mteb/BIRCO-ClinicalTrial-Test huggingface dataset:
Guidelines recommend inhaled corticosteroids (ICS) for patients with moderate to severe chronic obstructive pulmonary disease (COPD). Most COPD patients are managed in primary care and receive ICS long-term and irrespective of severity. The effect of withdrawing ICS from COPD patients in primary care is unknown.This randomised double-blind placebo-controlled trial will evaluate the effect of withdrawal of inhaled corticosteroids in patients with COPD recruited from general practice. Participants will have a clinical and spirometric diagnosis of COPD and will have been prescribed inhaled steroids for the 6 months before entry to the trial. They will be randomised to taking a fixed dose steroid inhaler (Flixotide Accuhaler) or an identical placebo inhaler. Patients will be monitored using diary cards for a year with 3 monthly follow-up visits at their general practice. The primary outcome measures will be exacerbation frequency and severity. Other outcomes are time to first exacerbation, costs, health status, lung function and unscheduled care. We tested the hypothesis that withdrawal of ICS in this population would lead to an increased number of exacerbations, earlier onset of exacerbation, and a worsening of symptoms. To determine whether withdrawal of inhaled corticosteroids in patients with COPD in general practice effects: - the frequency of exacerbations compared to a control group - differences in health status compared to a control group - differences in lung function compared to a control group - changes in unscheduled care compared to a control group - Direct and indirect costs compared to a control group Hypothesis The withdrawal of inhaled corticosteroids from patients with COPD identified in primary care will cause an increase in frequency and severity of exacerbations and is not cost-effective.
This study will evaluate the safety and effectiveness of methylphenidate in treating attention deficit hyperactivity disorder in children with both attention deficit hyperactivity disorder and Tourette syndrome. Tourette syndrome is a neurological disorder that is characterized by repetitive, involuntary movements and vocalizations called tics. Many children with Tourette syndrome also have attention deficit hyperactivity disorder (ADHD), which is one of the most common childhood mental disorders. Symptoms of ADHD usually include impulsiveness, inattention, and hyperactivity. ADHD is commonly treated with a stimulant medication, such as methylphenidate. It is under debate, however, whether using stimulants in children with Tourette syndrome exacerbates tics associated with the disorder. This study will evaluate the safety and effectiveness of methylphenidate in treating ADHD in children who have both ADHD and Tourette syndrome. Participants in this 6-week, double blind study will receive three doses of methylphenidate over the course of the study. Each dose will be taken twice daily, approximately 3.5 hours apart, for 2 weeks. Medication will be dispensed at study visits, which will occur once every 2 weeks. At each study visit, participants will take a dose of the medication. About an hour after ingesting the medication, they will be observed in a classroom setting by study physicians. Participants will then complete a Continuous Performance Test, which will measure their voluntary attention levels. The following will be assessed at study visits: ADHD symptoms; oppositional and aggressive behavior; frequency and severity of tics and obsessive compulsive disorder symptoms; rebound tic exacerbation; effects of methylphenidate on tic-related problems with self-esteem, family life, academic and social performance, and overall tic severity; anxiety and mood symptoms; and adverse drug reactions.
Treatment of COPD patients depends on the stage of the disease. First of all it is strongly recommended quit smoking, then bronchodilators drugs are added. In more advanced stages inhaled corticosteroids and pulmonary rehabilitation are added. In hypoxemic patients a long term supplemental oxygen is advised. The addition of sputum modifiers drugs is equivocal, since no objective improvement was documented. N-Acetylcystein (NAC) is a drug known for its anti-oxidant and mucolytic activity. In animal models of disease it showed its beneficial activity , whereas in human such changes weren’t demonstrated. In all the studies FEV1 was used to demonstrate the beneficial effect of the drug, although the disease changes are at the level of small airways which is almost not expressed by the measurement FEV1. Purpose of the study 1. To estimate the damage severity at the small airways. 2. To estimate the change in quality of life. 3. To assess the pulmonary function changes at rest and following exercise, including parameters of air trapping (hyperinflation) Methods & Materials Patients – Inclusion - 30 Moderate COPD (GOLD classification) , AGE 45-70, both sexes. Treated with inhaled steroids and long acting beta agonists. Exclusion – Active ischemic heart disease, heart failure, orthopedic problems that preclude ergometric bicycle activity. Questionnaire – The St. George questionnaire for quality of life will be used .
Diseases of the airways (bronchi) of the lungs include asthma and chronic obstructive pulmonary disease (COPD), which are leading causes of reduced quality of life, loss of work, hospital admissions and deaths and result in a major economic burden to the patient and society. Worsening (exacerbation) of these conditions is common and is frequently due to viral or bacterial infection, which causes inflammation in the bronchi, i.e. bronchitis. Ways to objectively measure the inflammation are needed to improve diagnosis, cause and severity and to guide treatment. The investigators also need to understand changes in the body's defense (immune) mechanisms that make some patients have more frequent infective bronchitis. At present, sputum cell counts are able to identify different types of bronchitis, their severity and may be able to differentiate viral from bacterial infection. Other measurements in sputum, exhaled breath, blood and urine are also available to measure this inflammation. Measurement of immune cells in the blood gives us an idea about the working capacity of the immune system of the body. The investigators plan to study patients with asthma or COPD at the time of worsening of their condition to identify, 1. To what extent viral or bacterial bronchitis can be diagnosed from tests of inflammation? 2. How clearing of infection relates to clearing of inflammation? 3. What are the changes in the body's defense mechanisms that make a patient more prone to frequent infective bronchitis?
