View clinical trials related to Interstitial Lung Diseases.
Filter by:Pathological comparisons of surgical open lung biopsies and cryobiopsies in non-IPF ILD. Patients with non-IPF ILD eligible for an open lung biopsy will undergo cryobiopsy in the same time. Between observers agreement will be assessed for each pairs of samples.
To study Fibrocytes in patients with Rheumatoid Arthritis, Interstitial lung disease and severe asthma and healthy controls.
Often, assessing a classifying diagnosis in patients with interstitial lung disease provides a diagnostic challenge. Currently HRCT, endoscopic or surgical video assisted thoracoscopic surgery(VATS) assessment including lung biopsies are diagnostic tools for patients with suspected ILD. However, tissue acquisition is associated with morbidity in these patients with an already compromised pulmonary function. In clinical practice this results in the fact that only a minor part of patients with an indication for tissue acquisition are actually undergoing biopsies. The aim of this study is to determine ILD-characteristics on imagign collected with minimal invasive novel optical techniques, to examine whether the addition of novel optical techniques to the diagnostic process of ILD could potentially limit the need for a tissue- (surgical) diagnosis and/or reduce the sampling error rate of biopsies by providing additional information on biopsy location.
Nanoparticles (NP) are particles whose length, width and height are less than 100 nanometres. Over the past decade, industrial applications of NP have increased dramatically. Despite their widespread use, their true impact on human health remains unknown and poorly studied. NP exposure in humans primarily occurs via inhalation through the respiratory system. The aim of this study is to estimate the relationships between the nanoparticle load in the lung and bronchi and some interstitial lung diseases. In the aftermath of human exposure to asbestos, the pathological consequences of environmental exposure to nanomaterials could be evaluated upon a mineralogical analysis of pulmonary samples.
Idiopathic pulmonary fibrosis (IPF) is a highly heterogeneous and lethal pathological process with limited therapeutic options, which is the most common and severe of the idiopathic interstitial pneumonias (IIPs). During the past 20 years, the incidence of IPF increased significantly. Most of IPF patients show a median survival time of 2-3 years after diagnosis. Five-year survival rate is 30%-50%. It's difficult to diagnose in the early stage of IPF. Once the patients go to hospital, it's already in the late stage. Now there is no effective therapy except lung transplant for IPF in clinical application. Acute exacerbation of idiopathic pulmonary fibrosis (AE-IPF) is a fatal condition with high mortality (over 80%). Its etiology and pathogenesis remain unknown. There is a lack of effective treatment for it. Based on the investigators' long-term clinical observation, most cases of AE-IPF initially got "common cold" and had coryza, more cough, nasal obstruction，rhinorrhea, sore throat, some patients had fever, headache, and etc. Some of these patients' condition developed very rapidly and then became very severe similar to the situation of acute respiratory distress syndrome (ARDS). Why these AE-IPF patients were so hypersensitive to "cold"? What were the immunologic and pathological mechanisms of their lung lesions after patients exposed to "common cold"? How to effectively offer interventional treatment for AE-IPF? All the above questions are yet to be explained clearly. In the investigators' previous retrospective study, the investigators found that there were some obviously imbalanced immune responses in IPF patients, including increased cluster of differentiation 4 (CD4) T cell population, immunoglobulin and complements. The investigators also found highly expressed inflammatory cytokines (IL-17, MIG and IL-9) and high detection rates of pathogens in AE-IPF patients, especially serum immunoglobulin M (IgM) antibody of some respiratory virus. These findings provide a strong suggestion that there are some imbalance of immunologic function in IPF and there are relationship between AE-IPF and infection, especially "Cold" virus infection might be a key trigger for AE-IPF.
Systemic sclerosis (SSc) is an orphan, multiorgan disease affecting the connective tissue of the skin and all internal organs. Interstitial lung disease is a frequent morbidity and mortality-driving manifestation in systemic sclerosis. This observational trial (OT) is part of the collaborative project "DeSScipher", one out of five OTs to decipher the optimal management of systemic sclerosis. Aim of this observational try is to identify: - The state of clinical practice in Europe for prevention and treatment of interstitial lung disease and its impact on lung function and disease progression - The potential predictors and confounders for response to therapy
Aim: To investigate whether ER stress is implicated in the pathogenesis of various pulmonary disorders Measurement: 1. Unfolded protein responses (UPRs) in blood (PBMCs)of patients 1. CHOP 2. GRP 78 and so on 2. Unfolded protein responses (UPRs) in blood (PBMCs)of healthy controls 1. CHOP 2. GRP 78 and so on
Interstitial lung diseases (ILD) is a collective noun for various chronic lung diseases, including sarcoidosis and idiopathic lung fibrosis (IPF). Sarcoidosis is a multi-systemic disease that includes damage to the lungs in 90% of the patients. Generally, the disease can be described as a systemic, granulomatous and antigen-driven disorder. IPF is a disease of only the lungs, in which an unknown cause induces a strong inflammation reaction leading to acute lung damage that ultimately results in the formation of scar tissue and stiffness of the lungs. Unfortunately, the exact cause of ILD is still unknown. It is suggested that environmental and work-related exposure to various triggers can exert an effect on the course of the diseases. Examples of such triggers include bacteria, organic agents such as pollen and cotton dust and inorganic agents like metals and talc. Due to this unknown cause, it is difficult to treat ILD. Consequently, the current guideline is no medication or anti-inflammatory agents in severe cases. Unfortunately, this therapy is not completely effective. Triggers that are suggested to cause ILD can exert their effects via various mechanisms. On the one hand, they can induce an inflammatory reaction as we recently demonstrated for various triggers including instillation material and sicila. During such an inflammatory reaction, cytokines are released that can induce oxidative stress, i.e. an imbalance between the formation of and the protection against reactive oxygen species (ROS). On the other hand, ILD-inducing triggers may directly cause an increased ROS production that subsequently can evoke an inflammatory reaction. The objective of the current study is to investigate the individual sensitivity for the development of ILD after exposure to various triggers. Main focus will be the differences in the formation of and the protection against ROS as well as the occurring inflammatory reaction after exposure to such triggers. Furthermore, a simple blood test will be developed to study and eventually even predict the individual reaction of subjects to various triggers. Finally, to fully characterize the development of ILD after exposure to various triggers, the exhaled air of patients will be studied in order to identify specific markers of oxidative stress and damage.
Reactive oxygen species (ROS) are suggested to play a pivotal role in ILD. Little is known, however, about the endogenous antioxidant levels in ILD that can offer protection against ROS. It is expected that the high amount of ROS present in ILD will reduce the antioxidant levels. Therefore, antioxidant therapy to strengthen this reduced antioxidant defense might be efficacious in ILD treatment. Since ROS are capable of initiating and mediating inflammation, antioxidant therapy might also mitigate elevated inflammation. A candidate for antioxidant therapy is the flavonoid quercetin that is known for its anti-oxidative and anti-inflammatory capacities. The aim of the present study is to determine the antioxidant and inflammatory status in ILD, i.e. sarcoidosis and idiopathic pulmonary fibrosis (IPF). Furthermore, to evaluate the possible anti-inflammatory effects of antioxidants, the effect of quercetin will be examined on the ex vivo LPS-induced cytokine production in ILD
In the present study inflammatory mediators will be isolated in induced sputum and exhaled breath condensate and will be correlated with particulate matter measured in these samples.Particulate matter will be assessed by partcle size distribution method and shape analysis. The aim of the study is to perform biological monitoring in environmental and occupational diseases in a non invassive fashion.