Active clinical trials for "Fibrosis"

The aim of this study is to determine the relationship between diets of children with cystic fibrosis and glycemic responses and some inflammatory markers.

Totals of 400 chronic hepatitis B or non-alcoholic fatty liver disease (NAFLD) patients with or without cirrhosis will be enrolled. Patients' clinical characteristics, including alanine aminotransferase, aspartic aminotransferase, total bilirubin, direct bilirubin, indirect bilirubin, triglyceride and total cholesterol, hepatitis B surface antigen, steatosis, and liver stiffness measurement will be collected. The consistence of liver fibrosis and steatosis assessment between Hepatus and FibroScan will be evaluated in this study.

Cystic fibrosis is a multi-organ disease. It most often results from a genetic mutation, the delta F508 mutation, which prevents the expression of the CFTR 'régulateur de conductance transmembranaire de la fibrose kystique) protein. If the poor prognosis of the disease is correlated to the pulmonary damage, we observe, at the naso-sinus level, a significant functional impact, with chronic rhino-sinusal damage that can alter the quality of life of patients. In addition to this functional impact, some studies suggest that these chronic naso-sinus attacks are involved in the creation of a bacterial reservoir that is secondarily responsible for pulmonary colonization and therefore partly responsible for the poor prognosis of the disease. The clinical and paraclinical examinations can be used to determine the extent of these disorders. Their functional impact can be assessed using quality of life questionnaires such as the SN-5 scale. Treatment with CFTR modulators in patients with mutations compatible with the treatment seems to transform their vital prognosis. The scientific rationale of this treatment consists in restoring the activity of the CFTR protein, allowing the recovery of the hydro-electrolytic balance of the mucous secretions, and thus reducing the viscosity of the biological fluids. The various studies carried out all prove a dramatic improvement in pulmonary parameters under treatment, with very limited toxicity. A marketing authorization for this treatment has been issued on the European market for patients over 18 years of age in 2020, for children over 12 years of age in 2021, and will soon be issued for children aged between 6 and 11 years. Since the pathophysiology of pulmonary and nasosinus involvement are similar, and since this treatment will be marketed for children between 6 and 11 years of age, we expect an improvement in rhino-sinus symptomatology. To date, clinical studies have focused primarily on pulmonary outcomes. There are only few publications dealing with the evolution of nasosinus symptomatology under treatment, and none concerning the pediatric population. The aim of our study is to evaluate the evolution of naso-sinusal symptomatology under treatment with CFTR modulators in children aged 6 to 11 years. This will allow us to confirm or deny the interest of these treatments in the extra-pulmonary manifestations of the disease.

The aims of this study will be to identify the clinical characteristics, the management and the outcomes of acute kidney injury in patients with cirrhosis worldwide. Specific aims: To establish the severity of AKI across different regions To identify precipitants of AKI across different centers To identify the phenotypes of AKI across different centers To evaluate differences in the management of AKI across different centers and their impact on clinical outcomes To assess outcomes of acute kidney injury (resolution of AKI, in-hospital mortality, 28-day mortality, 90-day mortality)

Cochlear fibrosis development can compromise the success and the outcomes of the cochlear implantation (CI) thus affecting the quality of life of the implanted patient. Correlating the results of the Transimpedance Matrix (TIM) measurements to the implant electrode location determined by the Cone Beam Computer Tomography (CBCT), this study aims to identify a range of TIM profiles within the implanted population, certain profiles suggesting the growth of the fibrosis tissue in cochlea