Chronic obstructive pulmonary disease (COPD) and asthma are common respiratory diseases in which people experience long-term inflammation of the lungs. Exacerbations, or prolonged worsening of symptoms, of asthma and COPD are often life-threatening and can lead to frequent need for hospitalization. Even with the proper use of bronchodilators, corticosteroids, and other currently available medications, clinical responses among people with COPD and asthma are variable. There remains a significant unmet clinical need for new therapeutic approaches and insights, including the identification of biomarkers to accurately assess the presence of airway infection and intensity of airway inflammation. This study will investigate potential natural biological causes and new biomarkers for increased susceptibility to persistent airway infection in asthma and COPD. COPD and asthma are chronic lung diseases that result in impaired air flow in the lungs, often causing coughing, wheezing, and shortness of breath. In uncontrolled COPD and asthma, people may experience a rapid worsening of symptoms, which may include fever, difficulty breathing, and chest pain. These exacerbations are the most serious expression of asthma and COPD and are usually caused by lung infections or air allergens. However, the biological basis for susceptibility to airway infection and inflammation is not well understood. Increased oxidative stress within the airways has been linked to several airway diseases. This increase in oxidative stress may reduce production of key fatty acid anti-inflammatory mediators.
Hyperglycemia is a common complication of corticosteroid (cortisone) therapy. It is estimated that more than a third of patients with chronic pulmonary disease (COPD) exacerbation (16). Despite its frequency, the impact of corticosteroid-induced diabetes on clinical outcome and mortality is not known. A computerized search of biomedical journal literature from MEDLINE, PubMed, and Ovid from 1966 to 2006 provided very little information on the prevalence and outcome of corticosteroid-induced diabetes in patients with COPD. Therefore, the present study aims to evaluate the impact of corticosteroid-induced diabetes on clinical outcome in patients with COPD exacerbation. We will perform a retrospective chart review of all patients admitted to the hospital with COPD exacerbation from 1/01/05 to 06/30/06 at Grady Memorial Hospital. Medical records of all patients with COPD exacerbation treated with corticosteroids will be analyzed. Data on demographics, laboratory values, mortality rate, rate of hypoglycemic events, length of stay, as well as disposition at discharge will be analyzed. Hypotheses: We hypothesize that COPD patients with corticosteroid-induced hyperglycemia experience higher morbidity (infections, ventilator associated pneumonia, length of stay, acute renal failure) and mortality compared to COPD patients with normal glucose levels. Specific Aim: To determine the impact of corticosteroid-induced hyperglycemia on clinical outcome (length of stay, disposition, APACHE score, need for ventilatory support and ICU admission, mortality) in patients with COPD exacerbation.
Background: Smoking cessation is the key element in the treatment of patients with Chronic Obstructive Pulmonary Disease (COPD). The role of the general practice in assisting these patients with successful quitting smoking was suboptimal. Therefore we evaluated the effectiveness of two smoking cessation programs (counseling and nicotine replacement) for smokers with COPD in routine general practice, one with (CNB) and one without (CN) the combination with bupropion-SR, compared to usual care (UC) and explored the role of COPD symptoms in successful smoking cessation. Method: RCT with 667 patients with COPD, 68 general practices were randomly allocated. The usual care group (UC) consisted of 148 patients (22 practices), the first intervention group (counseling plus nicotine replacement (CN) of 243 patients (21 practices) and the second intervention group of 276 patients (25 practices. Main outcome measure was (biochemically verified) point prevalence.
The overall purpose of PA-SCOPE is to determine why black and rural residents of Pennsylvania might be at higher risk for deadly, debilitating, and costly hospitalizations for chronic obstructive pulmonary disease (COPD)— and then to show that repeat acute exacerbations in high-risk patients can be reduced with one simple intervention. We believe that 1) COPD patients who are black or who live in rural areas of Pennsylvania are at higher risk of acute exacerbations requiring hospitalization and 2) this elevated risk can be reduced with one simple intervention: access to a 1-800 Temple Call Center where patients can get immediate customized advice on managing COPD exacerbations in their early stages. We will test these beliefs in PA-SCOPE. The collaborators with Temple University Hospital on the PA-SCOPE project are Lancaster General Hospital, Western Pennsylvania Hospital, and the Philadelphia College of Osteopathic Medicine. - Overall objective: To determine why African American and rural residents of Pennsylvania might be at higher risk for deadly, debilitating, and costly hospitalizations for COPD—and to show that repeat acute exacerbations in high-risk patients can be reduced with one simple intervention--access to a 1-800 Temple Call Center phone number where patients can get immediate customized advice on managing COPD exacerbations in their early stages. - Phase 1: To compare and contrast the influence of race and geographic location in COPD exacerbation in relation to severity, comorbidities, treatment patterns, infection rate.
