| 1. |
- Hjalmarsson, Claes, et al.
(författare)
-
Activated Protein C-Protein C Inhibitor Complex, Activation Peptide of Carboxypeptidase B and C-Reactive Protein as Predictors of Severe Acute Pancreatitis.
- 2009
-
Ingår i: Pancreatology. - : Elsevier BV. - 1424-3903. ; 9:5, s. 700-707
-
Tidskriftsartikel (refereegranskat)abstract
- Introduction: The concentration of carboxypeptidase B activation peptide (CAPAP) is proposed to be a predictor of severe acute pancreatitis. The activated protein C (APC)-protein C inhibitor (PCI; APC-PCI) complex in plasma could be useful in detecting the hypercoagulative condition in severe acute pancreatitis. Method: In this prospective study, mild (n = 50) and severe (n = 9) cases of acute pancreatitis were compared with respect to levels of CAPAP and APC-PCI, and sorted in time intervals from onset of symptoms to sampling. The peak values of the C-reactive protein (CRP) within the 1st week were also compared. Results: CRP detected the severe cases with a sensitivity of 0.89 and a specificity of 0.74 (cut-off level 200 mg/l). In the interval 0-72 h, CAPAP could predict the severity of the disease in serum and urine (sensitivity 0.52/0.29, specificity 0.73/0.93, cut-off 2 nM/60 nM). The level of APC-PCI in plasma could predict the severe condition in the interval 0-24 h after the onset of symptoms (sensitivity 0.6, specificity 0.66, cut-off level 0.54 mug/l). Conclusion: Of the parameters explored, CRP is still the best biochemical marker to distinguish between severe and mild acute pancreatitis. CAPAP could be useful in combination with other tests, but the APC-PCI complex's diagnostic time interval is too short to be used in the clinical routine. and IAP.
|
|
| 2. |
- Johansen, Dorthe, et al.
(författare)
-
Different Markers of Alcohol Consumption, Smoking and Body Mass Index in Relation to Risk of Pancreatic Cancer. A Prospective Cohort Study within the Malmö Preventive Project.
- 2009
-
Ingår i: Pancreatology. - : Elsevier BV. - 1424-3903. ; 9:5, s. 677-686
-
Tidskriftsartikel (refereegranskat)abstract
- Background/Aim: The association between alcohol consumption and pancreatic cancer is not clear. This study investigates different prediagnostic measurements of alcohol consumption, a laboratory marker (gamma-glutamyltransferase; gamma-GT), and a score measuring alcohol addiction (Mm-MAST), in relation to the risk of pancreatic cancer. Furthermore, the study investigated whether smoking and alcohol consumption interact with each other, or if the risk of pancreatic cancer associated with these factors is modified by obesity or weight gain. Methods: A cohort of 33,346 subjects provided prediagnostic information on the above factors. During a mean follow-up of 22.1 years, 183 cases of pancreatic cancer occurred. Cox's analysis yielded relative risks (RR) with 95% confidence intervals (CI). Results: The highest gamma-GT quartile was associated with a high risk of pancreatic cancer (RR = 2.15, 95% CI = 1.34-3.44), and this association was even stronger in subjects that reported a previous weight gain (RR = 3.61, 95% CI = 1.29-10.09). A high Mm-MAST score was also associated with pancreatic cancer (p = 0.02). Current smoking was associated with pancreatic cancer (RR = 2.34, 95% CI = 1.60-3.43), and obese smokers had an even higher risk (RR = 7.45, 95% CI = 1.65-33.64). Conclusion: High alcohol intake is associated with subsequent risk of pancreatic cancer and this risk may be higher following weight gain. The risk associated with smoking may be even higher in obese subjects. and IAP.
|
|
| 3. |
- Sadic, Jalal, et al.
(författare)
-
Bleeding peptic ulcer - time trends in incidence, treatment and mortality in Sweden.
