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)

Post-endoscopic retrograde cholangiopancreatography (ERCP) pancreatitis has been suggested as a model for acute pancreatitis (AP), which allows evaluation of early alterations in the time course of the disease. The influence of the clinical course on procalcitonin (PCT), serum amyloid A (SAA), and several proinflammatory and inhibitory cytokines was evaluated in patients with AP following ERCP. Blood samples were prospectively collected from patients undergoing ERCP. The incidence of ERCP-induced pancreatic damage, defined as abdominal complaints, a threefold increase of serum lipase, and elevation of CRP from <10 to >20 mg/liter was 12.8% (12/94). Only mild clinical courses of acute pancreatitis were observed. PCT significantly increased in subjects with post-ERCP pancreatitis after 24 hr. However, PCT levels did not exceed 0.5 ng/ml in any patient. Interleukin-1 receptor antagonist (IL-1RA) began to differ from baseline 2 hr after ERCP, followed by interleukin-6 (IL-6, 6 hr), solubilized tumor necrosis factor-alpha receptor II (sTNF-alphaRII, 24 hr) and SAA (24 hr). Interleukin 10 (IL-10) showed marked interindividual variations with no obvious peak. Among all parameters evaluated, only peak values of IL-6 and IL-10 showed significant correlations with the reported pain score (r2 = 0.62/0.78), degree of ampullar irritation (r2 = NS/0.87), and the duration of ERCP (r2 = 0.58/0.76). No correlation was found with the volume of the injected contrast agent. We conclude that IL-10 and IL-6 appear to be useful to monitor patients after ERCP. The absence of any PCT elevation in the present study is in accordance with the clinical course of the patients who suffered from mild pancreatic damage without systemic or infectious complications.
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PMID:Diagnostic relevance of interleukin pattern, acute-phase proteins, and procalcitonin in early phase of post-ERCP pancreatitis. 972 66

Phospholipase A2 (PLA2) is an enzyme that catalyzes the hydrolysis of membrane phospholipids. This article reviews the source and structure of PLA2, the involvement of the enzyme in various biological and pathological phenomena, and the usefulness of PLA2 assays in laboratory diagnostics. Of particular importance is the role of PLA2 in the cellular production of mediators of inflammatory response to various stimuli. Assays for PLA2 activity and mass concentration are discussed, and the results of enzyme determinations in plasma from patients with different pathological conditions are presented. The determination of activity and mass concentration in plasma is particularly useful in the diagnosis and prognosis of pancreatitis, multiple organ failure, septic shock, and rheumatoid arthritis. A very important result is the demonstration that PLA2 is an acute phase protein, like CRP. Indeed, there is a close correlation between PLA2 mass concentration and CRP levels in several pathological conditions. Although the determination of C-reactive protein is much easier to perform and is routinely carried out in most clinical laboratories, the assessment of PLA2 activity or mass concentration has to be considered as a reliable approach to obtain a deeper understanding of some pathological conditions and may offer additional information concerning the prognosis of several disorders.
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PMID:Phospholipase A2: its usefulness in laboratory diagnostics. 1043 55

Recently an ELISA using specific antibodies to detect elastase-1 in serum has become available. Earlier studies using a radioimmunoassay reported a prolonged elevation of serum elastase as compared to other pancreatic enzymes in acute pancreatitis. The aim of the present study was to compare the changes of serum levels of ELISA-elastase-1, lipase and amylase in acute pancreatic damage following ERCP. Blood samples were prospectively collected at five time points before and after the endoscopic procedures in 212 patients. Samples were analyzed for pancreatic serum enzymes, acute phase proteins and routine parameters. A pain score was used for clinical evaluation. Relevant post ERCP pancreatic damage was defined as CRP elevation from < 10 mg/l to > 10 mg/l in the presence of persistent abdominal pain without laboratory evidence of cholangitis and without clinical or laboratory signs of pancreatitis before the endoscopic procedures. Elastase-1 time course paralleled the courses of lipase and amylase peeking at six hrs. There was no prolonged elevation of elastase-1. Ten out of 204 patients (4.9%) were found to have relevant pancreatic damage. Depending on the cut off point used, sensitivity/specificity were as follows: lipase 80-100%/30.9-71.6%; amylase 70-90%/44.3-88.7%; elastase-1 60-90%/64.9-81.4%. In conclusion ELISA-elastase-1 is a marker of acute pancreatic damage similar to lipase and amylase. Although elastase-1 may show a better specificity than the other enzymes, this seems to be a matter of definition of the normal range. The determination of serum ELISA-elastase-1 does not provide additional information in acute pancreatic damage as compared to a combination of lipase and amylase.
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PMID:Determination of elastase-1 serum levels in post ERCP/EST pancreatic damage. 1049 4