People with Chronic Obstructive Pulmonary Disease (COPD) often have periods during the year when their symptoms become worse. These are often due to an infection and are called "exacerbations" by doctors. Exacerbations are more common in the winter and also seem to be related to particular types of weather. As well as forecasting the weather the UK Met Office has developed a system to try to predict when exacerbations are likely to occur. The main purpose of this research study is to find out whether the Met Office forecasting service can predict when exacerbations are more likely to occur and whether the advice given during the predicted higher risk periods leads to fewer patients having an exacerbation or if it reduces the impact of the exacerbation. The study will also assess if there is a link between viral or bacterial infection and breathing problems that occur during the study period. The study will also collect information about possible causes of the breathing problems and what happens to the person afterwards. The results of this study will help us learn more about breathing problems which may lead to new research studies that would aim to improve the care of people with COPD.
Antibiotic therapy has been shown to be beneficial in patients with severe acute exacerbation of chronic obstructive pulmonary disease (COPD). Although recent guidelines support the use of new antibiotics there is no evidence that newer antibiotics are any better than older agents. The choice of antibiotic to be used in this situation is challenging to the clinician who must choose between traditional antibiotics (cyclins, aminopénicillins, cotrimoxazole...) and new antimicrobial agents. Indeed, available comparative studies did not show an obvious superiority of new antibiotics compared to their predecessors . Taking into account bacterial agents associated to COPD exacerbations, one must choose an antibiotic which has the best activity against Haemophilus influenzae, Streptococcus pneumoniae and Branhamella catarrhalis. News quinolones are represented as an interesting alternative to standard antibiotics because of their large spectrum of action and of their pharmacokinetic advantages allowing high tissue penetration in the pulmonary parenchyma and tracheobronchial tree. Data on their use among patients having moderate exacerbation of COPD are encouraging but their effectiveness in more severe presentations is not established. The objective of this randomized controlled and double blind study is to evaluate the effectiveness and tolerance of ciprofloxacin compared to trimethoprim sulfamethoxazole in patients admitted to ICU for severe exacerbation of COPD requiring mechanical ventilation.
COPD is ranked number 3 by the WHO list of important diseases worldwide and is the only disease with increasing mortality. The pathogenesis of cigarette smoke-induced COPD is obscure, therefore more insight is needed to design effective anti-inflammatory agents. We hypothesize that healthy individuals who are susceptible to smoking demonstrate a higher and aberrant inflammatory response to cigarette smoke. This susceptibility is caused by heterogeneous factors and is associated with various polymorphic genes that interact with each other and with the environment. Objective: - To define mediators involved in the early induction of COPD in susceptible smokers (and so to define new drug targets) - To develop new biological and clinical markers for the early diagnosis and monitoring of COPD - To compare between susceptible and non-susceptible individuals the corticosteroid responsiveness of bronchial epithelial cells in vitro, and to study the mechanisms of smoking-induced corticosteroid unresponsiveness. - To study the role of candidate genes that may play a role in the development of fixed airway obstruction, and to identify clues for patient's responsiveness to specific drugs. Primary study parameters/outcome of the study: - Local inflammation before and after cigarette smoking assessed by exhaled breath condensate, microprobe sampling and bronchial biopsies. - Systemic inflammation before and after cigarette smoking assessed by the expression of established and newly developed markers on innate immune cells associated with pre-activation. - Extensive clinical characterisation including life style factors, lung function, CT scanning of the lung.
The purposes of this pilot safety study are to identify a dose of inhaled Clinical Center Reference Endotoxin (CCRE) that is well tolerated by allergic subjects that induces measurable increases in neutrophil content of induced sputum that can be employed to screen large populations for susceptibility to the inflammatory effect of inhaled endotoxin. Twenty-four or forty-eight hours (study day 1) prior to the inhalation challenge, subjects will undergo a physical examination of the ears, nose, throat and chest and will have an assessment of vital signs (temperature, pulse, respiratory rate, blood pressure), oxygen saturation, symptom score assessment and undergo spirometry to rule out acute illness prior to challenge. All female volunteers will undergo a urine pregnancy test. A similar examination will take place immediately prior to inhalation challenge with 10,000 EU of CCRE, as well as 30, 60, 120, 180, 240, 300 and 360 minutes and 24 hours after challenge (with the exception of a pregnancy test which will only be administered prior to sputum induction on study day 1). Induced sputum will be 24 to 48 hours prior to challenge, and again six hours after challenge on Study day 2. Sputum will be analyzed for PMN content, CD14 expression on airway macrophages and monocytes, soluble CD14 levels, cytokine levels in sputum and products of inflammatory cells (eosinophil, cationic protein, myeloperoxidase).
