Active clinical trials for "Fibrosis"

In December 2019 SARS-CoV-2 virus appeared in the world, mainly appearing as an acute infection of the lower respiratory tract. In March 2020, the World Health Organization (WHO) announced a pandemic in relation to the disease caused by the SARS-CoV-2 virus, known as COronaVIrus Disease 2019 (COVID-19). Since then, the efforts of scientists from around the world have focused on finding the right treatment and vaccine for the new disease. COVID-19 has spread rapidly in a few months, affecting patients in all ages. The disease has a varied course, patients can be 80% asymptomatic, but many develop respiratory failure, complicated by sepsis and ultimately death. One of the possible complications associated with COVID-19 lung involvement is pulmonary fibrosis, leading to chronic breathing difficulties and prolonged disability. No specific mechanisms leading to this phenomenon have been identified in COVID-19, but some information is derived from previous studies on the SARS and MERS epidemic. There have been several reports that the use of spironolactone may be important in preventing pulmonary fibrosis. The aim of the study is to evaluate the effectiveness of intravenous form of mineralocorticoid receptor antagonist canrenoate potassium (an aldosterone antagonist of the spirolactone group) in the treatment of COVID-19-associated pulmonary fibrosis based on the mechanisms of the immune response.

Idiopathic pulmonary fibrosis is the most severe form of interstitial lung disease. It is known that the prognosis is poor due to extensive inflammation and fibrosis of the lung parenchyma. In case of acute exacerbation, the prognosis becomes worse. In early studies, the 3-month mortality rate reached 50-80%, and in a recent study, the 1-month survival rate was 66%, and the 3-month survival rate was 41%. It is known that 20% of patients with IPF will experience acute exacerbations in their lifetime. The most commonly used treatment for such acute exacerbations is antibiotics and high-dose steroids, or steroid pulse therapy. However, its effectiveness is unclear, and the survival rate is still low. However, as there is no evident therapeutic agent other than steroids, it is included in the treatment guidelines, so conservative treatment is administered while steroids are administered to patients with acute exacerbation of idiopathic pulmonary fibrosis in most upper institutions. There is no precise treatment other than steroids for patients with idiopathic pulmonary fibrosis-acute exacerbation, but the side effects of steroid administration cannot be overlooked. Therefore, a study is needed to confirm whether steroid pulse therapy is necessary or not. Inclusion criteria Among patients with clinically or histologically confirmed idiopathic pulmonary fibrosis, patients who visited the emergency room with dyspnea symptoms Patients within 1 month of exacerbation of respiratory symptoms Patients with increased GGO or worsening of IPF on chest CT within the last 2 weeks Patients who understand the purpose of the clinical study and voluntarily agree to participate in this clinical study When it is determined that steroid administration is necessary under the judgment of the medical staff during the treatment process Exclusion criteria Patients who complain of dyspnea symptoms due to causes other than the respiratory system, such as fluid overload, congestive heart failure, pulmonary embolism, etc. Patients whose respiratory symptoms have worsened for more than 1 month Persons who cannot read consent forms (eg. illiterate, foreigners, etc.) Study design Using an open-label RCT randomization method, the administration will be divided into Group 1 (high-dose followed by low-dose steroid administration) and Group 2 (high-dose/low-dose steroid administration after steroid pulse therapy). Test group: Group 1 (high dose followed by low dose steroid administration) Control group: Group 2 (high-dose/low-dose steroid administration after steroid pulse therapy) ▶ Steroid administration Protocol Group 1: Methylprednisolone 1 mg/kg 7 days → 0.5 mg/kg 7 days → 0.25 mg kg 7 days Group 2: Methylprednisolone 10 mg/Kg (500 mg ~ 1g) pulse 3 days -> Methylprednisolone 1 mg/kg 7 days → 0.5 mg/kg 7 days → 0.25 mg/kg 7 days Response evaluation The level of inflammatory markers Imaging improvement: chest x-ray or CT Pulmonary function test: performed at the outpatient clinic before discharge or 12 weeks after the first visit for acute exacerbation

This study evaluates the Safety,Tolerability, Pharmacokinetics and Exploratory Efficacy Parameters of AIR DNase™in Patients with Cystic Fibrosis previously treated with Pulmozyme®.

Cavosonstat (N91115) is being studied as a potential novel therapy for cystic fibrosis (CF), and this study assesses a target population of patients who are heterozygous for F508del-CFTR and a gating mutation that is approved for treatment with ivacaftor (G551D, G1244E, G1349D, G178R, G551S, S1251N, S1255P, S549N, or S549R).

Mucus in the airways of patients with CF represents an area for bacteria proliferation, microbial infection and inflammation. Similar to the lung, the esophagus provides an environment for bacterial to grow. The overall goal of this proposal is to characterize the esophageal microbiota of children with CF that are treated or untreated with acid blockade medication and to measure its possible impact on respiratory disease to develop novel treatment strategies.

The purpose of this study is to evaluate the safety and efficacy of human umbilical cord mesenchymal stem cell(hUC-MSC) for Hepatic Cirrhosis.

This study will examine potential factors in the aqueous humor that may contribute to the development or progression of macular edema or fibrosis (due to any underlying disease) in patients suffering from these conditions.

Chronic liver injury leads to the accumulation of proteins in the liver that form dense scars. Liver scar formation is typically a slow process that leads to major organ damage and loss of function over the course of many years. During scar formation the extracellular matrix in the liver changes. The type and quantity of extracellular collagen and other proteins change during tissue remodeling. Some of these changes can be detected by analyzing factors present in blood. Because of the lengthy time course, changes in the rate of liver scar formation and regression are very difficult measure; however, accurate measurements are needed in order to conduct trials of interventions aimed at preventing scar formation and/or promotion scar regression. Current methods have sub-optimal specificity and selectivity. The long term objective of the study is to identify serum proteins that can be used to accurately estimate rates of liver fibrosis progression and regression. The project focusses on a novel methodology that uses stable isotope labeling with deuterated water, D2O, to tag newly-synthesized proteins. Mass spectroscopy is used to identify individual proteins and to quantify the ratio of labeled protein to total protein. This ratio provides information about the rate of synthesis of the protein of interest. This method will be applied to specimens from patients with hepatitis C virus (HCV) infection who are about to begin HCV treatment. Treatment is known to reduce liver inflammation and collagen content.

The aim of the study is to choose an optimal stent and to get further knowledge about the mechanisms of the engraftment of a stent. The occurrence of a hyperplasia of neointima can be minimized by application of a coated stent and a concurrent safety four weekly dual thrombocytes therapy

The primary biliary cholangitis (PBC), formerly known as primary biliary cirrhosis, treatment is based in the use of ursodeoxycholic acid (UDCA) at a daily dose of 13 to 15 mg/kg, without other treatment options. Patients with good or complete response to UDCA have more liver transplant-free survival and delay histologic progression compared to patients with partial or no response. Nowadays there is an estimated partial response to UDCA in approximately 30 to 50% of patients with PBC. There is a need for new second line management strategies for patients without a biochemical response to UDCA. The addition of bezafibrate to the treatment of PBC patients with partial biochemical response to UDCA, will increase the biochemical response and improve the long term prognosis? And if so, which are the efficacy and security of bezafibrate in PBC patients without biochemical response?