Active clinical trials for "Pancreatitis"

Background: Acute pancreatitis is characterized by a high mortality rate (10%-15%), and a remarkably unpredictable clinical course. Approximately 50% of deaths in acute pancreatitis occur early-within the first 14 days-and early mortality is attributable to sequelae of a severe systemic inflammatory response syndrome (SIRS), which is associated with multi-organ dysfunction syndrome (MODS) that can escalate to renal failure, respiratory failure, and death. Significant improvements in acute pancreatitis mortality will demand innovative approaches to counteract early organ failure. A series of destructive cellular processes begins within minutes of initial pancreatic injury, and the ensuing inflammatory cascade is compounded by disease sequelae including edema, ischemia, and tissue necrosis. Early interventions to reduce inflammation within the first 36 hours have been shown to have significant effects in minimizing progressive organ dysfunction. Hypothermia is clinically employed to combat cellular injury and systemic responses following ischemia-reperfusion, and is been studied as a mechanism of acute inflammatory inhibition in processes including cardiogenic shock, lung injury, local intestinal injury, and reperfusion injuries to the lung, liver, and endothelium. In numerous studies, effective immunomodulations have been observed including reduction of pro-inflammatory cytokines (TNF-α, IL-6), stimulation of anti-inflammatory cytokines (IL-10), inhibition of pro-apoptotic JNK signaling, reduction of systemic oxidative stress, and inhibition of neutrophils, monocytes, and monocyte-derived macrophages. Most saliently, in the caerulein model of murine acute pancreatitis, therapeutic hypothermia has been shown to reduce serum IL-1, IL-6, and TNF-α, increased serum IL-10, decrease serum amylase and lipase, lower the histological grade of pancreatic injury as compared to normothermic mice, and significant survival benefit. Although therapeutic hypothermia is actively employed in the treatment of traumatic brain injury, neonatal asphyxia, spinal cord injury, and cardiac arrest, no studies have yet been made of its application to acute pancreatitis. Hypothesis: Patients treated with therapeutic hypothermia (32-34°C) will sustain reduced organ-specific injury in acute pancreatitis. Proposal: In a Phase IIa pilot clinical trial, we will examine the effects of therapeutic hypothermia on organ-specific outcomes during the early stage of acute pancreatitis. We will recruit five patients aged 18 to 80 receiving medically-necessitated ventilator support under ICU monitoring with core temperatures ≥36°C and severe acute pancreatitis defined as either a Ranson Score ≥7, a CT indicating ≥50% pancreatic necrosis, or a significant deterioration in clinical status including dysfunction of two or more organ systems (defined by ACCP/SCCM Organ Failure Guidelines, Chest 2009). All patients will receive current standard management for severe acute pancreatitis and a standardized protocol for application of therapeutic hypothermia and rewarming. Our primary endpoints are organ-specific cardiovascular, respiratory, hematological, renal, and metabolic dysfunction as measured at 28 days. Logistic Organ Dysfunction Scores (LOD) will be compared before and after therapeutic hypothermia, establishing day 4 versus day 1 changes in LOD. Secondary endpoints include D-dimer, IL-6, C-reactive protein, APACHE II scores on day 1 and day 4, inpatient and ICU length-of-stay, infection, mortality, and hypothermia-associated side effects including cardiac arrhythmia, electrolyte imbalance, hyperglycemia, major bleeding, and acute pancreatitis. We believe that such a study will supply preliminary answers to our chief research questions: does therapeutic hypothermia reduce morbidity as assessed by organ-specific outcomes, does therapeutic hypothermia attenuate the steep rise in inflammation observed in severe acute pancreatitis, and does therapeutic hypothermia shorten the clinical course for these patients.

Post-ERCP pancreatitis can be a serious complication to ERCP. Two studies have shown a promising preventive effect of glyceryl nitrate. This study should provide a final answer to the clinical question: Does glyceryl nitrate prevent post-ERCP pancreatitis? The study is a prospective, randomized, double blind, placebo-controlled multicenter trial. The investigators intend to include 1600 patients from Norway, Sweden, Denmark, and France. The patients will receive either placebo or a glyceryl nitrate patch (15 mg/24 hours). Follow-up will occur after 7 days. The primary outcome measure will be post-ERCP pancreatitis, and secondary outcome measures will be mild, moderate and severe pancreatitis; post procedure pancreatitis-related mortality; and adverse events.

