Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0001339 (acute pancreatitis)
 10,593 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Infectious complications are the leading cause of death in acute pancreatitis. Individual factors of immune defence could be of significance, whether or not a patient develops a severe course with infectious complications. In a prospective 5-year trial including 72 patients, we investigated 29 cellular and humoral markers of the body's defence system for their potential to indicate the severity and course of acute pancreatitis. Complement factors C3 and C4 as well as immunoglobulins IgG, IgM and IgA were normal, in general. Measurable levels of IL-1 alpha, IL-1 beta, IL-2 and sIL-2R could be detected only occasionally. Values of alpha 1-AT, TNF-alpha, TNF alpha-Rp75, neopterin, sICAM-1, IL-8, IL-1RA and sIL-6R did not correlate with a severe course. Due to the high magnitude of increase, CRP, IL-6 and granulocyte elastase were the best indicators of the inflammatory process. Delayed-type hypersensitivity response was the only early predictor of a severe course. It was superior over other cellular markers such as monocyte count or CD4+/CD8+ ratio. In vitro function of polymorphonuclear granulocytes (PMN) was not adequate to the severity of the disease already during the first week of illness. During further course, PMN motility and capacities to produce reactive oxygen species even worsened. The compromized PMN function could explain the frequent development of infectious complications in patients suffering from severe pancreatitis. These results should encourage new concepts of infection prophylaxis using stimulants of cellular defence.
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PMID:[Cellular and humoral functions in acute pancreatitis]. 913

The interleukin 1 (IL-1) gene cluster has been implicated in acute pancreatitis. Penta-allelic and bi-allelic polymorphisms exist in the IL-1RN and IL-1B genes, respectively. The aim of the study was to investigate these polymorphisms in acute pancreatitis. Genotype and allele frequencies were determined in patients (n = 116) and healthy controls (n = 170) using the polymerase chain reaction. PCR products from the IL-1B study were further digested with Taq I restriction endonuclease. Patients were categorised according to aetiology, severity, and organ-failure scores. Allele 1 of the IL-1RN polymorphism was significantly increased in patients compared with controls (72.0 vs. 63.0%; p = 0.029, Pc = 0.029), in severe cases compared with controls (81.9 vs. 63.0%; p = 0.002, Pc = 0.004), in idiopathics compared with controls (82.4 vs. 63.0%; p = 0.002, Pc = 0.006), and in severe cases compared with mild cases (81.9 vs. 67.5%; p = 0.023, Pc = 0.046). Allele 2 was significantly decreased in severe cases compared with controls (18.1 vs. 33.0%; p = 0.013, Pc = 0.026), in idiopathics compared with controls (17.6 vs. 33%; p = 0.013, Pc = 0.039), and in severe cases compared with mild cases (18.1 vs. 32.5%; p = 0.023, Pc = 0.046). No significant differences were found for the Taq I allele or genotype frequencies between controls and patients/subgroups of patients. IL-1RN appears to determine severity of acute pancreatitis and susceptibility to idiopathic acute pancreatitis. No association was found between IL-1B and the disease.
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PMID:Investigation of the interleukin 1 gene cluster and its association with acute pancreatitis. 1076 48

Efforts to unravel the events in the evolution of tissue damage in acute pancreatitis have shown a number of inflammatory mediators to be involved. The pathways of damage are similar, whatever the etiology of pancreatitis, with three phases of progression: local acinar injury, systemic response, and generalized sepsis. The proinflammatory response is countered by an anti-inflammatory response, and an imbalance between these two systems leads to localized tissue destruction and distant organ damage. Cytokines lie at the heart of the problem and are involved in all aspects of the cascade leading to systemic inflammatory response syndrome and multiple organ dysfunction syndrome. This review discusses the present knowledge about the role of various mediators in this process, their genetic control, and the effects of their modulation. The major proinflammatory mediators are tumor necrosis factor, interleukins 1, 6, and 8, platelet activation factor, and the chemokines. The major anti-inflammatory factors include interleukin 10, and interleukin 1 receptor antagonist. Emerging knowledge of new mediators as well as future strategy of damage control is discussed.
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PMID:Cytokine storm in acute pancreatitis. 1248 60