Study purpose is to evaluate if subjects with chronic obstructive pulmonary disease (COPD) are more likely to be responsive to additional inhaled corticosteroids if they have a positive response to hyperosmolar challenge with mannitol than if their response is negative. In patients with chronic obstructive pulmonary disease (COPD), the treatment with inhaled corticosteroids (ICS) is controversial. Preliminary results of our recent pilot study in 30 COPD patients showed for the first time, that ICS response mey be predicted by a bronchoprovocation challenge test with mannitol. However, this finding needs to be proven in a placebo-controlled trial. For this cohort study, 100 corticosteroid-naive, non reversible (FEV1) patients with COPD will be recruited. Spirometry before and after bronchodilation will be measured at study entry and at four weeks run-in (only tiotropium) and at three month of treatment with tiotropium and ICS or placebo. Quality of life (St. George Respiratory Quality of Life Questionnaire) and exacerbation rate of COPD will be assessed. Measurement of exhaled nitric oxide and mannitol challenge will be performed at study entry and at 1 and 4 month. Primary endpoint will be improvement in FEV1 in each group (positive and negative mannitol challenge) after 3 months follow up. Secondary endpoints will be the difference in dose-response-curve in the mannitol challenge, exacerbation rate and change in quality of life after three month follow-up.
COPD exacerbations are characterized by an excessive accumulation and activation of inflammatory cells in the airways. It is not known whether this phenomenon represents a risk for for lung damage via the release in the extracellular environment of potent cytolitic cellular granular contents such as granzymes and perforin. The investigators assess the intracellular expression of granzymes and perforin in neutrophils and large granular lymphocytes (LGL) at the onset of exacerbations compared to stable disease. The investigators hypothesize that a greater release of intracellular perforin and granzymes from neutrophils and LGL into the extracellular environment occur at exacerbations compared to stable condition and that these changes are more pronounced in COPD patients than in subjects without COPD who undergo respiratory infection. The course of Chronic Obstructive Pulmonary Disease (COPD) is characterized by exacerbations which lead to significant clinical deterioration and morbidity.COPD exacerbations are characterized by an augmentation of the inflammation that is observed in the airways in stable condition, particularly by excessive accumulation of polymorphonuclear neutrophils and activation of lymphocytes. It has been suggested that this abnormal increase of inflammatory cells in the airways of COPD patients during exacerbations, might represent a significant risk for excessive proteolytic activity in the airways via the release of their granule contents into the extracellular environment. Large granular lymphocytes (LGL) which include NK and cytotoxic T- cells and neutrophils contain cytolytic molecules such as, granzymes and perforin. Therefore, the inflammatory process during exacerbations might be potentially toxic to the lung.
Chronic obstructive pulmonary disease (COPD) is a chronic progressive respiratory disorder causing disability with an increasing burden to the patient, his family and to the health services. Treatment of COPD patients depends on the stage of the disease. COPD responds poorly to corticosteroids, in spite of inflammation is a major component in its pathogenesis. A major barrier to therapy of COPD is resistance to the anti-inflammatory effects of corticosteroids. The molecular mechanisms for this corticosteroid resistance are now being elucidated, particularly as the molecular basis for the anti-inflammatory effects of corticosteroids is better understood (12). An important mechanism of corticosteroid resistance in COPD, which is also linked to amplification of the inflammatory process, is a reduction in the critical nuclear enzyme histone deacetylase (HDAC)2 . Since the major changes are at the level of small airways. We will examine the effect of addition of theophylline product to stable COPD patients treated with combined inhaler of inhaled corticosteroids.
Cigarette smoking is the major risk factor for chronic obstructive pulmonary disease (COPD, commonly known as chronic bronchitis and emphysema). Despite this clear link, only 15-20% of smokers develop COPD suggesting that genetic factors affect the lung's susceptibility to the stress of cigarette smoke. The cells lining the airways (epithelium) and cells that help defend the lung (alveolar macrophages) of smokers develop gene expression changes that are different from that of nonsmokers. In the investigators' previous studies they have demonstrated that there are greater than 200 genes that are responsive to cigarette smoke in these cells. But the investigators do not know whether the gene expression is static or changes as a function of time. Genes that show significant changes over time may be relevant to the progression of the disease. Even though quitting smoking reduces the rate at which the lungs decline, many-smokers still go on to develop COPD. This study will provide insights into the natural history of smoking-related gene expression of the lung cells in health and disease. Cigarette smoke is responsible for the majority of lung cancers and is the major cause of COPD, the fourth leading cause of death in the United States. Despite the well established causal role of cigarette smoking in lung cancer and COPD, only 10-20% of smokers actually develop these diseases. This suggests that there are genetic predisposing factors that place some individuals at greater risk.
