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Query: UMLS:C0001339 (acute pancreatitis)
 10,593 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Fresh frozen plasma (FFP) has been proposed as a specific therapy for acute pancreatitis. It may replenish important circulating proteins, particularly the naturally occurring anti-protease system. To investigate this potential therapy, 72 patients with predicted severe disease were selected from 301 admissions with acute pancreatitis using the modified Glasgow prognostic scoring system. They were randomised within 6 h of diagnosis to receive FFP (8 units daily for 3 days) or a similar volume of colloid control as part of their intravenous fluid therapy. Clinical progress was monitored and specific blood proteins were measured on days 1, 3 and 7. FFP therapy significantly increased the day 3 concentrations of some of the acute phase proteins (C1-reactive protein P less than 0.02, D-dimer P less than 0.05 and fibrinogen P less than 0.05) as well as some proteins which showed a fall in circulating concentration during the early stages of the disease (alpha 2 macroglobulin P less than 0.001, antithrombin III P less than 0.01 and fibronectin P less than 0.001). However, there was no significant difference between the two groups in terms of clinical outcome. Mortality was 20% in patients who received FFP and 18% in the colloid control group. Despite the ability of FFP therapy to supplement circulating concentrations of several potentially useful proteins during acute pancreatitis, it does not appear to improve clinical outcome.
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PMID:A multicentre controlled clinical trial of high-volume fresh frozen plasma therapy in prognostically severe acute pancreatitis. 171 53

Urinary excretions of hydroxyproline and fibronectin fragment (FN fragment) were serially investigated in the patients with acute pancreatitis or acute exacerbation of chronic pancreatitis. While urinary excretion of FN fragment showed the maximal level on the first day of admission, high levels of urinary hydroxyproline were observed on the second to fifth day. As to the changes in the individuals, peak level of urinary FN fragment always preceded that of hydroxyproline. And it was assumed that the elevation of FN fragment excretion on the early phase of pancreatitis reflected tissue damages of pancreas itself and complicated organs, and following elevation of hydroxyproline showed enhanced collagen metabolism induced by acute inflammation and tissue damage. According to the severity of pancreatitis, urinary excretion of FN fragment on the first day increased, and it was therefore suggested that urinary FN fragment would be one of the parameters for the assessment of the severity of acute pancreatitis.
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PMID:[Changes of the urinary excretions of hydroxyproline and fibronectin fragment in acute pancreatitis]. 194 12

Time-dependent serum concentrations of extracellular matrix proteins were studied in 32 patients with pancreatitis in order to find potential markers of the reparative response during the disease. Patients were subdivided by clinical and biochemical criteria: severe acute pancreatitis (n = 10), moderate acute pancreatitis (n = 17), and acute attack of chronic pancreatitis (n = 5). Serum and plasma samples were collected on days 1-7, 10, 14, and 21 for measurements of the aminoterminal propeptide of type III procollagen (PIIINP), hyaluronic acid, laminin, fibronectin, and routine clinical-chemical parameters. During an acute attack of chronic pancreatitis all parameters were within the reference range. In moderate acute pancreatitis concentrations of PIIINP, laminin, and hyaluronic acid fluctuated around the upper reference limit, but declined to mid-normal levels at day 21. In severe acute pancreatitis all three parameters increased. In patients who died as a consequence of sepsis and multi-organ failure the increase in PIIINP, laminin and hyaluronic acid was much more pronounced and paralleled by a decrease in plasma concentrations of fibronectin. In conclusion, this study revealed a relation between the severity of acute pancreatitis and the increase in serum concentrations of extracellular matrix components, especially PIIINP.
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PMID:Follow-up of the serum levels of extracellular matrix components in acute and chronic pancreatitis. 212 79

The effects of acute pancreatitis on the rat pancreatic connective tissue matrix were studied following intraductal pancreatic injection of trypsin solution and serial killing of the animals. Pancreatic tissue was examined using light microscopy, hydroxyproline measurement and indirect immunofluorescence, using antibodies against collagen types I, III, IV, procollagen III, fibronectin and laminin. Light microscopy revealed that acute pancreatitis was present for up to four days after injection and that perilobular and intralobular fibrosis appeared at four days and subsequently regressed. Immunofluorescence studies demonstrated an abnormal fibronectin deposit at one day in acute pancreatitis. At four days this deposit was co-located with fibrosis which was composed of collagen and procollagen type III. By eight days the immunofluorescence and light microscopic changes were minimal. Biochemical analysis confirmed a significant rise in hydroxyproline concentration at four days, which was maximal at eight days, subsequently decreasing. This peak at eight days probably reflects collagen breakdown products.
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PMID:Sequential connective matrix changes in experimental acute pancreatitis. An immunohistochemical and biochemical assessment in the rat. 331 29

