| 1. |
- Andrén Sandberg, Ake, et al.
(författare)
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Early prediction of severity in acute pancreatitis. Is this possible?
- 2002
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Ingår i: Journal of the Pancreas. - 1590-8577. ; 3:5, s. 25-116
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Tidskriftsartikel (refereegranskat)abstract
- One out of ten cases of acute pancreatitis develops into severe acute pancreatitis which is a life threatening disorder with a high mortality rate. The other nine cases are self limiting and need very little therapy. The specificity of good clinical judgement on admission, concerning the prognosis of the attack, is high (high specificity) but misses a lot of severe cases (low sensitivity). The prediction of severity in acute pancreatitis was first suggested by John HC Ranson in 1974. Much effort has been put into finding a simple scoring system or a good biochemical marker for selecting the severe cases of acute pancreatitis immediately on admission. Today C-reactive protein is the method of choice although this marker is not valid until 48-72 hours after the onset of pain. Inflammatory mediators upstream from CRP like interleukin-6 and other cytokines are likely to react faster and preliminary results for some of these mediators look promising. Another successful approach has been to study markers for the activation of trypsinogen such as TAP and CAPAP. This is based on studies showing that active trypsin is the initial motor of the inflammatory process in acute pancreatitis. In the near future a combined clinical and laboratory approach for early severity prediction will be the most reliable. Clinical judgement predicts 1/3 of the severe cases on admission and early markers for either inflammation or trypsinogen activation should accurately identify 50-60% of the mild cases among the rest, thus missing only 2-4% of the remaining severe cases. One problem is that there is no simple and fast method to analyze any of these parameters.
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| 2. |
- Hakansson, HO, et al.
(författare)
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Synthesis and localization of pancreatic secretory proteins in pancreatic acinar-like metaplasia in the distal part of the oesophagus
- 2003
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Ingår i: Scandinavian Journal of Gastroenterology. - : Informa UK Limited. - 1502-7708 .- 0036-5521. ; 38:1, s. 41560-41560
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Tidskriftsartikel (refereegranskat)abstract
- Background: Pancreatic acinar-like metaplasia has previously been described in the gastric mucosa and in the distal part of the oesophagus. The resemblance to pancreatic acinar cells prompted us to study the possible occurrence of secretory pancreatic proteins in these cells. Methods: Seven specimens obtained from the distal oesophagus at gastroscopy where routine microscopy showed pancreatic acinar-like metaplasia were selected for this study. Sections were subjected to immunohistochemical detection of trypsinogen, pancreatic elastase, procarboxypeptidase B and pancreatic secretory trypsin inhibitor using specific antisera. An alkaline-phosphatase-conjugated oligodeoxynucleotide probe, complementary to the transcript for trypsinogen 2 (anionic) was used for in situ hybridization. Results: Cells with pancreatic acinar-like metaplasia were immunoreactive to all pancreatic secretory proteins studied. In situ hybridization showed the presence of trypsinogen 2 mRNA in pancreatic acinar-like metaplasia. The pancreatic proteins were not seen in other cells in the distal oesophagus. Conclusion: Pancreatic acinar-like metaplasia is common in the distal oesophagus and pancreatic secretory proteins, including trypsininogen 2, are produced in the oesophageal metaplastic acinar cells. The biological significance of this finding has yet not been thoroughly studied.
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| 3. |
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| 4. |
- Muller, Christophe A., et al.
(författare)
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Corticosteroid-binding globulin: A possible early predictor of infection in acute necrotizing pancreatitis
- 2007
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Ingår i: Scandinavian Journal of Gastroenterology. - : Informa UK Limited. - 1502-7708 .- 0036-5521. ; 42:11, s. 1354-1361
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Tidskriftsartikel (refereegranskat)abstract
- Objective. Infected pancreatic necrosis is the main cause of death in patients with acute pancreatitis, and therefore its early prediction is of utmost importance. Endogenous cortisol metabolism plays a basic role both in the course of acute pancreatitis and in the process of infection. The purpose of this study was to analyze corticosteroid-binding globulin (CBG), total cortisol, calculated free cortisol and adrenocorticotropic hormone as potential early predictors in order to differentiate between infected pancreatic necrosis and sterile pancreatic necrosis in patients with acute pancreatitis. Material and methods. Serum levels of CBG, total cortisol, calculated free cortisol, and plasma levels of adrenocorticotropic hormone were determined in 109 consecutive patients with acute pancreatitis. C-reactive protein was measured as the control parameter. Thirty-five patients developed necrotizing pancreatitis and 10 developed infection of the necrosis. Blood was monitored for 6 days after the onset of pain; 30 healthy individuals served as controls. Results. Of all parameters only CBG showed a significant difference ( p = 0.0318) in its peak levels measured in the first 48 h in patients with sterile (26.5 mu g/ml, range 21.3-34.7) and infected (16.0 mu g/ml, range 15.2-25.0) necrosis at a cut-off level of 16.8 mu g/ml. That difference was further preserved for the first 6 days after onset of pain. Conclusions. In our group of patients, a decreased CBG level below 16.8 g/ml within the initial 48 h of acute pancreatitis was an early predictor of later infected pancreatic necrosis, with a positive predictive value of 100% and a negative predictive value of 87.5%.
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| 5. |
- Müller, C A, et al.