The final purpose of this study is to determine whether bronchodilation and cigarette smoking in Chronic Obstructive Pulmonary Disease (COPD) patients interact, resulting in an increase of cardiovascular disease. The aim of this part of the study is to demonstrate the basic mechanism: Does increased respiratory function after administration of a bronchodilator in patients with COPD lead to elevated pulmonary retention of the harmful compounds in inhaled cigarette smoke and to short-term biological effects associated with cardiovascular disease? COPD currently is one of the most frequent diseases. In more than 80% of COPD patients, the disease is caused by smoking. About half of the COPD patients are active smokers, although smoking is also the most important prognostic factor. Also, smoking is an important cause as well as an important prognostic factor in cardiovascular disease. The corner stone of medical treatment in COPD is bronchodilation; more than half of the patients use a long-acting bronchodilator. An increase of the pathogenic effect of smoking by an increased lung function after bronchodilation is likely though, since more pathogenic particles would penetrate the lung. We hypothesize that bronchodilators increase cardiovascular disease in COPD patients who smoke. In order to demonstrate the basic mechanism of our hypothesis, COPD patients receive a bronchodilator at one time and a placebo at another time, preceded and followed by cigarette smoking during one hour as by a strict time schedule.
To assess whether maintenance treatment with macrolide antibiotics in COPD patients with three or more exacerbations in the preceding year of inclusion can decrease the exacerbation rate in the year of treatment. COPD is characterized by progressive development of airflow limitation that is poorly reversible. Because of a poor understanding of COPD pathogenesis, treatment is mostly symptomatic and new therapeutic strategies are limited. There is a direct relationship between the severity of the disease and the intensity of the inflammatory response.One of the hypothesis for persistent airway inflammation is that the presence of recurrent infections is responsible for this condition. Macrolide antibiotics have a bacteriostatic as well as anti-inflammatory properties. This clinical trial will investigate whether maintenance treatment with macrolide antibiotics during 1 year in people with 3 or more exacerbations in the preceding year of inclusion can decrease the exacerbation rate in that same year of treatment.
COPD is one of the most important causes of morbidity and mortality and supposes a sanitary problem in Europe and USA. Patients with COPD usually have 1-2 episodes of acute exacerbation of COPD (AECOPD) per year, being these the principal causes of of hospitalizations, respiratory problems and medical visits. After an episode of AECOPD, the majority of patients develop a transitory (or permanent) worsening in their quality of life and 50% of them will require a new hospitalization. Globally, a 75%& of the exacerbations might be associated with a respiratory tract infection, and among them, 50% might be related to bacteria and in 45% an evidence of viral infection could be documented. Even though the antibiotic treatment might not be useful for a majority of patients with AECOPD, is generalized its use(almost an 85% in some series) in hospitalized patients. The non-controlled use of antibiotics in AECOPD results in a very expensive disease and raises the rate of resistance of bacteria. The available literature have shown that there's a relation between exacerbations and infections, based on sputum samples. In summary, is well known that at least a 50% of the episodes of AECOPD might be associated with pathogenic bacteria in the lower respiratory tract. Prescription of antibiotics is wide and generalized in hospitalized patients. Clinical trials have shown correlation between AECOPD with sputum purulence (which correlates with presence of bacteria), however they've not included NON-purulent AECOPD, even though they're a significative group of patients hospitalized by this cause too.
Exacerbations are important events in the natural history of chronic obstructive pulmonary disease (COPD). Beside the acute (and prolonged) clinical impact, there is evidence that exacerbations negatively affect the natural history of the disease; e.g. lung function decline is accelerated in patients with frequent exacerbations. Bacteria are considered the most relevant cause of exacerbations, but there is evidence that viral infections are equally contributing. Either alone or in combination with viruses, airway bacterial load in stable COPD correlates with both the frequency of exacerbations and the decline in lung function. A long-term clinical trial recently showed that the regular treatment with inhaled corticosteroids (ICS) increases the risk of infectious events such as pneumonia, whereas it reduces the frequency of acute COPD exacerbations in COPD. In a recent study it was found that airway bacterial load increases over time (1 yr follow up) in stable COPD. In this study, virtually all patients (93%) were treated with ICS. This study is designed to evaluate whether long-term (1 year) ICS treatment increases viral and/or bacterial load in the sputum of COPD patients.
Rationale: Acute exacerbations are key events in chronic obstructive pulmonary disease (COPD), resulting in poorer quality of life. Causes include irritants, viruses and bacterial pathogens. These exacerbations are often treated with a combination of corticosteroids, bronchodilators and antibiotics, but the benefit of antibiotic therapy remains controversial. Several trials studying antibiotic treatment in AECOPD showed conflicting data, with several large studies failing to demonstrate superiority of antibiotic therapy over placebo. Other trials indicated that antibiotic therapy is effective in patients who have at least two of the following symptoms: increased dyspnoea, increased sputum volume and increased sputum purulence. Ever since sputum purulence has been used as a predictive marker in AECOPD, a strategy that has been integrated in the GOLD guideline for treatment of AECOPD. However, the color of sputum reported by patients is not always reliable and inspection of sputum is not always possible. Several serum biomarkers such as C-reactive protein (CRP) and procalcitonin (PCT) are now available. In a recent trial of doxycycline in addition to systemic corticosteroids for patients hospitalized with AECOPD we found that CRP might be valuable as a marker predictive of response to antibiotic treatment in AECOPD. Objective: CRP-guided antibiotic therapy will be compared with standard antibiotic therapy in AECOPD. Our aim is that CRP guided therapy will lead to 20% reduction in antibiotic consumption. Study design: randomized controlled intervention trial Study population: Hospitalised COPD patients with acute exacerbation.