Altered polymorphonuclear leukocyte (PMN) function is thought to contribute to organ dysfunction during the systemic inflammatory response syndrome (SIRS). To test this hypothesis, we evaluated whole blood PMN function adherent to fibronectin or laminin in patients with mild or severe acute pancreatitis as a paradigm for sirs. Whole-blood PMN intracellular H2O2 production, expression of CD32w (Fc gamma R II), CD16 (Fc gamma R III), and phagocytosis were performed using dichlorofluorescein diacetate, fluorescein isothiocyanate-labeled anti-CD32w, CD16, and serum-opsonized fluorescent microspheres. Group I (n x 7) represents normal control individuals; group II (n x 11) represents patients with mild acute pancreatitis. Group III (n x 15) represents critically ill patients with severe acute pancreatitis. Adherence of PMN from groups I and II to matrix proteins resulted in a 5% to 20% increase in each PMN function assayed whereas adherence of PMN from group III to matrix proteins resulted in 50% to 75% increases in each PMN function assayed. Pertussis toxin, pentoxifylline, and dibutyryl cyclic adenosine monophosphate (cAMP) each reduced group I-II H2O2 production and phagocytosis. Pentoxifylline and dibutyryl cAMP but not pertussis toxin reduced group III H2O2 production. Both intracellular H2O2 and phagocytosis assays from group III but not groups I-II showed exaggerated upregulation when exposed to NaF (4 mmol/L). Anti-interleukin-6 reduced the increase in intracellular H2O2 production in group III patients and significantly altered the exaggerated oxidative response to NaF. Longitudinal studies of group III whole-blood PMN showed persistent upregulation of intracellular H2O2 production in those patients whose hospital courses were complicated by multiple system organ failure. These results demonstrate abnormal whole blood PMN function during the systemic inflammatory response syndrome in the presence of fibronectin, or laminin and that this is mediated in part via a pertussis toxin insensitive altered guanosine triphosphate-binding protein.
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PMID:Polymorphonuclear leukocyte dysregulation during the systemic inflammatory response syndrome. 811 41

The pathogenesis of chronic pancreatitis (CP) has been debated as to whether it is a de novo process or the consequence of acute pancreatitis (AP). We investigated whether recurrent AP in rats leads to CP, by sequential morphological and biochemical studies. Thirty male Wistar rats were fed a choline-deficient diet with intraperitoneal ethionine injections twice daily at a dose of 60 mg/100 g body weight twice weekly, and six rats were killed at 4, 6, and 8 weeks; the remaining 12 rats, followed without further treatment, were killed at 12 and 16 weeks. The pancreata from study and control groups were examined by histology, immunohistochemistry, and bio- and immunoassays. Histologically, moderate to severe intra- and perilobular fibrosis and other CP-like lesions appeared maximally at 8 weeks. Immunohistochemically, the earliest extracellular matrix change was strong fibronectin staining at 4 weeks, with a progressive increase to 8 weeks. Collagens I and III came to show strong, and collagen IV moderate, interstitial staining at 6-8 weeks. These morphological changes, however, returned to nearly normal at 16 weeks. Prolyl hydroxylase was significantly elevated at 4 and 6 weeks and normalized after 8 weeks, with no significant change in collagenase. In conclusion, our results suggest that even severe CP-like lesions induced by recurrent AP are reversible in the absence of persistently elevated prolyl hydroxylase and/or suppressed collagenase. The mechanism regulating these changes remains to be studied further.
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PMID:Does recurrent acute pancreatitis lead to chronic pancreatitis? Sequential morphological and biochemical studies. 916 78

