dysfunction, and progressive neuroventilatory dissociation, leading to reduced exercise tolerance, marked breathlessness during effort, and severe chronic dyspnea. N. G. Koulouris et al. in their paper discuss the expiratory flow limitation in COPD patients at rest (EFLT). EFLT, namely, attainment of maximal expiratory flow during tidal expiration, occurs when an increase in transpulmonary pressure causes no increase in expiratory flow. EFLT leads to small airway injury and promotes dynamic pulmonary hyperinflation with concurrent dyspnea and exercise limitation. Among the currently available techniques, the negative expiratory pressure (NEP) has been validated in a wide variety of settings and disorders. Consequently, it should be regarded as a simple, noninvasive, most practical, and accurate new technique. COPD is a complex pathological condition associated with an important reduction in physical activity and psychological problems that contribute to the patient's disability and poor health-related quality of life as it is stated in the paper of P. Santus et al. Pulmonary rehabilitation is aimed to eliminate or at least attenuate these difficulties, mainly by promoting muscular reconditioning. Pulmonary rehabilitation has a beneficial effect on dyspnea relief, improving muscle strength and endurance. Moreover, it appears to be a highly effective and safe treatment for reducing hospital admissions, mortality, and improving health-related quality of life in COPD patients. The paper of F. Krakontaki et al. attempts to show the impact of COPD on the cognitive functions of the patients. The findings provide evidence that stable COPD patients may manifest impaired information processing operations. Therefore, COPD patients should be warned of the potential danger and risk they face when they drive any kind of vehicle, even when they do not exhibit overt symptoms related to driving ability. The deterioration of quality of life of COPD smokers is illustrated by S. Joseph et al. in a study population from Lebanon. The Clinical COPD Questionnaire (CCQ) demonstrated excellent psychometric properties, with a very good adequacy to a cross-sectional sample and high consistency. Smokers had a decreased respiratory quality of life versus nonsmokers, independently of their respiratory disease status and severity. I. Tsangaris et al. show one of the most important complications of chronic hypoxemia in COPD, which is pulmonary hypertension. Interestingly, in types of PH that are encountered in parenchymal lung diseases such as interstitial lung diseases (ILDs), chronic obstructive pulmonary disease (COPD), and many other diffuse parenchymal lung diseases, some of which are very common, the available data is limited. The paper summarizes the latest available data regarding the occurrence, pathogenesis, and treatment of PH in chronic parenchymal lung diseases. Finally, M. Pecchiari discusses the role of heliox, which has been administered to stable chronic obstructive pulmonary disease (COPD) patients at rest and during exercise on the assumption that this low density mixture would have reduced work of breathing, dynamic hyperinflation, and, consequently, dyspnea sensation. Contrary to these expectations, beneficial effects of heliox in these patients at rest have been reported only sporadically. On the other hand, when it is administered to COPD patients exercising at a constant work rate, heliox systematically decreases dyspnea sensation and, often but not always, increases exercise tolerance. Therefore, further studies, aimed to the identification of mechanisms conditioning the response of exercising COPD patients to heliox, are warranted, before heliox administration, which is costly and cumbersome, can be routinely used in rehabilitation programs.

Aneurysms of the thoracoic aorta may on rare occasions lead to shortness of breath by external compression of the tracheobronchial tree. We report the case of a patient who presented with orthopnea due to extensive compression of the trachea and the major airways by a large aneurysm of the ascending aorta.

Background: Endothelin (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, falling with treatment of the exacerbations. Objective: The aim of this study was to examine the ET-1 blood levels in stable asthmatic patients and stable COPD patients during alertness and sleep. Materials and Methods: We examined 48 COPD and 20 asthmatic patients. All underwent forced spirometry, measurement of SaO2 and of arterial ET-1 levels and nocturnal polysomnography. ET-1 levels were also determined during nocturnal oxyhaemoglobin desaturation. Results: The daytime SaO2 level of our asthmatic patients was higher than that of our COPD patients (p < 0.001). Daytime SaO2 level of our non-desaturator COPD patients was higher than that measured in desaturator COPD patients. Nightime SaO2 level in our asthmatic patients was higher than that in our desaturator COPD patients (p < 0.001). Daytime ET-1 levels in desaturator COPD patients were higher than those observed in normal individuals, in non-desaturator COPD patients and in asthmatic patients. The COPD desaturator patients had higher levels of ET-1 during nighttime than during daytime (p < 0.001). Conclusion: Asthmatic patients did not exhibit desaturation of haemoglobin during the night. ET-1 levels are significantly higher in desaturator COPD patients compared with non-desaturator COPD patients, both during the day and during the night. ET-1 levels in stable COPD patients are significantly higher than in patients with stable asthma. These findings are consistent with the hypothesis that ET-1 is implicated in the pathogenesis of COPD and asthma.

