View clinical trials related to Sarcoidosis.
Filter by:This study is a prospective observational non-randomized clinical trial where all the participitants undergo the same procedure and every participitant's samples are compared to each other. The investigators conduct EBUS TBNA and EBUS TBMCB on all the study participants.The cryobiopsy samples are numbered to evaluate the number of biopsies needed to reach a definite diagnosis and to assess the added value of every sample taken from the same participitant. Every participitant's own samples are compared to each other and added value of EBUS TBMCB is defined as the difference in diagnostic yield between the EBUS TBNA alone and the combination of EBUS TBNA with EBUS TBMCB. Diagnostic yield is defined as the efficacy of the investigation module in reaching a definite diagnosis (percentage of cases with a definite diagnosis). Follow up four weeks after the procedure to assess the risk for postoperative complications.
To assess the frequency and risk factors of decreased bone mineral density (BMD) and vertebral fractures in Danish patients with sarcoidosis.
The goal of the study is to create a longitudinal study of patient reported outcomes for people living with sarcoidosis that maintains privacy. Patients report on the following: demographics, disease symptoms, diagnostic journey, provider experience, disease treatment, and burden of disease. The goal is to create a natural history of sarcoidosis, support research, and better understand the needs of the sarcoidosis community.
This randomized pilot clinical trial aims to examine whether sample collection with Franseen-type needles are effective for the diagnosis of sarcoidosis, as defined by improved sample quality for pathological diagnosis compared to the conventional Menghini-type needle.
This is a Phase 2, randomized, double-blind, placebo-controlled, adaptive, multicenter study to evaluate the efficacy, safety, tolerability, Pharmacodynamics (PD), and Pharmacokinetics (PK) of OATD-01 in the treatment of subjects with active pulmonary sarcoidosis.
The purpose of the CuDOSIS study is to examine the diagnostic value of activated macrophage imaging in patients with or under evaluation for cardiac sarcoidosis. The PET/CT tracer 64Cu-DOTATATE is used as a tool to identify activated macrophages. The trial is an open-label prospective study. The study will include 54 participants from the Department of Cardiology and the Department of Clinical Physiology, Nuclear Medicine, and PET at Rigshospitalet. Further, the study will include data from 22 patients with NET who have been scanned with 64Cu-DOTATATE PET/CT previously as negative controls. Participants will be included in the following groups: Group A: 22 patients with clinically suspected cardiac sarcoidosis Group B: 22 patients with known cardiac sarcoidosis Group C: Up to 10 patients with clinically suspected or confirmed acute lymphocytic myocarditis Group D: 22 patients with NET without known inflammatory heart disease who have previously been scanned with 64Cu-DOTATATE PET/CT as part of their routine diagnostic work-up or follow-up (control group)
Inhalation of beryllium can induce specific sensitization and diffuse pulmonary granulomatosis called chronic beryllium disease (CBD). The clinical, radiographic, and anatomopathological features of CBD are very similar to those of sarcoidosis, another granulomatosis, making its diagnosis difficult. In addition, the progression of CBD is poorly understood. The investigators hypothesis is that there are specific clinical, biological, anatomopathological, and radiological presentation specificities of CBD, as well as a worse prognosis compared to pulmonary sarcoidosis.
Sarcoidosis is a systemic inflammatory disease characterized by unspecific granuloma formation. Our hypothesis is that granuloma formation and maintenance mainly relies on the overactivation of monocytes (Mo) and macrophages (Ma). To this end, the study aims (i) to define MoMa systemic signature in sarcoidosis, (ii) to characterize this signature in situ on tissue samples, and (iii) to identify causative factors that participate to the MoMa chronic overactivation. Thus, a cohort of sarcoidosis patients will be compared with tuberculosis patients. The MoMa systemic signature will be defined on whole blood (TruCulture model) and then in situ through different methods (multi-parameter spectral flow cytometry, RNA-seq, Luminex, imaging mass cytometry). The epigenome of monocytes will be studied thanks to CUT&Tag. The MoMa systemic signature will be defined ex vivo at different time points during the course of the disease with phenotypic, transcriptomic, cytokine and functional approaches. The previously identified signature will be studied in situ and completed by the characterization of granuloma architecture and microenvironmental interactions, which could be modulated by epigenetic modifications. Hence, the epigenome of monocytes will be analyzed in two groups (sarcoidosis and tuberculosis). These results would allow to better understand sarcoidosis physiopathology and, in fine, may raise new therapeutic strategies. Finally, the study could challenge the dogma on innate immunity/auto-inflammation versus adaptive immunity/auto-immunity/memory.
A phase 1b/2 study of XTMAB-16 in patients with pulmonary sarcoidosis
Background: Sarcoidosis is an inflammatory disease, most commonly affecting the lungs and intrathoracic lymph nodes but can affect virtually any organ, sometimes manifesting as life threatening cardiac arrythmias. Some patients resolve spontaneously, whereas others get a chronic disease leading to for instance impaired lung function and cardiac failure. The most severe cases might need a transplantation. In the lungs, activated T cells are accumulated leading to release of cytokines, especially TNF-alpha is regarded as crucial for disease progression. Some segments of the T cell receptor and specific genes (HLA types) are connected to a resolving disease. More detailed knowledge about mechanisms why some experience a chronic disease course and others resolve spontaneously without treatment is to a large extent lacking. There is no cure, and despite treatment with immunosuppressants (often corticosteroids and cytotoxic agents), many patients experience a deteriorating disease. Aim: 1. Find biomarkers to be able to early predict which patients will develop a more severe/ chronic disease course and thereby enabeling early intervention before irreversible damage. 2. Predict which treatment is best for a specific patient, i.e. individualize treatment. 3. Find targets for new potential therapies. Methods: The majority of data is collected at investigations normally performed during diagnostic work-up for sarcoidosis. Most patients undergo a bronchoscopy with bronchoalveolar lavage (BAL) and some also lymph node punction through oesophagus with the help of ultrasound. The BAL fluid that remains after clinical analysis is used for research purpose. For patients undergoing lymph node punction, one extra punction is performed for research purpose. Extra blood samples are taken from all patients. The samples will mostly be used for studying T cells with immunohistochemistry, flow cytometry including activity markers, subtypes and receptors, but also cytokines and other cells (for instance B cells, NK and NKT cells). The patients are followed longitudinally, minimum 2 years. Some patients will undergo a second bronchoscopy 6-12 months after the first. Results from the immunological investigations will be correlated to disease course, genetics and result of treatment. Significance : By comparing the inflammation in several compartments (lung, lymph node , blood) at a molecular level with clinical disease course, genotype, and treatment response we hope to find biomarkers that can predict disease course and response to therapy. Thereby, we hope to be able to tailor therapy for each individual patient. By studying several compartments, the results may also help to improve understanding of how a systemic inflammation is distributed within the body, and thus also contribute to understanding of other inflammatory diseases.