View clinical trials related to Calprotectin.
Filter by:Crohn's disease (CD) is a chronic inflammatory bowel disease (IBD) that can dramatically affect the quality of life of patients. Due to its transmural nature (involvement of the entire thickness of the intestinal wall), it naturally progresses to intestinal destruction (stenosis, fistula) which requires intestinal resection in approximately half of patients during their follow-up. The long-term goal for patients is to maintain a normal life, that is, without symptoms and without intestinal destruction. For this, the short and medium term therapeutic objectives have evolved in recent years. Clinical remission is not a sufficient goal since it has failed to alter the natural history of the disease. The current objective to be achieved is the combination of clinical remission and endoscopic mucosal healing since it is associated with a reduced risk of progression (reappearance of symptoms, hospitalization, intestinal resection). Fecal calprotectin, better accepted than colonoscopy, is a non-invasive biomarker of endoscopic inflammatory activity in CD. The CALM study recently showed that close follow-up with clinical and biological evaluation (assays of CRP and fecal calprotectin), called "tight control", associated with therapeutic intensification in the absence of clinical or biological remission, was associated with a better rate of endoscopic mucosal healing at 1 year than follow-up based solely on symptoms. Thus, the "CALM" strategy is considered to be the current benchmark. Transmural healing evaluated by MRI is also a promising objective associated with a reduced risk of progression (reappearance of symptoms, hospitalization, bowel resection). In addition, it could prevent intestinal destruction. A recent study by our team suggested that calprotectin (mucosal assessment) and MRI (transmural assessment) may be complementary and be a better therapeutic goal. We hypothesize that a "CALM + MRI" strategy concomitantly targeting transmural healing would be superior to the "CALM" strategy alone in maintaining clinical remission without corticosteroids in patients with CD treated with biotherapies.
In the 21st century, the incidence of inflammatory bowel disease (IBD) globally increases. Higher incidence of IBD development may implicate that environmental factors played essential roles in IBD pathogenesis. One of the environmental factors is a westernized diet that contains a high amount of animal protein and a low amount of dietary fiber. This kind of diet can lead to gut microbial dysbiosis and increase susceptibility to IBD. A microbial dysbiosis pattern in IBD is a decrease in microbial diversity and the inversed ratio of local protective and pathologic bacteria. High animal protein was associated with an increased risk of IBD and increased risk of disease relapse meanwhile dietary fiber was associated with IBD risk reduction. A semi-vegetarian diet is a diet with high fiber and low red meat and processed food that may reduce inflammatory activity in IBD. The study in the semi-vegetarian diet in IBD activity is still limited. This study aimed to evaluate a semi-vegetarian diet's effect in maintaining IBD remission in disease quiescence patients.
Nosocomial diarrhea is a common problem.There are multiple ethiologies of nosocomial diarrhea in which can be divided into inflammatory and non inflammatory diarrhea. Fecal calprotectin is a good marker to identify inflammatory diarrhea in outpatient setting; for example, differentiating inflammatory bowel disease and irritable bowel syndrome. Its performance in inpatient setting has not been well established. This study aim to determine the efficacy of fecal calprotectin in distinguishing inflammatory nosocomial diarrhea from non-inflammatory nosocomial diarrhea.
Infants born with heart problems are at risk of developing gut disease due to reduced blood flow to the intestines which can result in poor weight gain, surgery and even death. At present, doctors are often unaware of any gut problems until clinical symptoms present (poor feed tolerance, blood stained stools or bloated stomach) which is often too late to prevent gut damage. Earlier diagnosis of gut disease may now be possible; calprotectin is produced when the gut is inflamed and can be found in faeces and blood. Calprotectin levels have been shown to be a reliable marker in diagnosing gut disease in premature infants. To date, calprotectin levels have not been monitored in infants with cardiac defects, who like premature infants are at high risk of gut disease but the cause of gut disease is different to that seen in premature infants and therefore requires specific monitoring. This study will implement a high risk feeding protocol which has been adapted from current feeding practices from the United States; the aim being to promote weight gain without increasing the risk of gut inflammation. Furthermore, the study will validate whether faecal calprotectin is a useful non-invasive marker in identifying gut disease in infants with cardiac defects. Currently, infants are diagnosed with necrotising enterocolitis by an abdominal X-ray (current 'Gold Standard'); infants who have a positive diagnosis will have faecal calprotectin levels cross-checked. From this data, cut-off values will be established which will provide data to diagnose necrotising enterocolitis eliminating the need for X-rays (radiation). Secondly, faecal calprotectin levels will be measured at strategic time points (longitudinal data) linked to increased risk of gut damage (following cardiac surgery and feeding) which will then be cross-checked against infants that developed NEC to identify whether high risk infants had raised calprotectin levels earlier.
For the main goal - the accuracy of calprotectin for the diagnosis of IBD - calprotectin levels will be compared between patients with and without a diagnosis of IBD and the sensitivity, specificity and accuracy will be determined. For the secondary aim - the correlation between calprotectin levels and disease activity - in patients with IBD selected from this cohort, we will determine the association between calprotectin levels and clinical IBD score, serological markers (WBC, Hgb, Platelets, ESR, CRP, Albumin), endoscopic (disease score, pathological activity) and radiological features (bowel wall thickening, enhancement, edema, mesenteric inflammation).