COPD patients frequently suffer intermittent exacerbations of their disease characterised by acute deterioration of symptoms. Acute exacerbations of COPD (AECOPD) are associated with significant impairment of health status, use of health care resources, poor prognosis and increased mortality. The development of simple and practical predictive tools would help to identify COPD patients at greater risk of suffering exacerbations, which is important since those patients would need more intense and early treatment. This one-year prospective cohort non-drug study will evaluate several COPD-specific questionnaires as predictive tools and the presence of cardiovascular comorbidities as risk factors, for the composite events in study cohorts. The trial duration consists of a screening period (4-6 weeks) and a follow-up period (12 months), 4 visits in total along the study.
Chronic Obstructive Pulmonary Disease (COPD) is a major health concern, with a substantial impact on a patient's life. However, the impact of COPD is currently under-recognised and, as a result, COPD is under-treated. An exacerbation of COPD is a major element that causes poor quality of life and loss of productivity. Therefore, minimizing the frequency of exacerbations is a short term treatment goal in COPD management and could improve Quality of Life (QoL) significantly in all severity groups of COPD. Although the use of spirometry for the determination of disease severity in COPD is supported by guidelines, a lung function test alone does not provide a measurement of the overall impact of COPD on health status and is not generally available especially in primary care centre. Therefore, a standardised and effective dialogue between patients and physicians in a consultation could address the impact of COPD on a patient's QoL in this situation. The COPD Assessment Test (CAT), recently launched in 2009, is a short and simple, self-administered questionnaire designed to assess the condition of patients and overall impact of COPD, and to improve patient-physician communication. It has been proven that the CAT has good repeatability and discriminative properties which suggest that it is sensitive to treatment effects at a group level. The CAT score with its better ability to assess the impact of COPD on patients, suggests potential to predict a significant change in COPD status such as acute exacerbations of COPD.
There is a mounting body of evidence suggesting that there is a large disparity between the development and the actual implementation of guideline-driven asthma care in primary and specialty care practices. To address this disparity, the American Academy of Allergy, Asthma & Immunology (AAAAI) developed a unique, comprehensive and easy-to-use Web-based tool for clinicians who treat asthma patients called "Asthma Specialist Tool to Help Manage Asthma and Improve Quality" (Asthma-IQ). This study will examine whether the use of the Asthma IQ primary care tool will improve asthma care and asthma outcomes using a randomized trial of the Asthma IQ system versus usual asthma care in the primary care setting over 1 year. At the end of 1 year, all patients will be managed using the Asthma-IQ tool for an additional year to determine if the patients managed by usual care in the first year improve when managed in conjunction with Asthma-IQ. The primary endpoint to determine if the use of the Asthma IQ tool will improve asthma patient outcomes is quarterly assessments of Asthma Control Test (ACT) scores via automated / electronic patient survey. The secondary endpoint is asthma exacerbations and there are a number of exploratory endpoints to further define the clinical utility of the primary care version of Asthma-IQ. This study will involve recruiting approximately 20 family medicine offices with approximately 20 patients each, to conduct this randomized, multiple time point intervention trial.
The sensitivity of a persons cough reflex can be measured by getting them to breath in (inhale) irritant chemicals. The purpose of this clinical research study is to test the sensitivity of the cough reflex to a variety of chemicals that can be inhaled to see if coughing responses are different between healthy people and people with respiratory problems that make them cough. Coughing is a distressing symptom which has a major impact on quality of life. It has been estimated that cough costs the UK economy £1 billion each year. Currently there are no effective anti-tussive agents to treat subjects with cough. Although drugs such as morphine may have some anti-tussive effect, side effects unacceptable. Currently our understanding of the mechanisms which lead to coughing in different diseases is poor. Many mechanistic studies rely on testing the sensitivity of the cough reflex by inhalation of capsaicin (chilli-pepper extract) or citric acid. These challenges do not differentiate well between health and disease or between different disease states. Other agents such as prostaglandins and bradykinin are known to stimulate a coughing but responses to these agents have rarely been used as a measure of cough reflex sensitivity and not been compared to standard challenges. It is clear that patients with common airway diseases such as COPD and asthma cough significantly more than healthy subjects. Moreover subjects presenting with chronic cough have cough rates an order of magnitude higher than most patients with airway disease.
