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

The prognosis of an individual attack of acute pancreatitis is dependent on its severity and whether or not sepsis develops in or around the pancreas. Approximately 20-25% of patients with acute pancreatitis have a severe form of the disease which usually necessitates high dependency or intensive care management in the first week or two of illness. While most of these patients can readily be identified by experienced clinical judgement a proportion of them do not appear unduly ill at first presentation. For this reason a number of objective grading systems have been devised which identified the group of patients with the greatest likelihood of developing major complications and being at risk of death. The most commonly utilised systems in the United Kingdom are the eight factor Glasgow scoring scale and the APACHE II system. The measurement of C-reactive protein is also helpful and it has recently been shown that the combining of the Glasgow scoring system with CRP results in 80% or better sensitivity and specificity for those who develop major clinical complications. The body mass index (BMI) when over 30 kgs/m2 is also a useful marker of an adverse outcome, and CT scanning is another method of grading severity. The newer markers of interleukin 6 and PMN elastase have yet to be proved in a large prospective clinical study but do show considerable promise as being of value in identifying the patient at risk.
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PMID:Prognosis of acute pancreatitis. 766 94

A number of laboratory and clinical studies have shown that interleukin-6 is the principal mediator of the acute phase protein response. In this study the relationship between serum concentrations of interleukin-6 and C-reactive protein in acute pancreatitis are examined and the ability of interleukin-6 to discriminate between severe and mild attacks is assessed. We have studied 24 patients (10 severe and 14 mild). Serum samples were collected on admission, six hourly for 48 hours and then 12 hourly for a further three days. When the areas under the curves of individual patients were compared there was a strong correlation between the total production of interleukin-6 and C-reactive protein (r = 0.73) (Spearman rank correlation) and peak interleukin-6 and C-reactive protein concentrations (r = 0.75), suggesting a close relationship between interleukin-6 and C-reactive protein production. Both on admission and peak interleukin-6 concentrations were significantly higher in patients with severe than mild disease. There was no significant difference in on admission C-reactive protein concentrations, although significant differences were seen when peak concentrations were considered. Utilising a peak interleukin-6 concentration of > 130 u/ml, we were able to distinguish between severe and mild attacks of acute pancreatitis with a sensitivity of 100% and specificity of 71%. These figures were comparable with those for peak C-reactive protein, a C-reactive protein of > 150 mg/l detecting severe attacks of acute pancreatitis with a sensitivity of 90% and specificity of 79%. In view of the fact that interleukin-6 concentrations peaked earlier than those of C-reactive protein, interleukin-6 is capable of providing comparable, but earlier severity prediction than C-reactive protein.
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PMID:Role of interleukin-6 in mediating the acute phase protein response and potential as an early means of severity assessment in acute pancreatitis. 824 23

With the aim of studying the clinical usefulness and applicability of circulating levels of protease inhibitors, complement factors, acute phase reactants, and leukocytic enzymes in the prognostic evaluation of acute pancreatitis (AP), the present prospective multicenter study has been carried out. A total of 182 patients with AP have been included, to whom an exhaustive evolutive protocol has been applied from the time of their hospital admission (2-12 hr from the onset of the disease) until the 15th day of evolution in order to clearly define them. The severe episodes exhibit a greater consumption of alpha 2-macroglobulin, and C3 and C4 complement factors, as well as a greater increase of alpha 1-protease inhibitor, C-reactive protein and polymorphonuclear elastase than mild events, with regards to the underlying pathophysiological condition. The determination of the plasma levels of leukocytic elastase in the first hours of evolution allows a prediction of the severity of the acute pancreatitis event with a high reliability (predictive values that become higher than 90%). The clinical value of the remaining parameters analyzed, in this aspect, is less, being applicable to the monitoring of the disease.
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PMID:Monitoring of serum proteinase--antiproteinase balance and systemic inflammatory response in prognostic evaluation of acute pancreatitis. Results of a prospective multicenter study. 768 Mar 2

Tumour necrosis factor (TNF) is an early mediator of sepsis and multiple organ failure; increased concentrations in serum are also observed in acute pancreatitis. In the present study the predictive value of TNF and C-reactive protein (CRP) concentrations on admission were compared in order to differentiate complicated cases of acute pancreatitis from the mild course in 77 patients. Serum TNF concentration exceeded the detectable level only in seven of 77 patients (9 per cent), although complicated pancreatitis developed in 18 (23 per cent). The sensitivity and overall accuracy of TNF concentration in predicting severe disease were only 16 and 74 per cent respectively. The corresponding values for CRP (concentrations greater than 100 mg/l) were 84 and 74 per cent respectively. These data suggest that, in contrast with CRP, the early determination of peripheral blood TNF concentration is of no clinical value in assessing the severity of acute pancreatitis.
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PMID:Serum tumour necrosis factor compared with C-reactive protein in the early assessment of severity of acute pancreatitis. 774 9