The goal of this research study is to learn more about the pancreas. The investigators want to use Magnetic Resonance Cholangiopancreatography (MRCP) to learn more about the size of a normal pancreas. MRCP is a special kind of MRI exam that produces detailed images of the pancreas. The investigators also want to figure out how much fluid the pancreas releases in response to secretin. Secretin is a chemical in the body that causes the pancreas to release fluid that helps with digestion. Secretin is used during the MRCP (MR-PFT) to help identify dysfunction of the pancreas. MR elastography (MRE) will be used to measure how hard the pancreas is. MRE is a special kind of MRI that uses vibrations to image tissue.

This randomized phase II trial studies how well simvastatin works in reducing pancreatitis (the inflammation of the pancreas) in patients with pancreatitis that occurs more than once (recurrent), has worsened quickly (acute), or has persisted or progressed over a long period of time (chronic). Simvastatin may decrease the inflammation of the pancreas by modulating the immune response responsible for inflammation. It is not yet known if simvastatin may be an effective treatment for pancreatitis.

Aggressive hydration with lactated Ringer's solution (LRS) has been shown in a preliminary research to reduce the incidence of post-endoscopic retrograde cholangiopancreatography (ERCP) pancreatitis. This randomized, controlled trial was designed to assess the effect of peri-procedural aggressive intravenous hydration with LRS on the incidence of post ERCP pancreatitis.

Acute pancreatitis is the most common and feared complication of ERCP, occurring after 1% to 30% of procedures. Since 2012, a multicenter RCT was published in NEJM, indomethacin use in high risk patients was considered a "standard" method to prevent PEP. However, the risk factors of PEP is not fully clear. Rectal indomethacin before ERCP for all patients, not just for selected high-risk patients, may preventing PEP maximum. The purpose of this study is to determine whether routine using of rectal indomethacin is more effective than the conditional strategy.

For 40 years, the post-ERCP (endoscopic retrograde cholangiopancreatography) pancreatitis has been the most frequent adverse effect of endoscopic transpapillary interventions. We sought to determine the efficacy of thoracic epidural analgesia for the prevention of post-ERCP pancreatitis. Between 2008 and 2013, a randomized study of the results of endoscopic treatment of 491 patients was conducted. The first group of patients (N=247) received thoracic epidural analgesia (TEA) during ERCP procedures, the patients of the second group (N=244) received a narcotic analgesic. To detect statistically significant differences between research groups adjusted odds ratios (OR) and their 95% confidence interval (CI) were calculated.

It is now established that indomethacin, a non-steroidal anti-inflammatory drug, at a dose of 100 mg, is effective in reducing the frequency and severity of pancreatitis (inflammation of the pancreas) after endoscopic retrograde cholangiopancreatography (ERCP) in high risk patients. However, the optimal dose required is not known. The purpose of this study is to determine whether a dose of 200 mg, administered as rectal suppositories, is more effective than the standard dose of 100 mg. An ERCP procedure is a scope procedure where a lighted tube with a camera is passed down the patient's throat and allows for evaluation of the bile duct and/or pancreatic duct. The most common side effect of this procedure is post-ERCP pancreatitis, or swelling of the pancreas. Some patients are at higher risk for this complication than others. Our hypothesis is to compare the efficacy of these two dose regimens (100 mg vs 200 mg) of prophylactic rectally-administered indomethacin on the frequency and severity of post-ERCP pancreatitis in high-risk patients.

The purpose of this study is to evaluate the safety and effectiveness of RG1068 (synthetic human secretin) with MRCP in subjects with abnormalities of the pancreas.

Post-ERCP pancreatitis is a well-known and sometimes life-threatening complication of ERCP. Both LR and rectal indomethacin have shown benefit in preventing post-ERCP pancreatitis. Despite this, no study to date has evaluated both of these measures for preventing post-ERCP pancreatitis. It is our hope to evaluate the combination of these two modalities for preventing post-ERCP pancreatitis compared with either modality alone.