The aim of this prospective case-control study is to investigate the prevalence, severity and incidence of systemic consequences in newly detected patients with mild and moderate Chronic obstructive pulmonary disease (COPD). Special attention will be paid to skeletal muscle dysfunction and physical inactivity as these factors are, together with smoking, potentially modifiable. Three groups will be included in this study: - Patients with COPD (cases) - Patients with smoking history but no COPD (smoking controls) - Patients with no smoking history and no COPD (non-smoking controls) An extensive test battery will be performed at baseline and after 3 years: Clinical assessment (height, weight and blood pressure)* Complete pulmonary function ((post-bronchodilator)spirometry + diffusion)* Sputum Induction Fasting venous blood sample (fasting glucose, cholesterol, triglycerides, inflammatory markers, creatinine, NT pro BNP, hemoglobin, testosterone, vitamin D) Vascular screening (arterial stiffness - arterial stenosis - CIMT) Muscle force (peripheral + respiratory)* Functional exercise capacity (6 MWT)** Maximal exercise capacity (incremental cycle test)** Dexa scan (osteoporosis - body composition) Spiral CT scan of the chest RX thorax - RX lumbar Questionnaires (MRC, CCQ, SF-36, EQ5D, HADS, Exacerbation, CATZ)** Physical activity monitoring (sensewear armband)* * test will be repeated every 6 months ** test will be repeated every year !
The objective of this study was to examine COPD-related outcomes for patients with comorbid depression/anxiety who are on combination fluticasone propionate/salmeterol xinafoate compared to those receiving anticholinergics. The prevalence of comorbid depression/anxiety in patients with chronic obstructive pulmonary disease (COPD) is estimated to be high and range from 10-40%, given that the risk of depression/anxiety symptoms is almost 3 times higher in patients with versus without COPD. Additionally, patients with comorbid COPD and depression/anxiety have higher COPD-related healthcare utilization and costs compared to those without depression/anxiety. Therapy with maintenance medications for COPD has been recommended to prevent future adverse COPD outcomes, but the impact of initiating these interventions has not yet been evaluated in a higher-risk population with comorbid COPD-depression/anxiety. The present study compares the risk of COPD exacerbations and COPD-related costs in patients initiating maintenance medications for treatment of COPD in a comorbid COPD/depression-anxiety population. Maintenance medications include inhaled corticosteroid (ICS), long-acting beta agonist (LABA), combination drug product of ICS+LABA, and anti-cholinergics (AC) including tiotropium (TIO) and ipratropium or combination ipratropium-albuterol (collectively abbreviated as IPR). This was a retrospective cohort study using a large administrative database (study period: 1/1/2003 through 6/30/2009). Date of first FSC or ACs (tiotropium; ipratropium alone or in combination with albuterol) was defined as the index date. Managed care enrollees (aged >40 years) having at least one medical claim with a primary diagnosis of COPD (ICD code 491.xx, 492.xx and 496.xx) and a diagnosis of depression (at least one claim with depression/anxiety or at least one prescription claim for depression/anxiety) in one-year pre-index and within 60-days post-index were defined in the comorbid population.
RATIONALE: Diagnostic procedures, such as an urgent chest x-ray, may help in planning cancer treatment. It is not yet known whether standard medical care is more effective than an urgent x-ray in diagnosing lung cancer in smokers with chest symptoms who are older than 60 years. PURPOSE: This randomized clinical trial is studying standard medical care to see how well it works compared with an urgent chest x-ray in diagnosing lung cancer in smokers with chest symptoms who are older than 60 years. OBJECTIVES: Primary - To determine the prevalence of extra-NICE symptoms in patients consulting in UK general practice. - To determine the proportion of patients who agree to participate in the trial. - To determine the proportion of patients who are diagnosed with lung cancer and the best sources of routine data for capturing lung cancers. Secondary - To determine the best way to train general practitioners to identify and recruit eligible patients into the trial. - To determine the most effective method of presenting the trial (and randomization) to patients. - To determine the barriers to recruitment and how to overcome those barriers. - To determine the best tools to use to measure anxiety/depression that may be caused by unnecessary chest-x-rays or no chest x-rays. - To determine the best measures of resource use to facilitate health economic analysis of the cost-effectiveness of 'extra-NICE'. - To determine the stage at diagnosis, performance status, and the proportion of patients receiving radical treatments in those diagnosed with lung cancer.
Streptococcus pneumoniae is the most common causes of community-acquired pneumonia and exacerbations in chronic obstructive pulmonary disease (COPD) patients, which are associated with morbidity, mortality, and higher health-care cost. In addition, recently high daily dose of inhaled corticosteroid (ICS) therapy became more evident to be beneficial in moderate-to-severe COPD patients, but excess risk of pneumonia shown in database analysis was worried about by primary physicians. The use of pneumococcal polysaccharide vaccination (PPSV23) has protective efficacy to eliminate infection of Streptococcus pneumoniae from previous studies. If the use of PPSV23 can reduce the incidence of pneumonia or exacerbations in COPD patients using high daily dose of ICS, the benefit of ICS can be preserved and risk of pneumonia can be reduced. However, there is only limited data supporting this hypothesis. In this study, the investigators will conduct a double-blinded, randomized controlled trial to evaluate the clinical efficacy of PPSV23 in severe COPD patients using high daily dose of ICS. Exacerbations are a common feature in moderate-to-severe chronic obstructive pulmonary disease (COPD). Morbidity, mortality and health-care costs of these patients largely result from exacerbations. The most common causes of an exacerbation are infection of tracheobronchial tree. Among them, Streptococcus pneumoniae is the most frequently isolated organism, accounting for 5-25% patients of COPD, while it is also the most commonly identified cause in community-acquired pneumonia (CAP), accounting for 16.5-38.9% of CAP patients.
