Active clinical trials for "Crohn Disease"

Purpose: Inflammatory bowel disease patients undergoing treatment with varying biologic agents will be evaluated for incidences of paradoxical immune reactions, the risk factors associated with those paradoxical immune reactions, and whether the paradoxical immune reactions and their associated risk factors differ based on formulation of biologic agent. Participants: All adults (≥18 year) with confirmed IBD on a biologic agent or with plans to initiate treatment in 1 month Procedures (methods): Subjects undergoing treatment with a biologic agent will be followed indefinitely for paradoxical immune reactions. Data will be collected at baseline as well as serum and plasma for banking. Subjects will be followed at 6 month intervals either via email, telephone interviews or at the time of clinic follow-up visits. In the event of a de-novo paradoxical reaction, specific information will be collected from sites in an event capture form, with data abstracted from routine clinical care for the paradoxical reaction. Subjects will continue to be followed every 3 months after the event via email, telephone contact to determine whether resolution and/or recurrence occurred, and to determine any changes in medical therapy. Serum and plasma will be re-collected at the time of first event for comparison to baseline samples and to samples from controls (those on biologics without study documented paradoxical immune reactions). At resolution of the event, patient will return to 6 month follow up schedule. Subjects can discontinue and/or fail a particular biologic treatment; therefore they will also be followed for paradoxical immune reactions, on any new biologic treatment they undergo while in the study.

This is a post-marketing observational study of patients with Inflammatory Bowel Disease (specifically, Crohn's disease or Ulcerative Colitis) who have been prescribed CT-P13 (infliximab) or Remicade (infliximab) for treatment. CT-P13 (brand names Inflectra and Remsima) is a biosimilar medicine to Remicade, meaning it is a biologic medicine that contains the same active substance as Remicade (infliximab). The key study objectives are as follows: To characterize the population and drug utilization patterns of patients treated with CT-P13 for Crohn's Disease (CD) or Ulcerative Colitis (UC) in the context of standard of care Remicade To explore the long-term safety profile of CT-P13 in the treatment of patients with CD or UC in the context of standard of care Remicade To assess the effectiveness of CT-P13 in the treatment of patients with CD or UC in the context of standard of care Remicade

The main purpose of this study is to assess ustekinumab's ability to induce clinical response and remission ("effectiveness") at Week 16 and remission at Week 52 and Week 104 in participants with Crohn's disease (CD). Response and remission will be assessed using clinical parameters. Retention rate at week 52 and 104 will also be studied.

Inflammatory Bowel Diseases (IBD) is a group of relapsing and remitting gut inflammatory conditions acquired due to genetic susceptibility and/or environmental triggers. The disease manifestations are being increasingly seen in young children and the life-long debilitation has a severe effect on quality of life. Limited evidence suggests, although rare, in some young IBD individuals vascular complications may ensue. This leads to increased risk of vascular problems such as thrombosis, arterial disease and stroke. In the present project we aim to study and highlight potential vascular changes in young Inflammatory Bowel Disease (IBD) patients and compare these changes with age and gender matched controls. Vasculature will be measured in multiple ways including blood analysis in the laboratory and non-invasive, physiological measures of arterial health (e.g. ultrasound arterial scan). Our overall goal is to identify biomarkers indicative of increased risk of vascular dysfunction as this will open new avenues for early therapeutic intervention.

For public health purposes disability is becoming increasingly important as an outcome measure. Despite this, there are few data on the effectiveness of adalimumab on disability outcomes in patients with immune-mediated inflammatory diseases (IMIDs), particularly in the Phase IV setting. There are even less data available in New Zealand, which did not have the opportunity to participate to a major extent in large, multinational, Phase III pivotal studies of adalimumab in IMIDs. The World Health Organisation Disability Assessment Schedule (WHODAS) 2.0 is a simple, validated, free and easy-to-use generic assessment instrument for health and disability. It is applicable across cultures, in all adult populations. It is a responsive measure that can show what difference a treatment makes. Results from study of effect of adalimumab on WHODAS scores and other patient-reported outcomes (PROs) of work activity and well-being will be of interest to a variety of stakeholders in the healthcare system including patients, healthcare practitioners and payers.

