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

Endoscopic retrograde cholangiopancreatography (ERCP) is complicated by acute pancreatitis in up to 12% of the examinations. One possible mechanism for this complication is the cannulation-induced sphincter of Oddi spasm with temporary pancreatic duct obstruction. Nifedipine is known to relax the sphincter of Oddi, thus possibly inhibiting or reducing post-ERCP +/- endoscopic sphincterotomy (EST) pancreatic irritation. To test this hypothesis 166 adult patients undergoing ERCP +/- EST were randomized to receive nifedipine (n = 82) 20 mg 3 times at 8-hour intervals during the day of ERCP +/- EST or placebo (n = 84) in a double-blind manner. Clinical pancreatitis developed in 6 patients (4%), in 3 patients in each group. Necrotizing pancreatitis developed in 3 patients, 2 (2%) in the nifedipine group and 1 (1%) in the placebo group. Overall 60 patients (36%) needed medication for post-ERCP +/- EST epigastric pain, 27 (33%) in the nifedipine group and 33 (39%) in the placebo group. Of the 87 patients, who did not need any pain medication before ERCP +/- EST, 34 (39%) needed pain medication after ERCP +/- EST. 14/47 (30%) in the nifedipine group and 20/40 (50%) in the placebo group (p = 0.044). Serum total amylase activity (median) increased from 189 U/l (range 39-11,950 U/l) before ERCP +/- EST to 299 U/l (range 43-11,824 U/l) at 12 h (p < 0.001) and 247 U/l (range 34-15,950 U/l) at 24 h (p < 0.001), with no differences between the two groups. Median serum C-reactive protein concentration and blood leukocyte count remained unchanged in both groups.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Prospective randomized trial of the effect of nifedipine on pancreatic irritation after endoscopic retrograde cholangiopancreatography. 831 38

Randomized clinical trials of antibiotic prophylaxis in acute pancreatitis are now warranted in the light of recent evidence of pancreatic penetration of certain antibiotics at therapeutic minimal inhibitory concentrations. The aim of the present prospective clinical study was to investigate whether there are detectable risk factors for pancreatic sepsis in acute pancreatitis that would allow better selection of patients for inclusion in clinical trials. Fifty-nine consecutive patients with acute pancreatitis were recruited and submitted to admission baseline and 48-h determinations of Ranson score, and assay of C-reactive protein at admission and weekly intervals thereafter. Contrast-enhanced computed tomography (CT) was also performed within 24 h of admission. Pancreatic sepsis, defined as infection of pancreatic and/or peripancreatic collections, was demonstrated in all cases by culture of samples obtained by needle aspiration and at laparotomy. Although all prognostic indices correlated significantly with sepsis, multivariate logistic regression analysis showed that the only variables predictive of the risk of subsequent sepsis were the presence and extent of necrosis. Early detection of pancreatic necrosis by CT should be the primary inclusion criterion in future clinical trials of antibiotic prophylaxis in acute pancreatitis.
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PMID:Prospective comparison of C-reactive protein level, Ranson score and contrast-enhanced computed tomography in the prediction of septic complications of acute pancreatitis. 833 Jan 67

In this review, the relative values of serum pancreatic enzyme assays and other laboratory tests for diagnosis and prognosis of acute pancreatitis have been evaluated. It is concluded that serum lipase measurement should be the preferred diagnostic method since it is as simple and accurate as amylase assay, all the while being more specific. As for prognosis, among the several biochemical tests now available, the most useful for clinical practice is serum C-reactive protein determination.
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PMID:Update on laboratory diagnosis and prognosis of acute pancreatitis. 837 Jan 44

It has been proposed that endotoxin contributes to the development of multiple organ failure (MOF) in acute pancreatitis. Endotoxaemia is transient and may not be detected by intermittent blood sampling. By contrast, not only can changes in the patient's endogenous antiendotoxin core antibody pool persist for many days, but depletion of this pool may be a key event in determining the physiological significance of endotoxaemia. A series of 33 patients with acute pancreatitis had daily measurement of Acute Physiology Score (APS) and levels of C-reactive protein, interleukin 6, endotoxin, immunoglobulin (Ig) G and IgM antiendotoxin core antibodies, and prospective documentation of complications. Endotoxin was detected in the serum of 13 patients, while a significant change in levels of endogenous antiendotoxin core antibodies was detected in all those with severe pancreatitis and in 28 overall. MOF developed in seven patients, five of whom died. The combination of a rising APS over the first 48 h of admission and a significant fall in endogenous IgG antibody level was observed in all patients who developed MOF (seven of seven), but in only one of 16 without MOF (P = 0.00003; overall predictive value 91 per cent). This study suggests that measuring the initial trend in APS and the concentration of endogenous IgG antiendotoxin core antibody provides a means of identifying patients with acute severe pancreatitis who are at high risk of developing MOF. This group might benefit from passive immunotherapy with antiendotoxin antibodies.
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PMID:Role of serum endotoxin and antiendotoxin core antibody levels in predicting the development of multiple organ failure in acute pancreatitis. 840 63

