View clinical trials related to Fibrosis.
Filter by:To compare the efficacy of Triamcinolone with Pentoxifylline and Vitamin E in patients with stage two and three oral submucous fibrosis.
Idiopathic pulmonary fibrosis (IPF) is a serious chronic (long term) disease with injury of lung tissues. REGEND001 Autologous Therapy Product, made from bronchial basal cells with ability to regenerate lung tissue, is promising to IPF treatment. In this study, a single-armed clinical trial is ongoing to assess the safety and tolerability of REGEND001 Autologous Therapy Product in treatment of IPF. Different doses of REGEND001 Autologous Therapy Product is evaluated to establish a dose-response relationship and to recommend appropriate dose for subsequent clinical trials.
Cystic fibrosis (CF) is a multi-system inherited disease. It's a common autosomal recessive illness. It mostly affects the lungs, liver, and pancreatic exocrine glands, as well as the intestines. The production of viscous mucus and an environment prone to chronic airway blockage. This allows harmful microorganisms to infect the lungs. The role of Exercise as a prognostic indicator or therapeutic aid is important in CF research around the world. The objective of this study is to find out the Effects of Breathing Exercises Combined with Endurance and Strength Training on Dyspnea and Quality of Life of patients with Cystic Fibrosis. It will be Quasi Experimental study. Treatment will be given to all participants 3 sessions in a week for 4 weeks. Pre and Post treat-meant evaluation will be checked by CFQ-R+14. All patients will be treated with exercise program of Active cycle breathing techniques(ACBT), Pursed lip breathing, Endurance Exercise 20 to 30 min ( walking, cycling) and strength training with Thera-Bands (Bilateral arm raising, Bilateral knee extension). Exercise capacity will be measured with 6MWT. Dyspnea and fatigue will be measured with Borg scale.
In this study we aim to evaluate the radiological and functional changes in post-acute covid-19 pulmonary fibrosis patients in relation to anti-inflammatory and/or antifibrotic drugs prescribed during and after covid-19 pneumonia.
This is a randomized, double-blind, placebo-controlled, parallel-group, multicenter trial. Participants will be in the trial for up to 24 weeks, including a screening period lasting up to 8 weeks, a 12-week treatment period, and a 4-week safety follow-up period Participants are not expected to directly benefit from treatment during this trial. Participants will help researchers learn more about and how to develop AZD4831 to treat NASH.
Fibrosis is the final common pathway of solid organ diseases and accounts for ~45% of deaths in the developed world. Fibrosis is characterized by excessive deposition of extracellular matrix that replaces normal organ parenchyma, leading to loss of function. Chronic kidney disease is invariably characterized by fibrosis and affects >3 million Canadians. Although fibrosis can affect all compartments in the kidney. Interstitial fibrosis/tubular atrophy (IFTA) is the most potent predictor of kidney disease progression, regardless of its underlying cause. In addition to affecting native kidneys, IFTA also occurs in kidney allografts in transplanted patients, resulting in progressive kidney allograft dysfunction and, finally allograft loss with significant implications for patients' care and also financial implications for the healthcare system. However, early, noninvasive markers of IFTA or ongoing hypoxia in the kidney grafts are lacking. This is particularly problematic, since diagnosis of IFTA is often made late in the course of disease, and once IFTA develops, it is generally considered irreversible. There is thus an unmet clinical need to identify early markers of IFTA that could guide the use of novel anti-fibrotic therapies. In patients with clinically decreasing allograft function or protienuria, indication (or for cause) biopsies are the gold standard test used to identify the cause for the functional decrease. However, biopsies carry significant procedural risk (e.g. bleeding and death) and suffer from a sampling bias - not all areas of the kidneys are accessible for biopsy and there is currently no way to target the fibrotic / hypoxic areas. Urine protein measurements are obviously also not suitable to resolve this clinical dilemma. There would thus be great clinical interest in developing non-invasive tools that could provide more information compared to traditional tests for monitoring renal hypoxia and injury through imaging and urinary biomarkers. Our aims would be to image patients with different states of allograft function impairment and ideally find an imaging-based way to monitor those patients after transplantation. This way, an early detection of evolving interstitial fibrosis/tubular atrophy (IFTA) might be possible in a non-invasive way.The goal of this trial is to validate FAZA-PET/MR as a biomarker of hypoxia by correlating its uptake in patients with kidney allograft fibrosis with mass spectrometry based quantitative assays for monitoring of fibrotic markers in the urine of those same patients. There would thus be great clinical interest in developing non-invasive tools that could provide more information compared to traditional tests for monitoring renal hypoxia and injury through imaging and urinary biomarkers. Whereas currently only allograft biopsy can be performed to detect (rather late stage) interstitial fibrosis/ tubular atrophy. The study subjects' clinical management will not be changed based on the PET-MR scan within the trial.
This is a Phase 2a, single -center, randomized, double-blind, placebo-controlled study to evaluate type 1 collagen deposition in the lungs following once-daily treatment with PLN-74809 for 12-weeks. This study is occurring at Massachusetts General Hospital.
This randomized controlled study aimed to determine the effect of the exercise program to be applied in patients with cirrhosis on the patient's biochemistry parameters, quality of life, fatigue level, depression, and sleep quality.
Cystic fibrosis (CF) is an autosomal recessive genetic disorder caused by mutations in the gene encoding CF transmembrane conductance regulator (CFTR), which is located at 7q31.2 and encodes 1480 amino acids. CFTR protein is responsible for regulating the transport of electrolytes and chloride across epithelial and mucus-producing cell membranes.
This prospective case-control study was planned to evaluate the efficacy of antibiotic therapy selected with the AtbFinder® in persons with cystic fibrosis.