The proportion of peripheral blood mononuclear cells expressing the T helper cell phenotype and levels of antiendotoxin core antibody, interleukin (IL) 6 and C-reactive protein (CRP) were determined within 48 h of admission in a group of 29 patients with acute pancreatitis (16 mild, 13 severe attacks). There was a significant decrease in the proportion of T helper cells (12.2 versus 34.9 per cent, P < 0.01) and significant increases in levels of IL-6 (69.5 versus < 10 pg/ml, P < 0.01) and CRP (119 versus 30.5 mg/l, P < 0.01) in severe compared with mild attacks. During the convalescent stage at 3 months after admission, severe attacks were characterized by a significant increase in the proportion of T helper cells compared with the acute period (22.4 versus 10.6 per cent, P < 0.01). A persistently low proportion of T helper cells was associated with residual pancreatic necrosis. The presence of circulating endotoxin was demonstrated in two mild and two severe attacks using the Limulus amoebocyte lysate assay, and abnormal levels of antiendotoxin core antibodies were found in 70 and 92 per cent of mild and severe attacks respectively. There was a strong inverse correlation between levels of CRP and the proportion of T helper cells in severe disease (r = -0.76, P = 0.004). Translocation of endotoxin from the gastrointestinal tract may partly explain the abnormal levels of T helper cells, IL-6 and CRP.
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PMID:Reduction in circulating levels of CD4-positive lymphocytes in acute pancreatitis: relationship to endotoxin, interleukin 6 and disease severity. 790 47

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

Currently, there is no specific therapy for acute pancreatitis. The management of the disease is supportive in approximately 80% of patients who suffer mild to moderate attacks. The remaining 20% of patients develop one or more major complications and require intensive care. Classification of acute pancreatitis according to severity is, therefore, necessary for proper management. Severe acute pancreatitis is detected early by the determination of circulating levels of polymorphonuclear elastase (PMN-E) and/or C-reactive protein (CRP). Patients with low levels of both PMN-E and CRP who have no major local or systemic complication of the disease can be classified as having mild acute pancreatitis. These patients require only supportive therapy and basic monitoring of vital functions. Patients with high levels of PMN-E and/or CRP and disease-related complications should be classified as severe. These patients should be managed in an intensive care unit for close monitoring of cardiovascular, respiratory, renal, metabolic, and hematological functions, and for early treatment of complications. Any organic dysfunction needs to be specifically treated. Development of extrapancreatic organ failure is closely related to the extent of pancreatic necrosis. Therefore, contrast-enhanced computed tomography (CT) should be performed in every patient classified as having severe acute pancreatitis. If sepsis develops, fine-needle ultrasound or CT-guided aspiration of necrotic tissue for bacteriological examination should be performed. Infected necrosis and persistent systemic failure under maximal intensive treatment require surgical treatment by necrosectomy and continuous lavage of the lesser sac. Late local complications of acute pancreatitis (i.e., abscesses and persistent pseudocyst) must be drained percutaneously or, more often, surgically.
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PMID:Management of severe acute pancreatitis. 805 21

Serum amylase continues to be the most widely used test to diagnose acute pancreatitis; however, its popularity does not appear to be justified. The serum amylase test has a poor sensitivity and specificity. Furthermore, it has an extremely low sensitivity in detecting acute alcoholic pancreatitis, which is the most common cause of acute pancreatitis in city hospitals. Older assay techniques for serum lipase were cumbersome and time-consuming. The newer methods seem to have overcome the disadvantages of the previous techniques. They are quick, reliable, and inexpensive. Recent studies indicate that serum lipase may be a better test to diagnose acute pancreatitis. Therefore, serum lipase should be used more frequently in the diagnosis of acute pancreatitis. Serum trypsin, although sensitive, is difficult to estimate and is not routinely available. Serum elastase offers no additional benefit over the serum amylase or lipase tests. Markers such as alpha 2-macroglobulin, RNase, phospholipase, and polymorphonuclear elastase predict severity of disease, but assay techniques for these agents are still experimental and confined to specialized centers. C-reactive protein is a reasonably reliable indicator of severity and, because it is universally available, should be used more frequently. Of the imaging techniques, computerized tomography scanning is the best method to delineate the pancreas; however, ultrasound is more cost-effective in clinical practice.
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PMID:Diagnostic tests for acute pancreatitis. 805 37

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

Dynamic computed tomography (CT) is the most accurate method for determining the extent of necrosis in acute pancreatitis. Debate exists, however, regarding patient selection and the optimal timing of CT. This study examined selection based on biochemical and/or clinical criteria and the influence of delayed dynamic CT performed 5-10 days after the onset of an attack. A total of 120 patients with acute pancreatitis were studied. Dynamic CT was performed if any of the following criteria were identified: a biochemically severe attack (according to Glasgow criteria) in the first 24 h, C-reactive protein (CRP) level above 120 mg/l in the first 3 days or failure of clinical resolution within 7 days. Of 42 patients selected for CT, five died from multisystem organ failure before day 5. There were no deaths or delayed complications in the 78 patients not selected for scanning. Positive Glasgow criteria alone in the scanned group had a sensitivity for predicting necrosis (as recognized by CT) of 22 per cent and a specificity of 20 per cent. Measurement of CRP level alone had a sensitivity of 26 per cent and specificity of 80 per cent. Failure of clinical resolution had a sensitivity of only 7 per cent but a specificity of 100 per cent. The combination of Glasgow criteria and CRP level had a sensitivity of 44 per cent and specificity of 100 per cent. Delayed complications (pseudocyst, five; infection, six) occurred only in patients with necrosis, and there were two deaths. An 'at-risk' group can be identified for CT on the basis of biochemical and clinical observations. Neither routine nor emergency dynamic CT in acute pancreatitis seems justified.
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PMID:Patient selection and timing of dynamic computed tomography in acute pancreatitis. 825 45


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