Mucosal immunology during helminth infection

Food intake is mainly controlled through interactions between the gut and brain (the homeostatic control) and through our environment, with food exposure, mood and past experiences (the hedonic control) playing a major role. The link between the gut and the brain is mainly controlled through enteroendocrine cells (EC). These cells in the bowel sense nutrients in the food and link with the brain to control how much we eat. They make a number of hormones that link with the brain to control one's eating habits. Crohn's disease (CD) is an inflammatory disease of the bowel which can present with a number of symptoms including weight loss and loss of appetite. We thought some time ago that an increase in the number and function of these EC could play a central role. Since then we have carried out work which has shown that in CD these EC increase in number and produce more hormones after a meal. This finding could have a negative effect on food intake. This would be one explanation to the symptoms so commonly experienced by these patients. In CD we thus feel that there might be an imbalance in the appetite control. We expect an increasingly sensitive gut to food intake and a subdued mood and perception to food reward and that this imbalance will lead to a decrease in food reward and consequently a decrease in food intake. This study will be carried out using Healthy Volunteers and CD patients. We plan to measure food intake though telephone interviews and plan to analyse eating behaviour through 5 questionnaires.This study will help us to improve our understanding of what it is that controls food intake. This will be particularly important to patients with CD who routinely lose weight and appetite.

Vedolizumab is a new medication being used for the treatment of Crohn's disease and Ulcerative colitis. It works by blocking specific white blood cells (alpha 4-beta7 lymphocytes) from migrating to areas of inflammation in the gastrointestinal tract. Previous studies have shown that patients who have previous exposure to another type of medication for Crohn's disease and Ulcerative colitis (anti-TNF medications) do not respond to vedolizumab as well as those who have never been exposed. This study will investigate biologic markers in the blood and tissue the help identify possible reasons for this difference.

The inflammatory tumor micro-environment is a consequence and a driver of tumorogenesis. On one hand it promotes antitumor immune responses and on the other hand it favors development and progression of cancerous lesions. Factors regulating the complex interplay between epithelial and immune cells are still poorly characterized. Extracellular ATP (eATP) acting on the purinergic P2X7 receptors (P2RX7) has recently emerged as a key signaling pathway in the immune response. Recent data have revealed the crucial role of P2RX7-NLRP3-Caspase-1 for priming dendritic cells (DC) within the tumor microenvironment upon treatment with certain types of chemotherapy drugs. Despite this important discovery, no previous study has so far investigated the global in vivo effect of P2RX7 modulation in inflammation-induced carcinogenesis of mucosal tissues. Our consortium, endowed by a long standing experience in the field of mucosal immunology, inflammation and signaling, already demonstrated that the P2RX7 is differentially expressed in the mucosa of patients with active and quiescent inflammatory bowel disease (IBD), where eATP is present at very high concentration, and that P2RX7 controls an amplification loop of the inflammatory response (Cesaro et al., 2010). Furthermore, we uncovered that P2RX7 controls homeostasis, survival and function of regulatory T cells (Hubert et al., 2010). In addition, our recent demonstration that P2RX7 deficiency lowered mucosal inflammation but unexpectedly enhanced tumor formation in vivo warrants additional efforts to explore the molecular and cellular mechanisms accounting for this effect and suggest that enhancing P2RX7 function may have an anti-tumor therapeutic effect. These observations emphasize the tumor suppressor role of P2X7 receptor, warrant further investigation to better understand the molecular mechanisms responsible for this anti-tumor effect and suggest that enhancing the function of P2X7R could have a therapeutic effect significant antitumor. Our main objectives is to explore the role of P2RX7 in healthy, inflammatory and cancerous colonic mucosa. For this we will map the expression of the protein P2RX7 and realize genotype of P2RX7 forms in inflammatory diseases and cancer of the colon.

The objective of this observational study was to assess changes in fecal calprotectin levels and its suitability as a monitoring tool in participants with moderate-to-severe Crohn's Disease who were treated with adalimumab.