Despite the clinical importance of pancreatic necrosis in the course of acute pancreatitis, little is known about when it develops. Serum C-reactive protein (CRP) is a reliable parameter with a high deduction rate for pancreatic necrosis. We analyzed 199 patients with acute pancreatitis. The development of pancreatic necrosis was ascertained by a daily measurement of serum CRP in 45 patients with contrast-enhanced computed tomographic-proven necrotizing pancreatitis. In all 45 cases, the criteria for pancreatic necrosis were satisfied within the first 4 days of the onset of symptoms. This indicates that pancreatic necrosis is an early finding that develops within hours.
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PMID:Pancreatic necrosis: an early finding in severe acute pancreatitis. 848 78

The intercellular adhesion molecule-1 (ICAM-1), a membrane glycoprotein, is important in the adhesion of cytokine-stimulated leukocytes to the endothelium of microvessels and their transendothelial migration. Circulating isoforms of ICAM-1 (cICAM-1) are known to be elevated in human serum as an indirect consequence of inflammatory responses. The aim of this study was to investigate whether cICAM-1 levels are elevated in patients with acute pancreatitis within 48 h of the onset of abdominal pain and whether cICAM-1 levels correlate with the severity of the tissue damage. Twenty-five consecutive patients admitted to a medical ICU had elevated cCAM-1 concentrations of 548 +/- 68 ng/ml, significantly different when compared to a control group of 18 healthy subjects (343 +/- 29; p = 0.018). According to the findings of contrast-enhanced CT or laparotomy patients were further divided in a group with acute edematous pancreatitis and a group with acute necrotizing pancreatitis. Pancreatic necrosis was associated with cICAM-1 levels of 729 +/- 106 ng/ml, significantly different from patients with mild disease (367 +/- 48) and controls (p < 0.001). Plasma cICAM-1 levels were not significantly different between healthy subjects and patients with mild pancreatitis. A significant correlation was found between cICAM-1 and C-reactive protein, an acute phase reactant and marker of necrotizing pancreatitis (r = 0.62; p < 0.01). The sensitivity and specificity for the detection of edematous or necrotizing pancreatitis of cICAM-1 plasma concentrations (cutoff point at 500 ng/ml) were 75% and 85%, respectively. These results suggest an enhanced release of ICAM-1 into plasma in the early stage of acute necrotizing pancreatitis. Leukocyte-endothelial cell adhesion may be associated with the inflammatory process of necrotizing tissue damage in acute pancreatitis. It could thus serve as a marker or predictor of a severe clinical course of pancreatitis.
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PMID:Increased plasma concentrations of circulating intercellular adhesion molecule-1 (cICAM-1) in patients with necrotizing pancreatitis. 887 97

Forty-eight patients with severe acute pancreatitis were treated with intraperitoneal lavage in a double-blind randomized multi-center trial. One group (aprotinin group, n = 22) was also treated intraperitoneally with high doses of the protease inhibitor aprotinin. In the group not treated with aprotinin (control group), 6 patients were operated on because of pancreatic necrosis, compared with none in the treated group. Complement activation and the acute phase response were studied with measurements of anaphylatoxin C3a, C1 inhibitor (C1 Inh), interleukin 6 (IL-6), and C-reactive protein (CRP). The control group had higher plasma levels of C3a and lower levels of C1 Inh compared with the aprotinin group. The differences were statistically significant for C3a but not for C1 Inh. Both groups had high plasma levels of IL-6 and CRP. There were no differences between the groups in CRP levels, but the control group had higher IL-6 levels (not statistically significant) than the aprotinin group. This was caused by very high levels in the 6 patients operated on because of pancreatic necrosis, indicating that IL-6 could be a good plasma marker of pancreatic necrosis. The results also show that massive antiprotease treatment reduces complement activation, as illustrated by the lower C3a levels in the aprotinin group. The lower C1 Inh levels in the control group could have been caused by an increased consumption of the inhibitor.
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PMID:Effects of high-dose intraperitoneal aprotinin treatment on complement activation and acute phase response in acute severe pancreatitis. 888 38

