This trial is evaluating whether Namilumab will improve 1 primary outcome and 14 secondary outcomes in patients with Sarcoidosis. Measurement will happen over the course of Baseline of double-blind to week 26.
This trial requires 100 total participants across 2 different treatment groups
This trial involves 2 different treatments. Namilumab is the primary treatment being studied. Participants will all receive the same treatment. Some patients will receive a placebo treatment. The treatments being tested are in Phase 2 and have already been tested with other people.
Though no single factor can explain the cause of sarcoidosis, there are several associated factors in its multifactorial etiology. This implies that various factors act in concert to cause its manifestation. question: Is sarcoidosis in women associated with decreased circulating levels of S100A12? answer: Although the exact role of S100A12 in sarcoidosis was not elucidated, our study found a significantly lower S100A12 serum level in female sarcoidosis patients, suggesting a S100A12 modulating role and S100A12 involvement in the etiopathogenesis of sarcoidosis. S100A12 has a special role in innate immune responses.
Sarcoidosis is a chronic disease, which usually may be spontaneously and completely self-limited. If sarcoidosis recurs in a patient with a history of complete and sustained remission, it is the time to start the therapy again and keep it constant on the time.
Arthritis is present in almost 10% of adult patients being evaluated for symptoms attributed to sarcoidosis. This frequency is relatively high in our sarcoidosis population.
Sarcoidosis is a disease characterized by chronic inflammation of the skin (erythema nodosum), lungs, or eyes as well as of internal organs (extrathoracic involvement). About 7 in 10 Americans have this disease at some point in their lives.\n
Immunomodulatory treatments are the most effective antifungal agents used. Common antifungal medications include ketoconazole and itraconazole, respectively. Steroid therapy is frequently used, mostly with oral prednisone. Treatment of pulmonary manifestations of sarcoidosis is dependent on disease severity. Patients with severe disease may be treated with biologic therapies, like IFNβ, which are administered intranasally for persistent pulmonary involvement. Patients with pulmonary involvement may be prescribed inhaled corticosteroids, such as Budesonide, fluticasone, and budesonide.
Sarcoidosis may cause physical abnormalities such as shortness of breath, sweating (palmar erythema), and fever. These signs are typically seen in advanced disease, and there is usually an interval of 6–8 weeks between the first manifestation and development of overt clinical disease. Patients with chronic sarcoidosis may also have skin pigmentation and a thickened chest wall.
Namilumab is a monoclonal antibody against programmed-cell death 1 (PD-1), produced by the Mayo Clinic. Since its approval in April 2015, data in Phase 2 and 3 clinical trials of multiple autoimmune diseases in children have been published, and namilumab has been well-tolerated in clinical trials.
Although other clinical studies are in progress, the FDA was not yet considering a review. A second-generation anti-IL-17Ab, androstanolone acetonide are two therapeutic options in clinical trials, which may have been helpful in preventing or treating sarcoidosis, but the lack of current data on side effects of the drugs makes us unable to recommend these therapies to the extent that it could be considered an option for the treatment of sarcoidosis. Patients are encouraged to take these trials more seriously, when the research results are published.
The findings suggest that namilumab's efficacy is due to both its ability to inhibit IFN-γ production and its intrinsic immunomodulatory function. This information will be useful for the development of new therapies that target IFN-γ or its downstream effectors.
The findings of the present study support the hypothesis that sarcoidosis-like lesions are probably inherited. The inheritance pattern suggests that a genetic component may control the development of sarcoidosis, and that there are multiple genes that play a role in the development of the disease.
Sarcoidosis has almost always been reported as occurring more commonly in people ≥ 25 yr old. In a previous survey in the United States from 1973 to 1988, sarcoidosis prevalence was highest (approximately 5%) in those ages 18 to 24 yr. This survey did not include data from Asians or in the last 10 yr. The current findings, however, suggest that the average age of disease onset is decreasing in these more recent decades as a result of better living situations and a changing attitude toward health and medicine.
Results from a recent paper represents a significant advance in our understanding of the role of TNF-α in sarcoidosis and indicates a number of important therapeutic implications. Additionally, our data suggest that pharmacologic blockade of TNF-α may be a viable alternative to corticosteroids in treating sarcoidosis patients. Results from a recent paper have potential to inform future sarcoidosis clinical trials for namilumab.