Active clinical trials for "Sarcoidosis, Pulmonary"

to determine the genetic pathways operating at the tissue level to cause granulomatous inflammation in the lungs and lymph nodes of patients with sarcoidosis. By so doing, we hope to identify unique genetic mechanisms which will aid in the diagnosis of sarcoidosis and will help us understand the pathogenesis of this poorly understood disease.

The goal of this observational study is to elucidate the role of serum amyloid A (SAA) in the diagnosis and follow-up of sarcoidosis, including its prognostic value. The main questions it aims to answer are: Whether, at the time of diagnosis, SAA is in correlation with other serum markers of granulomatous inflammation, interstitial disease and pulmonary fibrosis, lung function and radiologic characteristics of intrathoracic sarcoidosis, Whether increased serum concentrations of SAA at the time of diagnosis act as a prognostic marker of progressive granulomatous inflammation and pulmonary interstitial disease. Patients will undergo standard diagnostic procedures for intrathoracic sarcoidosis, according to WASOG (World association of sarcoidosis and other granulomatous disorders) criteria. Two additional vials of blood will be taken at diagnosis and one vial at follow-up for serum processing and biomarker analysis. Healthy blood donors will represent our group of healthy controls.

The goal of the current study is to evaluate the potential of the selected PET tracers to detect sarcoidotic lesions in lungs. The tracers are already in clinical use for the detection of certain inflammatory processes or malignant tumors, and their targets present similarities with molecular mechanisms of sarcoidosis.

Sarcoidosis is a disease of unknown cause which affects adults of all ethnic backgrounds. Clumps of tissue called granulomas develop primarily in the lungs, but can damage other organs, especially the heart. Anecdotal evidence from autopsy studies suggests the heart is affected in up to 68% of patients, but there is much uncertainty about this figure. If undetected and untreated, it can lead to serious complications or even sudden death. The current recommendation is to perform heart tracings (ECG s) on all patients, but this detects fewer than half of those with heart involvement. Blood markers traditionally used to diagnose heart disease are unreliable, meaning there is no simple blood test in use. The investigators propose a study with three aims. Firstly, identify the true prevalence of heart disease by performing Magnetic Resonance Imaging (MRI) scans on a group of patients with newly diagnosed lung sarcoidosis. Those found to have heart disease will have specialist (but routine) electrical heart tests. Secondly, (and perhaps the most immediate and clinically relevant) to identify the best method of diagnosing heart involvement using a combination of three simple tests: advanced ECG, 24-hour continuous ECG and a new type of computerised ultrasound scan. Thirdly, to identify proteins in the blood that could be used to develop a simple blood test for heart involvement in patients with lung sarcoidosis.

Interstitial lung disease (ILD) is a restrictive lung disease characterized by impaired lung function, exercise limitation and skeletal muscle dysfunction. There is limited data on skeletal muscle function in ILD, most of which are focused on the lower limb muscles. The aim of this study were to evaluated the change of pectoralis muscle strength and relationship of pulmonary function with pectoralis muscle strength.

Sarcoidosis is a heterogeneous multisystem disorder of unknown etiology which often presents with bilateral hilar lymphadenopathy, pulmonary infiltration and ocular and skin lesions. In addition to possible changes in forced vital capacity (FVC) and carbon monoxide transfer factor (TLCO), a higher prevalence of clinical depression, reduced health status and exercise intolerance have been observed in patients with sarcoidosis. Reduced health status has been related to decreased pulmonary function, depressive symptoms, and to respiratory muscle weakness. Exercise capacity is believed to be limited by dyspnea, an insufficient heart rate response, decreased arterial oxygen tension during exercise, excessive and inefficient ventilation and by respiratory muscle weakness. In the past, exercise capacity was shown to be limited by skeletal muscle weakness in patients with chronic pulmonary or cardiac disease. 67% of the sarcoidosis patients studied by Miller et al terminated their peak exercise test due to "leg complaints". Skeletal muscle weakness is therefore still assumed to be present in patients with sarcoidosis. Treatment with oral corticosteroids, clinical symptoms of depression, myositis, self-reported complaints of fatigue and high circulating levels of tumour necrosis factor-α (TNF-α) are all present in patients with sarcoidosis and can all affect skeletal muscle force and exercise capacity. Additionally, low levels of circulating insulin-like growth factor I (IGF-I), which can be induced by high levels of TNF-α, and high circulating levels of interleukin (IL)-6 and IL-8 (CXCL8) have been associated with skeletal muscle weakness. These interleukins are part of the current concept of the immunopathogenesis of sarcoidosis16 and may be raised in patients with stable sarcoidosis. Recent studies have shown that pulmonary rehabilitation program can lead to improve in the health status and anxiety among patients with chronic obstructive lung disease .However, no study has evaluated the role of pulmonary rehabilitation among patients with sarcoidosis.