It has been supposed that there are differences with regard to clinical course and outcome due to the underlying etiological factor in acute pancreatitis. Therefore, the objective of this study was to analyze the severity of the disease, serum enzymes, indicators of necrosis, systemic complications, and mortality in acute pancreatitis with regard to the etiology. One hundred ninety patients with acute pancreatitis (127 male, 63 female) were studied prospectively and subdivided into three etiological groups: (i) alcohol, (ii) gallstones, and (iii) other causes and idiopathic acute pancreatitis. Severity scores (Ranson and Bank) and findings by contrast-enhanced computed tomography were similar in all three groups. Analysis of serum enzymes [lipase, aspartate aminotransferase (ASAT)] and indicators of necrosis (C-reactive protein, alpha 1-antitrypsin, alpha 2-macroglobulin, and lactate dehydrogenase) showed only for ASAT within 24 h significantly higher levels in biliary acute pancreatitis in comparison with the other groups. There were no differences in the rate of infected pancreatic necrosis and mortality in alcohol-related acute pancreatitis (31 and 5.3%), biliary acute pancreatitis (38 and 10%) and acute pancreatitis due to other etiological factors (43 and 5.5%). In conclusion, this study clearly showed that once the pathogenetic mechanisms have initiated the disease, the course and outcome of acute pancreatitis are not influenced by the underlying etiological factor.
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PMID:Influence of etiology on the course and outcome of acute pancreatitis. 889 93

Twelve patients with acute pancreatitis admitted to our department between January 1993 and December 1994 were studied prospectively and classified into two groups (severe group, five patients; mild group, seven patients), according to the criteria for grading severity of acute pancreatitis proposed by the Research Committee for Intractable Diseases of the Pancreas, Japanese Ministry of Health and Welfare (1990). To evaluate markers for early estimation of the severity of acute pancreatitis, we measured serum changes in various parameters. In the severe group interleukin-6 (IL-6) levels were increased significantly 5, 24, 72, and 120 h after the onset (p < 0.01), compared with the mild group. C-reactive protein (CRP), thrombin antithrombin III, and alpha 2-plasmin inhibitor plasmin complex levels were significantly increased only at the 72-h time point. Peak values of interleukin-8 (IL-8) and soluble human E selectin were observed at 5 and 72 h, respectively, after the onset. There was a significant correlation between IL-6 at 5 h and both pancreatic secretory trypsin inhibitor (r = 0.85) and CRP (r = 0.94) at 72 h. We therefore conclude that IL-6 is a useful marker for assessment of the severity of acute pancreatitis in its early stages.
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PMID:Interleukin-6 is a useful marker for early prediction of the severity of acute pancreatitis. 959 21

Serum levels of hepatocyte growth factor (HGF), C-reactive protein (CRP), and interleukin-6 (IL-6) were determined at the time of admission in 38 patients with acute pancreatitis. The clinical utility of HGF for the detection of severe pancreatitis and for predicting prognosis, bacterial infection (infected pancreatic necrosis or sepsis), and organ dysfunction (liver, kidney, and lung) during the clinical course of acute pancreatitis was compared with the clinical utility of CRP and IL-6 by analysis of receiver operator characteristic (ROC) curves. The optimum cutoff levels of HGF for severity, prognosis, infection, hepatic dysfunction, renal dysfunction, and respiratory dysfunction were 0.9, 1.1, 1.0, 1.1, 1.1, and 1.0 ng/ml, respectively. HGF was as useful as CRP and more useful than IL-6 for detection of severe pancreatitis and for predicting hepatic dysfunction. Moreover, HGF was more useful than CRP or IL-6 for predicting prognosis, renal dysfunction, and respiratory dysfunction. However, for predicting infection, CRP was more useful than HGF. These results suggest that serum HGF levels on admission may be a useful new clinical parameter for determining the prognosis of acute pancreatitis and that HGF may be closely related to the organ dysfunction of acute pancreatitis.
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PMID:Hepatocyte growth factor in assessment of acute pancreatitis: comparison with C-reactive protein and interleukin-6. 905 97


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