In healthy subjects, the 3 known pancreatic trypsinogens, which are endopeptidases belonging to the chymotrypsin superfamily, are activated by enterokinase and partial autoactivation in the duodenum. The premature activation of trypsinogen in the pancreatic interstitium, with the subsequent activation of other pancreatic zymogens, is believed to lead to the autodigestion of the gland, this being the first event in acute pancreatitis. The mechanisms that lead to trypsinogen, activation in acute pancreatitis are largely unknown. However, ischemia, hypercalcemia and the activation of cathepsin B (by cholecystokinin) are thought to be of importance. The easiest and most reliable way to assess trypsinogen activation is the measurement of the activation peptide, TAP, in urine, plasma, pancreatic tissue or ascitic fluid. In the animal model of acute pancreatitis, TAP in ascites and pancreatic tissue has been shown to correlate with the presence and extent of necroses. It has proven to be a good marker for the severity of pancreatitis and is a useful marker in examining the pathophysiology and possible treatment modalities in the animal model of acute pancreatitis. Studies on TAP in human acute pancreatitis were most commonly focused on urinary TAP. Within a 48-hour time frame after the onset of the disease, TAP was a good predictor of the severity of acute pancreatitis. The main advantage over other markers, such as CRP, is that TAP is the earliest marker of necrosis to be increased. Also, increased levels of TAP in ascitic fluid were shown to correlate well with pancreatic necroses. In our experience, plasma TAP was found to have a "diagnostic window" within the first 3 days predicting pancreatic necroses. Positive TAP gave a very good positive prediction and a high specificity towards the development of pancreatic necroses, but did not differ between necrotizing pancreatitis with systemic complications or uncomplicated necrotizing pancreatitis. We therefore think that plasma TAP is a very good marker for local complication in acute pancreatitis and its routine measurements may help to identify patients at a high risk within the first days of the disease.
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PMID:Mechanism and role of trypsinogen activation in acute pancreatitis. 1057 41

A wide variety of adverse effects of methimazole (MMI) have been reported. Here we report a new MMI-induced disorder, acute pancreatitis and parotitis. Three weeks after a woman started MMI treatment for Graves' disease, she developed a high fever, painful parotid swelling and dull pain in the upper abdomen with elevation of the serum levels of salivary and pancreatic enzymes. These abnormalities disappeared soon after the withdrawal of MMI. However, the same abnormalities were rapidly provoked when MMI was reintroduced. Marked increases in the leucocyte count and CRP were also observed during these episodes. The possible mechanisms of MMI-induced pancreatitis/parotitis are discussed.
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PMID:Acute pancreatitis and parotitis induced by methimazole in a patient with Graves' disease. 1059 30

Normal serum PAP levels on admission to the hospital in patiens with acute pancreatitis has been proposed to help select the patients who are not going to develop complications. The aims of this study were, first, to assess the specificity of serum pancreatitis associated protein (PAP) serology test and second, to evalute the usefulness of the test for prediciting complications in acute pancreatitis on admission to the hospital. The sensitivity of the PAP ELISA in patiens with acute pancreatitis on admission to the hospital was 70% and the serum PAP levels significantly higher than in healthy controls (p < 0.0001). However, the serum PAP levels in patients with acute pancreatitis were not significantly different from values in patients with various abdominal diseases (p < 0.58). Serum PAP levels gave good correlation to APACHE II (p = 0.02) and CRP (p = 0.01). Two patients with local complications (necrotizing pancreatitis, pancreatic fluid collection) had elevated serum PAP levels on admission to the hospital (> 100 ng/ml). The diagnostic specififity of PAP ELISA is low. Patients, who develop local complications in acute pancreatitis can not be excluded by normal serum PAP levels on admission to the hospital.
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PMID:Low Serum Pancreatitis-Associated Protein Does not Exclude Complications in Mild Acute Pancreatitis. 1117 21

Although we have reported the beneficial effect of continuous regional arterial infusion (CRAI) of protease inhibitor and antibiotic on acute necrotizing pancreatitis (ANP), the optimal timing of the initiation of CRAI therapy has not been clarified. The present study was conducted to evaluate whether the difference of the timing of CRAI therapy may affect the clinical course and outcome in ANP. 73 patients with ANP were stratified into three groups according to the interval between the onset and initiation of CRAI therapy as follows: group I (32 patients in whom CRAI therapy was initiated within 48 h after the onset); group II (22 patients in whom CRAI therapy was initiated between 48 and 72 h after the onset), and group III (19 patients in whom CRAI was initiated more than 72 h after the onset). The mortality rate was 3.2% in group I, 9.1% in group II, and 26.3% in group III. The mortality rate was significantly low in group I compared with that in group III. The frequency of respiratory failure in group I was also significantly low compared with that in group III. CRP and APACHE II score were reduced rapidly in both groups I and II after the initiation of CRAI therapy. These results suggested that the optimal timing of CRAI therapy in ANP should be considered to be within 72 h after the onset.
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PMID:Benefit of continuous regional arterial infusion of protease inhibitor and antibiotic in the management of acute necrotizing pancreatitis. 1212 Feb 52

