Active clinical trials for "Emphysema"

Pneumonia is a recurrent element of COVID-19 infection, it is often associated with development of respiratory failure and patients frequently need various degrees of oxygen therapy up to non invasive ventilation (NIV-CPAP) and invasive mechanical ventilation (IMV). Main purpose of this study is to evaluate with non invasive clinical instruments (pletysmography, Diffusion lung capacity for carbon monoxide -DLCO-, six minute walking test and dyspnea scores) and radiological tools (chest X-ray and chest CT scan) the development of medium-to-long term pulmonary sequelae caused by SARS-CoV-2 pneumonia.

The goal of this study is to better understand why some Alpha-1 genotype MZ (PiMZ) individuals develop chronic obstructive pulmonary disease (COPD) while others do not. This study will examine portions of the Alpha-1 gene that are not routinely tested to determine whether other changes in this gene correlate with development and progression of COPD. Participation involves responding to questionnaires about lung health and history, and performing an at-home finger stick to obtain blood spots using a test kit that is mailed. The blood provided will be used for genetic testing and correlation of results with COPD history. Participants will receive their results and access to genetic counseling at the conclusion of the study.

Chronic obstructive pulmonary disease (COPD) is a lung disease that is primarily caused by cigarette smoking. The breakdown of elastin, a protein found in the lungs, can cause lung damage and may contribute to the development of COPD. Some people may be more prone to elastin damage and in turn to developing COPD than others. This study will examine whether genetic factors are responsible for altering elastin function and increasing the risk of developing COPD.

Emphysema, a common type of chronic obstructive pulmonary disease (COPD), is a long-term lung disease that is usually caused by cigarette smoking. This study will examine both current smokers and former smokers who have emphysema, as well as current and former smokers who do not have emphysema, to determine if certain factors found in the blood are related to the risk of developing emphysema.

Studying the airway microenvironment in patients undergoing surgical and bronchoscopic interventions for COPD

The purpose of this cross-sectional, observational study is to evaluate the site and mechanism(s) for expiratory airflow limitation in chronic, treated, current or former smokers (>15 pack years) with COPD, Emphysema, and Asthma-COPD Overlap with mild to severe expiratory airflow limitation. Treatment may include short and long acting inhaled beta2agonists, short and long acting inhaled muscarinic receptor antagonists, inhaled and or oral corticosteroid, oral antibiotic, supplemental oxygen, and PDE type 4 inhibitor. In some cases, the patient may have had a history of asthma preceding the development of COPD (Asthma COPD Overlap).

This is a Post-Market Evaluation of the Zephyr Valve 5.5-LP EBV to assess Treated Lobar Volume Reduction (TLVR), changes in lung function and the safety profile of the Zephyr Valve treatment with the use of at least one Zephyr Valve 5.5-LP EBV.

Background: Elastin is a unique protein providing elasticity, resilience and deformability to dynamic tissues, such as lungs and vasculature. Elastin fibers are characterized by their high affinity for calcium. However, calcified elastin is more prone to the degrading effects of proteases and, in turn, partially degraded elastin has an even higher affinity for calcium. A disturbed balance between proteases and anti-proteases is a major underlying mechanism in the development of chronic obstructive pulmonary disease (COPD). Virtually the only protein that can protect elastin from calcification is matrix Gla-protein (MGP), which needs vitamin K for its activation. In COPD patients, a lower vitamin K status is found when compared to control subjects and an inverse association exists between vitamin K status and elastin degradation. In addition, vitamin K status is lower and elastin degradation is accelerated in Vitamin K antagonist (VKA) users. VKAs are widely used. Nowadays, an increasing number of patients uses direct oral anticoagulants (DOACs), which do not influence vitamin K status. The hypothesis of this study is that discontinuation of VKAs results in an improved vitamin K status and deceleration of elastin degradation. In order to test this hypothesis, an observational pilot study will be conducted in which the change in elastin degradation- quantified by plasma desmosine concentrations - in patients who discontinue use of VKAs will be used as primary endpoint. Study design: Observational study. Study population: A total of 30 VKA users who will discontinue the use of VKAs. Elastin degradation rate (quantified by plasma desmosine levels) and vitamin K status (quantified by measuring plasma levels of dephosphorylated uncarboxylated (dp-uc)MGP) will be measured during the use of VKAs and approximately 6 months after discontinuation of VKAs. Furthermore, the VKORC1 polymorphisms will be determined. Main study parameters: The primary endpoint is the change in the rate of elastin degradation quantified by the plasma desmosine assay. Secondary endpoints are the change in vitamin K status quantified by measuring plasma levels of dp-ucMGP, the relation between desmosine and dp-ucMGP and differences of desmosine and dp-ucMGP levels among subjects with different polymorphisms of the vitamin K 2,3-epoxide reductase complex 1 (VKORC1) gene.

Chronic obstructive pulmonary disease (COPD) is a lung disease caused by cigarette smoke that affects millions of people. In the United States, COPD is the 3rd leading cause of death making it one of our most important public health problems. Some people with COPD get disease flares that are called acute exacerbations of COPD - or AECOPDs for short. When people get an AECOPD they experience increased shortness of breath, wheezing and cough; symptoms that often require urgent or emergent treatment by healthcare providers. In the most severe, life-threatening situations, people with AECOPDs are put on a ventilator in the emergency department and admitted to the intensive care unit. Most AECOPDs can be treated with low doses of medications called steroids. This is good because high doses of steroids can cause unwanted side effects. Unfortunately, recent studies suggest that the sickest people, those admitted to the intensive care unit needing ventilator support, need higher doses of steroids because they may have resistance to these important medications. The investigators are studying steroid resistance during very severe AECOPDs so that we can eventually develop better and safer therapies for these vulnerable people.

The purpose of this observational study is to investigate the efficacy of 9 mm intrabronchial valve treatment in patients with heterogeneous emphysema and to gain further insights and experience on the treatment with this valve size.