Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0030305 (pancreatitis)
 16,014 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 purpose of this study was to evaluate the role of cytokines in septic conditions following acute pancreatitis and to elaborate a new strategy in the treatment. Increased TNF and IL-6 serum levels were found in 30% of the patients (n = 40), while the IL-6 level was elevated in all of them. There was a positive correlation between the serum IL-6 and sICAM-1 levels. The in vitro TNF and IL-6 producing capacities were initially higher in the study group, but decreased on subsequent days, especially in fatal cases (n = 3). Administration of pentoxifylline [PTX] (400 mg/day) to septic patients following necrotizing pancreatitis resulted in TNF and IL-6 production similar to that observed in control donors. The level of sICAM-1 also decreased following PTX therapy. These results suggest that cytokines produced by activated leucocytes are important in the pathogenesis of infected pancreatic necrosis, and their inhibition might be of therapeutic advantage.
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PMID:Relevance of cytokine production to infected pancreatic necrosis. 940 98

Ulinastatin is widely used in the treatment of pancreatitis and sepsis, because of its excellent anti-inflammatory and antioxidant effects. However, its effects on atherosclerosis, an inflammatory vascular disease, are rarely reported. Therefore, in present study, we explored effects of ulinastatin on monocyte-endothelial adhesion, the initiator of atherosclerosis. We used U937 monocytes and angiotensin II-stimulated human umbilical vein endothelial cells (HUVECs) to build the model of monocyte-endothelial adhesion. Different methods were used to change the function of connexin43 (Cx43), the level of ROS, the activation of JAK2/STAT3 signaling pathway and its downstream MMP2 and MMP9 expression, and then the influences of ulinastatin on U937-HUVECs adhesion and the adhesion molecules were observed. The results showed that ulinastatin could attenuate ROS transmission between the neighboring HUVECs via inhibiting Cx43 function. With the decrease of ROS, JAK2/STAT3 signaling pathway and its downstream MMP2 and MMP9 expression were downregulated. Ultimately, important adhesion molecules expression, such as VCAM-1, ICAM-1, sVCAM-1 and sICAM-1, and U937-HUVECs adhesion, were both reduced. Thus, we can conclude that ulinastatin attenuates adhesion molecules expression and monocyte-endothelial adhesion, mechanism of which is related that ulinastatin inhibits ROS transfer between the neighboring vascular endothelial cells mediated by Cx43, resulting in the inactivation of JAK2/STAT3 signaling pathway, and its downstream MMP2 and MMP9 expression decrease.
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PMID:Ulinastatin attenuates monocyte-endothelial adhesion via inhibiting ROS transfer between the neighboring vascular endothelial cells mediated by Cx43. 3291 8