Portal hypertension contributed to the main complications of liver cirrhosis. Currently, hepatic venous pressure gradient (HVPG) was the reference standard for evaluating portal pressure in patients with cirrhosis. However, the practice of HVPG is limited to require the extensive experience and highly specialized centers. In recent years, non-invasive methods were proposed to predict the degree of cirrhotic portal hypertension. Of them, liver stiffness measured by transient elastography had shown good performance for predicting clinically significant portal hypertension. However, liver stiffness only has a good correlation with portal pressure in the early stage of portal hypertension (HVPG<10 mmHg), because liver fibrosis is the main cause of portal hypertension in this period. In the stage of clinically significant portal hypertension (CSPH) (HVPG≥10 mmHg), increased portal vein inflow due to splanchnic vasodilation and hyperdynamic circulation, spleen stiffness may have a better correlation with HVPG than that of liver stiffness. Several studies have explored the combination of liver stiffness, platelet count and spleen stiffness for varices screening. However, there are few studies to report the above parameters for assessing CSPH and unneeded HVPG avoiding. Since the spleen was stiffer than the liver, the current vibration-controlled transient elastography examination is dedicated to the liver, rather than the spleen. Very recently, a novel spleen-dedicated stiffness measured by transient elastography was proposed. The prospective, multicenter study aims to add spleen stiffness as a supplementary parameter to establish new criteria for identify CSPH in patients with compensated cirrhosis, with a dedicated probe on transient elastography equipment to assess spleen stiffness and liver stiffness, and further develop a novel model based on spleen stiffness for predicting the liver decompensation in patients with compensated cirrhosis.

In this research study the investigators want to learn more about how well the investigators can visualize scar tissue in the heart by MRI. In patients with congenital heart disease who need a procedure in the electrophysiology laboratory, how the MRI findings match the findings in the electrophysiology laboratory is not known. This study works to answer these questions. Participants will undergo a cardiac MRI as part of the routine clinical care that was ordered by their doctors and additional imaging by cardiac MRI will be performed.

The investigators use machine learning capabilities on massive electronic health records for the purpose of developing a model that prioritizes individuals at high risk of progressing to liver cirrhosis, and validating it with participants that the model found to be at high risk. constructing and validating a reliable model, with sufficient accuracy to justify further and expensive means of detection, will enable treating patients with damaged liver at an early enough stage to allow improvement of the liver condition.

Cirrhosis, as the end stage of most chronic liver diseases, is an important clinical landmark portending high risk of death. Early identification and accurate prognostic scores is critical issue to improve survival rate. Loss of muscle mass and other body features, which can be determined from CT, have been associated with mortality in cirrhosis or hepatic carcinoma. In this study, we sought to investigate serial changes of CT imaging parameters, such as the skeletal muscle index (SMI), liver volume, adiposity density and so forth, to develop a new prognostic model for long-term motality in patients with liver cirrhosis. The final predictive model was developed under the Cox regression framework with MELD, Child-Pugh score, baseline and serial changes of CT imaging parameters. The discrimination of the new risk score was assessed by the overall C index.

Background: - Noncirrhotic Portal Hypertension (NCPH) is caused by liver diseases that increase pressure in the blood vessels of the liver. It seems to start slowly and not have many warning signs. Many people may not even know that they have a liver disease. There are no specific treatments for NCPH. Objectives: - To learn more about how NCPH develops over time. Eligibility: - People age 12 and older who have NCPH or are at risk for getting it. In the past year, they cannot have had other types of liver disease that typically result in cirrhosis, liver cancer, or active substance abuse. Design: Participants will have 2 screening visits. Visit 1: to see if they have or may develop NCPH. Medical history Physical exam Urine and stool studies Abdominal ultrasound Fibroscan. Sound waves measure liver stiffness. <TAB>- Visit 2: Blood tests Abdominal MRI Echocardiogram Questionnaire Liver blood vessel pressure (hepatic venous portal gradient (HVPG)) measurement. This is done with a small tube inserted in a neck vein. They may have a liver biopsy. All participants will visit the clinic every 6 months for a history, physical exam, and blood tests. They will also repeat some of the screening tests yearly. Participants with NCPH will also have: Upper endoscopy test. A tube inserted in the mouth goes through the esophagus and stomach. At least every 2 years: Esophagogastroduodenoscopy. At least every 4 years: testing including HVPG measurements and liver biopsy. Participants without NCPH will also have: Liver biopsy and HVPG measurements to see if they have NCPH. Every 2 years: abdominal MRI and stool studies. The study will last indefinitely.