View clinical trials related to Pancreatitis.
Filter by:Azathioprine (AZA) and its metabolite 6-mercaptopurine (6-MP) were developed over 50 years ago by Gertrude Elion and George Hitchings and were initially used clinically in the management of childhood leukemia and organ transplantation. The first case report of 6-MP use in inflammatory bowel disease (IBD) was from 1962 , and since then the use of thiopurines has been well established in the management of moderate to severe IBD. Thiopurines offer an inexpensive and effective treatment option for maintenance of remission of IBD in comparison to biological agents which may be 30 times more expensive . Although 50-60% of IBD patients respond to thiopurines, a significant proportion of patients will not tolerate them due to various adverse effects . The adverse effects of thiopurines may be dose related, patient related or idiosyncratic. The immunosuppressive effects of thiopurines also increase the rates of opportunistic infections. Thiopurines are also associated with a higher rate of malignancies, particularly a malignant Burkitt-like lymphoma, related to Epstein-Barr virus infection . Other adverse effects of thiopurine relate to allergic phenomenon. An idiosyncratic adverse effect of thiopurine use is acute pancreatitis (AP). Acute inflammation of the pancreas defined by INSPPIRE criteria: requiring 2 of: 1. Abdominal pain compatible with AP 2. Serum amylase and/or lipase ≥ 3 times upper limits of normal 3. Imaging findings of AP Drug induced AP is the assumed diagnosis when no other cause of AP can be found, the patient is taking a drug known to be associated with AP, and symptoms resolve after drug discontinuation. If pancreatitis re-occurs on re-exposure, the drug is definitely considered the cause. While drugs are considered a rare cause of AP and most cases are mild and self limited , there is an 8 fold higher risk of AP in IBD patients treated with AZA . Thiopurine induced AP is usually detected within 4 weeks of starting treatment. However in the case of thiopurine induced AP, there has been no clear understanding of the mechanism. Thiopurine induced AP is generally considered an indication to cease thiopurine therapy, due to the assumed risk of recurrence of AP on reintroduction. There exists several case reports and anecdotal evidence that reintroducing thiopurines following an assumed thiopurine associated AP can be well tolerated. The investigators hypothesize that AZA and/or 6-MP can be safely reintroduced in the management of IBD patients following thiopurine-induced pancreatitis. If in the past the patients were treated with AZA, they will now be commenced on 6-MP, and if in the past they were treated with 6-MP, they will be commenced on AZA.
This investigation develops an online, patient self-assessment system, called "CarePrep" to support the care and clinical research of patients with chronic pancreatic disease and chronic pancreatic pain. This web-based assessment presents patients with questions that address medical, psychological, social, behavioral, and quality-of-life issues that are relevant to pancreatic disease. Patients will be given the opportunity to enter and track their symptoms over the Internet from home or clinic. The system is also designed to gather clues to identify neuropathic pain, which occurs when the nervous system fails to properly regulate pain signals. Any of these factors can contribute to chronic pain and may point the way to more effective treatment. The broad objective of this study is to extend CarePrep to cover a full range of topics that are relevant to chronic pancreatic disease. The study team will refine this content based on the system's accuracy in real clinical settings and direct efforts to maximize its feasibility.
This study is testing whether the addition of a noninvasive form of brain stimulation called transcranial direct current stimulation (tDCS) when combined with meditation helps decrease the abdominal pain in patients with chronic pancreatitis. The device involved in this study, transcranial direct current stimulation (tDCS) is investigational. This means that the study device is still being tested in research studies and is not approved by the Food and Drug Administration [FDA].
BACKGROUND: Auto immune pancreatitis (AIP), a benign pancreatic disease has certain morphological forms which mimics pancreatic malignancy in radiological appearance. There is no singe diagnostic test which can accurately differentiate these two conditions. In the past, AIP accounted for up to 27% of Whipple resections performed for suspected adenocarcinoma. AIMS: To evaluate the efficacy of Secretin assisted Magnetic resonance cholangio pancreatography (MRCP) in differentiating AIP and pancreatic malignancy. METHODS: 100 patients suspected with AIP will be consented to participate in the study to undergo secretin MRCP in addition to their other standard investigations. Patients will be categorized as those with AIP and with pancreatic malignancy based on these results and will be followed. Follow up will eventually give the true diagnosis when patients with pancreatic malignancy undergo pancreatic surgery and their pancreatic tissue is examined by histopathologist. AIP patients will undergo steroid trial which will give the true diagnosis. The preliminary diagnosis results based on standard investigations with and without inclusion of secretin MRCP will be compared to the true diagnosis.
The primary objective for this study is to compare the image quality of two endoscopic ultrasound (EUS) processors used for imaging of the pancreas. Processor images are used to make a correct clinical diagnosis and higher quality imaging is related to more accurate results. Patient care may be improved due to the information collected as part of this study. The quality of imaging is of utmost importance for diagnosing early neoplasms in the pancreas and diseases such as chronic pancreatitis. Image quality is dictated by two factors: image resolution and depth of penetration. Good imaging enables diagnosis of early stage disease and thereby facilitates early treatment.
Acute pancreatitis (AP) is one of the most common diseases in routine clinical practice of surgeons and gastroenterologists throughout the world. The high rate of pain relapse after oral refeeding contributes to high consumption of healthcare resources and prolonged hospital stay in AP patients. The data from the pilot MIMOSA trial suggest that early administration of nasogastric tube feeding may prevent pain relapse after oral refeeding in AP. The potential beneficial effects of enteral tube feeding include induction of postprandial gastrointestinal motility and improving the tolerance of oral refeeding. This may reduce the risk of pain relapse, thereby shortening length of hospital stay and reducing cost of treatment. The primary endpoint of the ORION trial will be the incidence of oral food intolerance. All eligible AP patients will be randomly allocated to either the Early Nasogastric Tube (ENT) group or Conventional Nutritional Management group (CNM) at 24h of hospital admission.
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.
The disruption of the pancreatic duct seems to be a major cause pseudocyst formation and persistence in patients suffering from acute/chronic pancreatitis. No prospective randomized studies have been conducted on the influence of pancreatic duct stenting for the patients' benefits and recurrence rates. The aim fo this study is therefore to evaluate prospectively in a randomized, controlled fashion in patients wit pancreatic pseudocysts, wether pancreatic duct stenting of a disrupted pancreatic duct is beneficial in terms of quicker clinical recovery and avoidance of recurrence of pancreatic pseudocysts.
This pilot trial will evaluate the following in patients with acute pancreatitis: 1. Safety profile of early treatment with intravenous dexamethasone 2. Impact of dexamethasone on systemic inflammation in patients with acute pancreatitis 3. Provide preliminary data on potential impact of early treatment with steroids on clinical outcomes
The purpose of the study is to determine if adding Benadryl improves sedation for patients scheduled to undergo ERCP or EUS procedures.