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| Name | Class |
|---|---|
| National University of Singapore | OTHER |
| National Medical Research Council (NMRC), Singapore | OTHER_GOV |
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Acute pancreatitis refers to inflammation of the pancreas and is associated with sudden onset of severe abdominal pain, often accompanied by transient systemic manifestations, including fever. In the majority of cases, the inflammatory process is self limiting and patient recovers uneventfully; however, in about 20% to 30% of the cases, a protracted clinical course ensues and the disease may progress to a severe necrotizing form, often triggering a systemic inflammatory response syndrome during which time, acute respiratory distress syndrome, renal failure, shock, and disseminated intravascular coagulation may occur. In the worst sequelae, multiple organ dysfunctions may follow and death supervene. The clinical outcome of patients suffering from severe acute pancreatitis depends to a great extent on the early diagnosis and prediction of severity and timely therapeutic intervention to prevent local and systemic complications. However, the course of the disease is often difficult to predict from the outset. Currently, there is still no single clinical or laboratory test that can be considered the "gold standard" for diagnosis and/or assessment of severity of acute pancreatitis. For a disease that may progress rapidly without apparent sign, the ideal marker for the prediction of disease severity in a patient would be one that is measurable rapidly and easily, besides being able to fulfill all the other criteria required of a good biological marker. To identify such a potential marker for acute pancreatitis requires understanding of the pathophysiological process underlying the rapid progression of a fulminant course of the disease. Although much remains to be elucidated, recent studies in animals have suggested that inflammatory mediators substance P and hydrogen sulfide may play critical roles. This study will evaluate if inflammatory mediators substance P and hydrogen sulfide are upregulated early on in the disease process, and if the levels of their elevation predict disease severity.
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| Label | Type | Description | Intervention Names |
|---|---|---|---|
| Acute Pancreatitis Patients | Patients presenting with clinical features compatible with acute pancreatitis | ||
| Control | Preoperative patients going for elective cholecystectomy |
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| Measure | Description | Time Frame |
|---|---|---|
| Levels of substance P and hydrogen sulfide in blood measured 6-hourly over a time course of 3 days | On admission to hospital, blood sampling will be done every 6 hours for 3 days |
| Measure | Description | Time Frame |
|---|---|---|
| Disease severity index derived from: (i) Ranson score; (ii) Acute Physiology and Chronic Health Evaluation (APACHE) II scores; (iv) Glasgow and (v) Multi-Organ System Failure (MOSF) Score | Within 3 days of hospital admission |
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Inclusion Criteria:
The patient should fulfill all of the following criteria:
Exclusion Criteria:
The patient should not present any of the following criteria:
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Patients with clinical presentation suggestive of acute pancreatitis
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| Name | Affiliation | Role |
|---|---|---|
| Khek Yu Ho, MD | National University Hospital, Singapore | Principal Investigator |
| Facility | Status | City | State | ZIP | Country | Contacts |
|---|---|---|---|---|---|---|
| National University Hospital | Singapore | 119074 | Singapore |
| PubMed Identifier | Type | Citation | Retractions |
|---|---|---|---|
| 17488480 | Background | Tamizhselvi R, Moore PK, Bhatia M. Hydrogen sulfide acts as a mediator of inflammation in acute pancreatitis: in vitro studies using isolated mouse pancreatic acinar cells. J Cell Mol Med. 2007 Mar-Apr;11(2):315-26. doi: 10.1111/j.1582-4934.2007.00024.x. | |
| 16798781 | Background | Bhatia M, Zhi L, Zhang H, Ng SW, Moore PK. Role of substance P in hydrogen sulfide-induced pulmonary inflammation in mice. Am J Physiol Lung Cell Mol Physiol. 2006 Nov;291(5):L896-904. doi: 10.1152/ajplung.00053.2006. Epub 2006 Jun 23. |
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| ID | Term |
|---|---|
| D010195 | Pancreatitis |
| ID | Term |
|---|---|
| D010182 | Pancreatic Diseases |
| D004066 | Digestive System Diseases |
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Whole blood; Serum
| 16186661 | Background | Hegde A, Bhatia M. Neurogenic inflammation in acute pancreatitis. JOP. 2005 Sep 10;6(5):417-21. |
| 15629143 | Background | Lau HY, Wong FL, Bhatia M. A key role of neurokinin 1 receptors in acute pancreatitis and associated lung injury. Biochem Biophys Res Commun. 2005 Feb 11;327(2):509-15. doi: 10.1016/j.bbrc.2004.12.030. |
| 10821777 | Background | Grady EF, Yoshimi SK, Maa J, Valeroso D, Vartanian RK, Rahim S, Kim EH, Gerard C, Gerard N, Bunnett NW, Kirkwood KS. Substance P mediates inflammatory oedema in acute pancreatitis via activation of the neurokinin-1 receptor in rats and mice. Br J Pharmacol. 2000 Jun;130(3):505-12. doi: 10.1038/sj.bjp.0703343. |
| 9539812 | Background | Bhatia M, Saluja AK, Hofbauer B, Frossard JL, Lee HS, Castagliuolo I, Wang CC, Gerard N, Pothoulakis C, Steer ML. Role of substance P and the neurokinin 1 receptor in acute pancreatitis and pancreatitis-associated lung injury. Proc Natl Acad Sci U S A. 1998 Apr 14;95(8):4760-5. doi: 10.1073/pnas.95.8.4760. |