View clinical trials related to Pulmonary Fibrosis.
Filter by:The goal of this study is to use the tissues from the explanted lungs in order to better study the cause of pulmonary fibrosis at a cellular level.
The general purpose of this trial is to investigate the efficacy and safety of 4 dose strategies of BIBF 1120 treatment for 12 months, compared to placebo in patients with idiopathic pulmonary fibrosis. The primary objective of this study is to demonstrate whether at least one dose strategy is superior to placebo in patients with IPF, in modifying the rate of decline of Forced Vital Capacity (FVC). As a secondary objective, additional parameters will be assessed in order to differentiate between dose strategies on the basis of safety and efficacy
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
A number of studies have shown that the quality of life of two common interstitial lung diseases (ild), sarcoidosis and pulmonary fibrosis patients, is impaired and that fatigue is a substantial problem for those patients. Furthermore, breathlessness is an additional major problem in pulmonary fibrosis. In the field of cardiovascular disease and breast cancer, personality factors have shown to play a role in patient's morbidity, mortality, quality of life, fatigue, depressive symptoms, and one study showed a predictive role of personality factors in health care consumption. No studies examining personality factors have been performed in sarcoidosis or pulmonary fibrosis. Therefore, the aim of the present study is to examine the role of personality factors as predictors of fatigue, quality of life, prognosis, and health care consumption in sarcoidosis and pulmonary fibrosis. In this study a number of possible moderators, such as social support, will also be examined, aiming to get a full picture of the relationship between the various factors examined. Known and new sarcoidosis and pulmonary fibrosis patients (inclusion period 1 year) of ild care team of the outpatient clinic of the department of Respiratory Medicine of the University Hospital Maastricht will be asked to participate through completing questionnaires at baseline and every six months for 18 months, and allowing the researchers access to their medical records for the purpose of this study.
We propose to acquire data and blood samples on all patients being cared for by the Interstitial Lung Disease (ILD) program. Additionally, we will collect data and blood samples from a control group for comparator purposes. In doing so, we will be able to describe the "phenotypic" expression of these diseases.
This study will examine whether five drugs (pravastatin, Losartan, Zileuton, N-acetylcysteine and erythromycin) used together can slow the course of pulmonary fibrosis (scarring of the lung tissue) in patients with Hermansky-Pudlak Syndrome (HPS). Patients with this disease have decreased skin color (albinism), bleeding problems, and sometimes colon problems. Two of the known types of Hermansky Pudlak syndrome, type 1 and type 4, are at high risk of pulmonary fibrosis between the ages of 30 and 50. Patients 18 to 70 years of age who have Hermansky-Pudlak Syndrome with a serious loss of lung function due to pulmonary fibrosis may be eligible for this study. Participants begin taking pravastatin on study day 2 and start a new drug every 3 days. Patients who experience no problems with the medicines return home and continue on the drugs for the next 2 years. They return to the NIH Clinical Center every 3 months for a medical history, physical examination, and blood, urine and lung function tests. CT and bone density scans are done every year. The study may continue for up to 3 years.
Octreotide is a somatostatin analog with a long half-life in vivo. Octreotide has interesting anti-inflammatory and anti-fibrotic properties in vitro and in vivo. Somatostatin receptors are increased and Octreotide uptake is increased in the lung in patients with idiopathic pulmonary fibrosis. Our hypothesis is that octreotide may slow the degradation of lung function in patients with IPF. In this proof of concept study, patients with IPF will receive an intramuscular injection of slow release octreotide (Sandostatin LP, 30 mg)every 4 weeks for 48 weeks. Lung function (FVC, DLCO), HRCT scores for fibrosis and ground glass, 6 minute walking test,quality of life and survival will be monitored.
The objective of this study is to assess the effects of using HRQL measures in the clinical care of pre- and post-lung transplant patients. The hypotheses are that the inclusion of HRQL measures, the Health Utilities Index System Mark 2(HUI2) and Mark 3 (HUI3), in routine clinical care of pre- and post-lung transplant patients, will: 1) improve patient-clinician communication;2) affect patient management; 3) improve patients' HRQL.
The study is aimed to assess safety of Depelestat treatment, as well as efficacy on prevention and treatment of alveolar inflammation in early pulmonary fibrosis in patients suffering from persistent Acute Respiratory Distress Syndrome.
The purpose of this study is to identify factors that contribute to higher mortality rates among blacks and Hispanics with diffuse parenchymal lung disease.