At present, the cell-cell interactions and molecular mechanisms of pancreas fibrogenesis are largely unknown. The purpose of this study was to investigate paracrine stimulatory loops between platelets and pancreatic stellate cells (PSC). Human PSC were obtained by outgrowth from fibrotic human pancreas. Native platelet lysate (nPL) and transiently acidified platelet lysate (aPL) were added to cultured PSC (passage 4 to 7) in the absence of serum. The synthesis of collagen types I and III and c-fibronectin (cFN) was demonstrated on protein (immunofluorescence and quantitative immunoassay) and mRNA (Northern blot) level. Using sections of human pancreas with acute pancreatitis, platelet aggregates in capillaries were demonstrated by transmission electron microscopy. nPL, and to an even greater extent aPL, significantly increased the synthesis of collagen types I and III and of c-FN (120 microl/ml aPL increased collagen type I concentration in PSC supernatants by 1.99 +/- 0.17 times and c-FN of 2.49 +/- 0.28 times, mean +/- SD, n = 3). nPL and aPL also significantly stimulated cell proliferation (increased bromodeoxyuridine (BrdU) incorporation by 6.4 +/- 0.78 times and 10 +/- 0.29 times, respectively). By preincubating aPL with transforming growth factor beta (TGFbeta)- and platelet-derived growth factor (PDGF)-neutralizing antibodies and the TGFbeta-latency associated peptide, respectively, TGFbeta1 was identified as the main mediator stimulating matrix synthesis and PDGF as the responsible mitogen. Our data demonstrate that platelets contain fibrogenic mediators that stimulate proliferation (PDGF) and matrix synthesis (TGFbeta1) of cultured PSC. We suggest that platelets and PSC cooperate in the development of pancreas fibrosis.
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PMID:Platelet-derived growth factors stimulate proliferation and extracellular matrix synthesis of pancreatic stellate cells: implications in pathogenesis of pancreas fibrosis. 1065 2

The fibronectin content dynamics in the blood serum was estimated in patients with various clinical forms of an acute pancreatitis. The fibronectin level lowering may be a predictor of occurrence and diagnostical criterion for infective complications in patients with destructive pancreatitis. Application of clexane had promoted the fibronectin level raising in the blood serum in patients with sterile and infected pancreatic necrosis.
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PMID:[The influence of clexane on the fibronectin content in the blood plasma in patients with destructive pancreatitis]. 1148 7

Acute pancreatitis (AP) in humans can lead to increased vascular permeability in the lungs and respiratory failure. Fibronectin plays an important role in maintaining the structural integrity of the pulmonary epithelium and endothelium. However, its importance in pancreatitis-associated lung injury has not been defined. AP was produced by infusing caerulein (5 ug/kg/hr) in rats for 8 or 24 hr. Lung injury was assessed histologically and by determining lung microvascular permeability by bronchoalveolar lavage (BAL) analysis. Organ distribution of a target particle given intravenously was determined by the vascular clearance of magnetic iron oxide particles. Plasma fibronectin was measured by the enzyme-linked immunosorbent assay technique. After 8 hr of cerulein infusion, serum amylase increased 8-fold. Pancreatitis correlated with lung injury. BAL at 8 hr showed a 90% increase (P < 0.05) in albumin levels. Histological analysis at 8 hr revealed an increased number of leukocytes within the lungs. By 8 hr, plasma fibronectin significantly decreased 25% (P < 0.05) and the pulmonary uptake of iron oxide increased 111% (P < 0.05). By 24 hr, these effects had nearly resolved. These results indicate that decreases in serum fibronectin and increases in pulmonary leukocyte margination during acute pancreatitis may compromise the integrity of the air-blood barrier and also increase the pulmonary uptake of circulating pathogenic materials, thus making lung injury more likely.
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PMID:Role of fibronectin in pancreatitis-associated lung injury. 1292 35

Phagocytosis of polymer microspheres both modified and unmodified by bioligands (gelatin, fibronectin and A protein) by leukocytic blood cells of patients with acute pancreatitis. The presence of bioligands in the surface of polymer microspheres and their activity were monitored by the reaction of latex agglutination with an appropriate ligand being involved. The study resulted in designing a method of phagocytosis implementation that can be used to evaluate the content of certain receptors in cellular membranes and, subsequently, to define the changed receptor cell apparatus caused by a disease. The nature of polymer microspheric bioligands immobilized to the surface was shown to influence significantly the activity of leukocytic blood cells.
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PMID:[Phagocytosis of polymer microspheres immobilized with bioligands by peripheral blood leukocytes in patients with acute pancreatitis]. 1466 82


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