(författare)
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Serum levels of procarboxypeptidase B and its activation peptide in patients with acute pancreatitis and non-pancreatic diseases
- 2002
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Ingår i: Gut. - : BMJ. - 1468-3288 .- 0017-5749. ; 51:2, s. 229-235
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Tidskriftsartikel (refereegranskat)abstract
- Background: Carboxypeptidase B from the pancreatic gland may exist in three different molecular and immunoreactive forms: the proenzyme, the active enzyme, and the activation peptide. Aims: To investigate levels of procarboxypeptidase B (proCAPB) and its activation peptide in serum in acute pancreatitis to test the accuracy of these two variables as markers for the diagnosis of acute pancreatitis and for prediction of pancreatic necrosis. To elucidate whether leakage of proenzymes and activation of proenzymes reflect two different pathophysiological events in acute pancreatitis. Methods: Sera from patients with acute pancreatitis (n=85) and acute abdominal pain of non-pancreatic origin (n=53) were analysed for proCAPB and its activation peptide. Patients with pancreatitis were divided into necrotising (n=33) and oedematous attacks (n=52) using contrast enhanced computed tomography. Accuracy was determined using receiver operating characteristic curve analysis. Results: Immunoreactive carboxypeptidase B activation peptide (ir-CAPAP) concentration in serum on admission was 0.7 nmol/l (0-18.1) in patients with oedematous pancreatitis compared with 5.8 nmol/l (1.9-34) in patients with later development of pancreatic necrosis. Elevated levels of the activation peptide on admission correlated with an accuracy of 92% to later development of pancreatic necrosis. Ir-proCAPB concentration in serum on admission was 16.0 nmol/l (1.4-50.5) in all patients with acute pancreatitis versus 0.3 nmol/l (0-3.6) in patients with non-pancreatic acute abdominal disorders. Cases with oedematous pancreatitis had ir-proCAPB levels of 15.4 nmol/l (1.4-50.5) versus 19.1 nmol/l (2.7-36.1) in cases with later development of pancreatic necrosis. Measurement of the proenzyme can thus be useful for the diagnosis of acute pancreatitis (accuracy 99%) but levels did not correlate with later development of pancreatic necrosis (accuracy 56%). Conclusion: Leakage of proenzymes occurs in acute pancreatitis, irrespective of severity, while development of pancreatic necrosis occurs only when there is activation of the proenzymes.
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| 6. |
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| 7. |
- Sadic, Jalal, et al.
(författare)
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Bleeding peptic ulcer - time trends in incidence, treatment and mortality in Sweden.
- 2009
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Ingår i: Alimentary pharmacology & therapeutics. - : Wiley. - 1365-2036 .- 0269-2813. ; 30, s. 392-398
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Tidskriftsartikel (refereegranskat)abstract
- Abstract Background: The incidence of peptic ulcer disease was expected to decrease following the introduction of acid inhibitors and H. pylori eradication. Aim: This study analyses possible changes in the incidence of bleeding peptic ulcer, treatment and mortality over time. Methods: Residents of Malmö hospitalised for bleeding gastric or duodenal ulcer disease1987-2004 were identified in hospital databases (n=1610). The material was divided in 6-year periods in order to identify changes over time. All patients who had been submitted to emergency surgery (n=137) were reviewed. Results: The incidence rate for bleeding gastric or duodenal ulcers decreased by one half in males and by one third in females and emergency operations decreased significantly (9.2, 7.5 and 5.7% during the three time periods respectively (p<0.05). The postoperative mortality tended to decrease (9.7, 2.4 and 3.7% respectively) and the 30-day mortality rates in the whole material were 1.2, 3.6 and 3.4% during the different time periods. Conclusion: The incidence of bleeding gastric and duodenal ulcer disease has decreased markedly. Operative treatment has been replaced by endoscopic treatment. The bleeding ulcer related mortality was less than 4% and has not changed over time.
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| 8. |
- Segal, I, et al.
(författare)
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Acute pancreatitis in Soweto, South Africa: Relationship between trypsinogen load, trypsinogen activation, and fibrinolysis
- 2002
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Ingår i: American Journal of Gastroenterology. - 1572-0241. ; 97:4, s. 883-892
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Tidskriftsartikel (refereegranskat)abstract
- Objective: It is not known why acute pancreatitis in Soweto, South Africa, pursues an aggressive course. We sought clues from circulating trypsinogen load at admission as marker of initial acinar injury, trypsinogen activation using the carboxypeptidase B activation peptide as surrogate, proteinase inhibitors, the coagulation-fibrinolysis axis, indicators of inflammation, oxidative stress markers, and antioxidant status. This article reports on the first four aspects. Methods: The study involved 24 consecutive patients with a first attack. All of them were admitted within 24 h, and 22 were alcoholic. Urine was analyzed for anionic trypsinogen and the carboxypeptidase B activation peptide. Serum was tested for anionic and cationic trypsinogen, alpha(1) proteinase inhibitor and alpha(2) macroglobulin. Plasma from a subset was assayed for soluble fibrin, cross-linked fibrin degradation products (surrogates for thrombin and plasmin activity, respectively), and tissue-type plasminogen activator and inhibitor. Results: Soweto controls had higher serum anionic trypsinogen (p=0.004) and plasminogen activator:inhibitor ratio (p=0.047) than U.K. controls. The outcome of acute pancreatitis was mild in 17 but severe in seven with three deaths, two on day 2. In mild pancreatitis, intense plasmin activity (p<0.001) accompanied the surge in trypsinogen, especially anionic (p<0.001), but without increased thrombin activity and in five patients without trypsinogen activation. In severe pancreatitis, further significant increments in plasmin activity and trypsinogens were accompanied by increased thrombin activity (p=0.013) and trypsinogen activation (p=0.046). There was no correlation between surrogates of plasmin and thrombin activity, or between either and the carboxypeptidase B activation peptide. which showed a curvilinear relationship to total serum trypsinogen. Conclusions: The aggressive nature of alcoholic acute pancreatitis in Soweto seems to reflect early profound fibrinolysis, which precedes coagulation and is initially independent of trypsin. Subclinical acinar-cell injury and a profibrinolytic diathesis in outwardly healthy Sowetans may predispose to this problem.
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