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)

We assessed the ability of serum human pancreatic secretory trypsin inhibitor (hPSTI) to establish the severity of acute pancreatitis and compared it in this respect to that of serum C-reactive protein (CRP). Of 26 patients studied with acute pancreatitis, 16 had mild pancreatitis, and 10, severe disease. Initial studies were performed at onset of the disease in 20 patients, on the second day of illness in two, and on the third day of illness in the remaining four. In all, serum hPSTI and CRP concentrations were determined on admission and daily for the following 5 days using commercial kits; Ranson's score was evaluated within the first 48 h of admission. Sixty-three healthy subjects and 31 patients with nonpancreatic acute abdomen were also studied. Values of 70 ng/ml for serum hPSTI and 10 mg/dl for serum CRP were taken as limits to distinguish severe from mild-to-moderate acute pancreatitis. When assessed within the first 24 h of pain, serum hPSTI correctly classified 71% of the patients with severe acute pancreatitis, whereas serum CRP did so for 29%. In subsequent days, the two markers showed a similar sensitivity in predicting severe acute pancreatitis. Serum hPSTI and CRP were alike in excluding a diagnosis of severe acute pancreatitis. Ranson's score correctly identified 50% of patients with severe illness and 63% of patients with mild pancreatitis. This study indicates that, when assessed within 24 h of pain onset, serum hPSTI is a better predictor of the severity of acute pancreatitis than serum CRP or Ranson's criteria.
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PMID:Human pancreatic secretory trypsin inhibitor in the assessment of the severity of acute pancreatitis. A comparison with C-reactive protein. 796 55

To investigate the role played by cytokines in chronic pancreatitis, we examined serum levels of interleukin-1 beta (IL-1 beta) and interleukin-6 (IL-6) by radioimmunoassay (RIA) and enzyme-linked immunosorbent assay (ELISA) in 33 patients with definitively diagnosed chronic pancreatitis. All the patients, who had received either no treatment or only digestive enzyme products for their chronic pancreatitis, had significantly elevated serum IL-1 beta levels (38.5 +/- 28.8 pg/ml, mean +/- SD), compared to normal controls (16.0 +/- 6.7 pg/ml; P < 0.01); however they showed no changes in serum IL-6 levels. Changes in IL-1 beta and IL-6 serum levels were not correlated with the etiological features of pancreatitis or with complications due to liver diseases. Serum IL-1 beta and IL-6 levels were also not correlated with the activity of any pancreatic enzymes in blood or urine. However, in the patients with chronic pancreatitis, serum IL-6 levels were correlated with C-reactive protein (CRP), whereas serum IL-1 beta levels were not correlated with CRP or with erythrocyte sedimentation rate. These results suggest that serum IL-1 beta is involved in the progression and reduction of chronic inflammation of the pancreas, and that the serum IL-1 beta level may be useful as a marker for chronic pancreatitis.
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PMID:Serum levels of interleukin-1 beta and interleukin-6 in patients with chronic pancreatitis. 806

The most important diagnostic step in the management of patients with acute pancreatitis is to discriminate between interstitial-edematous and necrotizing pancreatitis. Measurement of C-reactive protein or PMN-elastase is useful in detecting the necrotizing course of acute pancreatitis. While patients with acute edematous pancreatitis can be treated on a regular ward, patients with a necrotizing course should be treated in the ICU. Surgical decision-making in necrotizing pancreatitis should be based on the extent of necroses found by contrast-enhanced CT, and on the development of septic signs due to bacterial infection of the necroses. Information about the latter can be obtained by a bedside ultrasound-guided fine needle aspiration and bacteriological examination of the aspirate. Patients with no organic complications and with focal necrosis should be treated conservatively, while patients with persistent organic insufficiencies or progressive multiple organ failure despite maximum intensive care are candidates for surgical therapy. The procedure of choice in necrotizing pancreatitis is the careful removal of necrotic tissue (necrosectomy) followed and supplemented by a postoperative regimen for the continuous evacuation of further necrotic debris. Hospital mortality rate has been reduced to less than 20% by this procedure.
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PMID:Surgical strategies in acute pancreatitis. 811 41

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

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

Serum concentrations of free fatty acids (FFA) were assayed in 20 patients with acute necrotizing pancreatitis (ANP). Pancreatic and peripancreatic fat necrosis was verified on operation and/or by contrast-enhanced computed tomography. For comparison, 20 patients with acute edematous pancreatitis (AEP) were examined. On admission, FFA serum levels were 1.14 +/- 0.12 (SEM) mmol/L in ANP and, thus, significantly (p < 0.03) higher than in AEP (0.78 +/- 0.09 mmol/L). The two groups also differed in the later course: in ANP, the FFA values remained raised (d 5-11:0.86 +/- 0.13 mmol/L; p > 0.05 vs day 1), whereas in AEP, the FFA concentrations normalized within 1 wk (d 2-4:0.52 +/- 0.11 mmol/L; d 5-11:0.39 +/- 0.05 mmol/L; p < 0.05 vs day 1 and p < 0.01 vs ANP). Serum FFA correlated positively with C-reactive protein levels (rs = 0.42; p < 0.01), but has less discriminating potency between ANP and AEP. In AEP, the initial peak may correspond to the disease outburst itself and to unspecific stress. In ANP, the higher and sustained elevation of FFA may predominantly mirror the ongoing pancreatic parenchymal and extrapancreatic fat necrosis, and be pathophysiologically relevant, especially in view of significantly reduced serum albumin levels in ANP.
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PMID:Free fatty acids in serum of patients with acute necrotizing or edematous pancreatitis. 850 51

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

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

The detection of cytokines may elucidate the pathophysiological mechanisms that produce early systemic complications in acute interstitial (i) or necrotizing (n) pancreatitis (AP). The increase in the level of cytokines in the blood of patients with AP may correlate with the severity of the disease. In a prospective clinical trial from October 1992 to August 1993, 23 patients with AP were recruited and blood samples taken for cytokine detection by commercially available Elisa kits and C-reactive protein (CRP) by laser nephelometry. Six of 11 patients with nAP died either early (n = 1) or of late septic complications. None died of iAP. The peak of cytokine and CRP level in the first 3 days of hospitalization was used for calculation. The IL-6 concentration in the blood reached up to 2600 pg/ml in the 1st few days, depending on the severity of AP, and dropped to almost zero in the next days, independently of the clinical course. The differentiation of i- versus nAP, using a cut-off line of 600 pg/ml, was correct in 20 patients [87%, sensitivity (SE): 82%, specificity (SP): 91%, P < 0.001]. The blood levels of IL-8 reached a maximum of 1381 pg/ml in the 1st few days, depending on the severity of AP, and showed a correlation with the clinical course in the following days. The peak of IL-8 blood levels indicated correctly the severity of AP in 18 out of 23 patients using a cutoff level of 200 pg/ml (accuracy: 78%, SE: 82%, SP: 75%, P < 0.01). The CRP levels increased up to a maximum of 535 mg/l and indicated the course of AP correctly in 18 out of 22 patients (SE and SP 82%, P < 0.01). There was no correlation between cytokine blood levels and mortality. In the blood samples of five patients with i- or nAP, no TNF-alpha was detectable. The blood levels of IL-6, and to a lesser extent of IL-8 and CRP, can predict the severity and early systemic complications of AP. The excessive rise in cytokines can be explained by the stimulation of immunological cells (macrophages, lymphocytes and endothelial cells) in the course of AP, inducing early systemic complications.
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PMID:[Clinical significance of cytokines Il-6, Il-8 and C-reactive protein in serum of patients with acute pancreatitis]. 908 85


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