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.

The feasibility and reliability of the combination of several noninvasive methods using a multivariate method of analysis to predict pulmonary artery hypertension (PAH) is evaluated in 20 patients with chronic obstructive pulmonary disease. These methods comprised arterial blood gases (Pao2, Paco2), pulmonary functional parameters (FEV1), echo-Doppler parameters (tricuspid regurgitation jets, acceleration time on pulmonary valve), computed tomography measurements (transhilar distance, hilar thoracic index, and measurement of the descending branch of the right pulmonary artery to the lower lobe). A multiple stepwise regression analysis (including one Doppler parameter, two parameters of arterial blood gases, and one functional parameter) revealed a coefficient of determination (R2) equal to 0.954 for mean pulmonary artery pressure (MPAP) with a standard error of estimate (S.E.E.) of 5.25 mmHg. A stepwise regression analysis including computed tomography and radiographic parameters revealed an R2 equal to 0.970 for PAP with a S.E.E. of 4.26 mmHg. Logistical regression analysis classified correctly 80% of patients with PAH using noninvasive methods such as the diameter of the main pulmonary artery and the diameter of the left pulmonary arterial branch calculated by computed tomography. Not only the presence of PAH but also the level of MPAP can be estimated by the combination of multiple stepwise and logistical regression analyses.

Following percutaneous lung biopsy (PLB), we used fibrin glue as a sealant in 26 patients for the purpose of decreasing the incidence of pneumothorax.All 26 patients (group A) had chronic obstructive pulmonary disease (COPD). The results for group A were compared with a control group of 32 patients (group B), also with COPD and in whom fibrin glue was not used. All biopsies were conducted under computed tomography (CT) using a coaxial needle system consisting of 19-gauge and 22-gauge needles.Pneumothorax developed in five patients (19.2%) in group A and in one instance, drainage was required (3.8%). In group B, pneumothorax developed in 13 patients (40.6%) and in six instances (18.8%) drainage was required. Comparing the use of chest-tube drainage in the two groups, a statistical significance was observed, p0.0025). No adverse reactions related to the fibrin glue were observed.Our results indicate that fibrin glue is a safe sealing material for lung PLB and serves to decrease the incidence and, in particular, the severity of pneumothorax, especially in high-risk patients.

The concentration of secretory immunoglobulin A (IgA) has been measured by the immunodiffusion method in 28 chronic bronchitis patients (group A) and in 11 comparable patients receiving corticosteroid therapy (0.5 mg/kg/day prednisone; group B). The measurements have been taken before and after oral administration of Broncho-Vaxom which is an extract of bacteria that usually cause infection of the respiratory tract. The mean concentration of secretory IgA in the saliva was increased by over 130% after the 10-day administration of the preparation to group A patients. This increase was statistically significant between the 12th and 40th day after the beginning of the treatment (p0.001). It fell to initial levels after 1 month in 15 patients (group A2) who received a single treatment course. In 13 patients (group A1) who received a second treatment course, beginning 1 month after termination of the first course, the high concentration of IgA in saliva persisted for at least 3 months. The saliva IgA was increased by over 35% in 11 chronic bronchitis patients (group B) who received corticosteroid therapy. In this group of patients the rise of IgA levels began later than in group A. The IgA fell to initial level after 1 month in 5 patients (group B2) who received a single treatment course. In 6 patients (group B1) who received a second treatment course the high concentration persisted longer. The saliva level of IgA in groups A and A1 was higher than in groups B and B1 (p0.05 and p0.001, respectively). No differences of IgA in the saliva between groups A2 and B2 were found during the study.