Acute pancreatitis is one of the major complications of ERCP. It is of paramount importance that we accurately identify which patients will go on to develop post-ERCP pancreatitis. As most ERCPs are performed on an outpatient basis, early evaluation can allow safe discharge of the majority of patients who will not develop post-ERCP pancreatitis or develop only mild symptoms that will be self-limited. Alternatively, early detection of those patients who will go on to develop moderate or severe post-ERCP pancreatitis can guide decisions regarding hospital admission and aggressive management and can help direct the use of targeted therapies that have the potential to prevent or mitigate pancreatic inflammation. Thus, significant efforts have focused on trying to identify predictors of post-ERCP pancreatitis. These parameters can be organized into three categories of tests: 1) pancreatic enzymes as markers of pancreatic injury: serum amylase/urine amylase; 2) markers of proteolytic activation: trypsinogen, trypsinogen activation peptide; 3) markers of systemic inflammation: C-reactive protein, various interleukins such as IL-6 and IL-10. A serum amylase level greater than 4-5 times the upper reference limit in conjunction with clinical symptoms has been shown to be an accurate and reliable predictor of post-ERCP pancreatitis. However, the exact timing and level of amylase elevation remains debatable. Urine testing of amylase and trypsinogen-2 in post-ERCP patients has also been shown to be highly sensitive and specific for detecting pancreatitis. The main advantage of these urinary markers is that they are available as rapid dipstick tests. Serum trypsinogen-2 levels have also been studied in post-ERCP pancreatitis patients; high levels seem to correlate with severity of disease. Among the markers of systemic inflammation, serum CRP is an accurate and readily available laboratory test for predicting severity of post-ERCP pancreatitis, but it appears to be helpful at 24-48 hours and, therefore, is not an early marker. Several other markers remain investigational and have not yet found wide clinical applicability.
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PMID:What are the predictors of post-ERCP pancreatitis, and how useful are they? 1243 85

Intestinal barrier failure and subsequent bacterial translocation have been implicated in the development of organ dysfunction and septic complications associated with severe acute pancreatitis. Splanchnic hypoperfusion and ischemia/reperfusion injury have been postulated as a cause of increased intestinal permeability. The urinary concentration of intestinal fatty acid binding protein (IFABP) has been shown to be a sensitive marker of intestinal ischemia, with increased levels being associated with ischemia/reperfusion. The aim of the current study was to assess the relationship between excretion of IFABP in urine, gut mucosal barrier failure (intestinal hyperpermeability and systemic exposure to endotoxemia), and clinical severity. Patients with a clinical and biochemical diagnosis of acute pancreatitis were studied within 72 hours of onset of pain. Polyethylene glycol probes of 3350 kDa and 400 kDa were administered enterally, and the ratio of the percentage of retrieval of each probe after renal excretion was used as a measure of intestinal macromolecular permeability. Collected urine was also used to determine the IFABP concentration (IFABP-c) and total IFABP (IFABP-t) excreted over the 24-hour period, using an enzyme-linked immunosorbent assay technique. The systemic inflammatory response was estimated from peak 0 to 72-hour plasma C-reactive protein levels, and systemic exposure to endotoxins was measured using serum IgM endotoxin cytoplasmic antibody (EndoCAb) levels. The severity of the attack was assessed on the basis of the Atlanta criteria. Sixty-one patients with acute pancreatitis (severe in 19) and 12 healthy control subjects were studied. Compared to mild attacks, severe attacks were associated with significantly higher urinary IFABP-c (median 1092 pg/ml vs. 84 pg/ml; P < 0.001) and IFABP-t (median 1.14 microg vs. 0.21 microg; P = 0.003). Furthermore, the control group had significantly lower IFABP-c (median 37 pg/ml; P = 0.029) and IFABP-t (median 0.06 microg; P = 0.005) than patients with mild attacks. IFABP correlated positively with the polyethylene glycol 3350 percentage retrieval (r = 0.50; P < 0.001), CRP (r = 0.51; P < 0.001), and inversely with serum IgM EndoCAb levels (r = -0.32; P = 0.02). The results of this study support the hypothesis that splanchnic hypoperfusion contributes to the loss of intestinal mucosal integrity associated with a severe attack of pancreatitis.
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PMID:Intestinal hypoperfusion contributes to gut barrier failure in severe acute pancreatitis. 1255 82

We report on a 68-year-old female patient who was admitted with abdominal pain. Elevated lipase and CRP caused us to suspect pancreatitis. Because an enlarged pancreas head was found on ultrasound, an endoscopic retrograde cholangio- and pancreaticography was performed with a pethidine-containing premedication. Thereafter, bilirubin, gamma-glutamyl transpeptidase and alkaline phosphatase increased dramatically. There was also a moderate elevation of aspartate aminotransferase and alanine aminotransferase. A second endoscopic retrograde cholangio- and pancreaticography with the same premedication was performed in order to exclude an undetected concretion. This led to a further increase of bilirubin. An association with the drugs given as premedication was therefore suspected, and in fact, a hypersensitivity reaction towards pethidine was confirmed by the lymphocyte transformation test. We thus conclude that pethidine caused an immunologically mediated hepatic injury.
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PMID:Dramatic increase in bilirubin after ERCP - pethidine as a possible cause of drug-induced hepatitis. 1466 Nov 25


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