Patients with moderate COPD as defined by GOLD guidelines constitute almost 46% to 54% of all diagnosed COPD patients. Yet limited data exists on characterizing this study population in terms of drug therapy patterns and COPD-related resource use and costs. The objective of the following study was to conduct an analysis in the real-world setting to (1) identify and characterize COPD patients with moderate exacerbations and (2) evaluate the impact of initiating different maintenance therapies in this population. Maintenance therapy medications include inhaled corticosteroids (ICS), long-acting beta agonists (LABAs), combination of ICS+LABA, and anticholinergics (ACs) including tiotropium (TIO) and ipratropium or combination ipratropium-albuterol (collectively referred to as ipratropium [IPR]). Data from January 1, 2003 to March 31, 2009 will be available and termed as the study period. Patients with at least one moderate exacerbation defined as a physician/outpatient visit with a primary diagnosis of COPD and having an oral corticosteroid (OCS) or antibiotic prescription (ABX) within 5 days of physician/outpatient visit will be identified as the target population. The date of the first moderate exacerbation will serve as the patient's index date, and will be identified during the identification period of January 1, 2004 through February 28, 2009. Furthermore this moderate exacerbation should be the first medical claim with a primary diagnosis of COPD to ensure that only patients with moderate exacerbations will be captured.
Validation of Vital Signs and Symptoms for the Diagnosis of Serious Infections in Acutely Ill Children in a High Prevalent Setting: The Paediatric Accidents & Emergencies through prospective observational data collection concerning specific items from the clinical and technical examination in diagnosing serious infections, such as meningitis, sepsis, pneumonia, pyelonephritis, bronchiolitis with hypoxia. Eventually we will attempt to validate a vital signs and symptoms rule derived from multiple low to high prevalent settings of acutely ill children.
The timing of initiating short-term treatment for COPD exacerbations with oral corticosteroids and/or antibiotic therapy has been shown to influence the recovery time of exacerbations with early initiation of exacerbation therapy having a faster symptom recovery compared to delayed initiation. While oral corticosteroids and/or antibiotic therapy are crucial for immediate exacerbation therapy, maintenance therapy with controller medications for COPD has been recommended to reduce the risk of future exacerbations. The initiation of maintenance therapy after a COPD exacerbation has been shown to be beneficial in the reduction of risk of future exacerbations. However, there is a lack of information on whether the timing of this initiation influences the risk of future exacerbations. The following study evaluates the impact of early versus delayed initiation of controller medication therapy for maintenance treatment following a COPD-related exacerbation on outcomes of future exacerbations and costs in patients with COPD. Study period for this analysis will range from January 2003 through June 2009. Patients with at least one COPD exacerbation will be selected as the initial population. Three types of COPD exacerbations will be identified: 1) hospitalization with a primary discharge diagnosis code for COPD, 2) an emergency department (ED) visit with a primary diagnosis code for COPD, 3) physician visit with a dispensing of oral corticosteroid (OCS) or antibiotic (ABX) within 5 days of the visit. Only the first two will be selected as index exacerbations, which is defined as the first chronologically occurring exacerbation for a patient.
The purpose of the study is to determine a possible association between the clinical entity of exacerbation, markers of systemic inflammation and endothelial dysfunction in patients with COPD. Chronic obstructive pulmonary disease (COPD) is a chronic inflammatory disease of the lungs; however, there is cumulating data suggesting that the inflammatory reaction associated with COPD is not restricted to the lungs but has systemic effects. Patients with COPD have increased cardiovascular morbidity and mortality. The suspected link between increased cardiovascular mortality and systemic inflammation is endothelial dysfunction, which in turn is caused by impaired activity of NO. Endothelial dysfunction has been demonstrated in patients with COPD. Furthermore there is a close correlation between endothelial dysfunction in coronary and peripheral vessels, which allows assessing flow-mediated dilation (FMD) in the brachial artery via high resolution ultrasound as an early predictor of atherosclerosis. Moreover, systemic inflammatory markers correlate with endothelial dysfunction in patients with stable COPD. Exacerbations of COPD are episodes of worsening symptoms characterized by increased airway and systemic inflammation. If systemic inflammation is a cause of endothelial dysfunction in COPD, endothelial function would be suspected to be further impaired during exacerbation and recover thereafter. The purpose of this study is to determine a possible association between the clinical entity of exacerbation, markers of systemic inflammation and endothelial dysfunction in patients with COPD.