- 2009
-
Ingår i: Alimentary pharmacology & therapeutics. - : Wiley. - 1365-2036 .- 0269-2813. ; 30, s. 392-398
-
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.
|
|
| 4. |
- Lindkvist, Björn, et al.
(författare)
-
A Prospective Cohort Study of Smoking in Acute Pancreatitis.
- 2008
-
Ingår i: Pancreatology. - : Elsevier BV. - 1424-3903. ; 8:1, s. 63-70
-
Tidskriftsartikel (refereegranskat)abstract
- Background/Aims: Little is known about risk factors for acute pancreatitis other than gallstones and alcohol consumption. The aim of this study was to investigate if smoking or body mass index (BMI) are associated with acute pancreatitis and to determine relative risks (RR) for acute pancreatitis related to smoking, BMI, and alcohol consumption. Methods: From 1974 to 1992, selected birth-year cohorts of residents in Malmo, Sweden (born 1921-1949) were invited to a health-screening investigation including physical examination, blood sampling and a questionnaire. In total, 33,346 individuals participated. Cases of acute pancreatitis were identified from diagnosis registries (n = 179). Incidence rates were calculated in different risk factor categories. A Cox's analysis revealed RR. Results: Current versus never smoking at baseline was associated with acute pancreatitis (RR 2.14, 95% confidence interval (CI) 1.48-3.09) after adjustment for age, sex, BMI and alcohol consumption. This association was stronger in heavy smokers (20-30 cigarettes/day) (RR 3.19, 95% CI 2.03-5.00). Smoking was associated with a RR of 3.57 (95% CI 0.98-13.0) for acute pancreatitis in subjects who reported no alcohol consumption. An increased risk for acute pancreatitis was also found for high versus low risk, self-reported alcohol consumption (RR 2.55, 95% CI 1.59-4.08) and for gamma-GT levels in the highest versus the lowest quartile (RR 2.14, 95% CI 1.32-3.49). There was also a weak correlation between BMI and acute pancreatitis. Conclusions: Smoking is associated with the incidence of acute pancreatitis in a dose-response manner. Copyright (c) 2008 S. Karger AG, Basel and IAP.
|
|
| 5. |
|
|
| 6. |
- Lindkvist, Björn, et al.
(författare)
-
Long-term nicotine exposure causes increased concentrations of trypsinogens and amylase in pancreatic extracts in the rat.
- 2008
-
Ingår i: Pancreas. - 0885-3177. ; 37:3, s. 288-294
-
Tidskriftsartikel (refereegranskat)abstract
- To develop radioimmunoassays (RIAs) for rat trypsinogens 1 and 2 and to investigate the effect of nicotine exposure on concentration and production of pancreatic zymogens in the rat. METHODS: Male Sprague-Dawley rats were supplied with either normal or nicotine-containing (0.77 mM) water for 28 days and were then killed. Rabbit antibodies for the activation peptides of trypsinogens 1 and 2 were obtained for use in the RIAs. Concentrations of the both trypsinogens in pancreatic extracts were measured by the RIAs after activation by enterokinase. DNA and amylase were measured using commercial kits. mRNA for trypsinogens 1 and 2, procolipase, and cholecystokinin receptor was measured by in situ hybridization. RESULTS: The specificity of the RIA for the trypsinogen 1 activation peptide was satisfactory. The RIA for the trypsinogen 2 activation peptide showed a limited cross-reaction toward the synthetic trypsinogen 1 activation peptide, but the importance of this cross-reaction was moderate when investigated in samples of activated trypsinogens. Weight gain was reduced in nicotine-treated animals. Concentrations of amylase, trypsinogen 1, trypsinogen 2, and the ratio of trypsinogen 2 to 1 were all increased in pancreatic extracts of nicotine-fed animals. Total DNA and mRNA for the trypsinogens, procolipase, and cholecystokinin receptor were not affected by nicotine exposure. CONCLUSIONS: The combination of increased proenzyme concentrations and unaffected mRNA levels suggests that nicotine impairs secretion rather than production of pancreatic zymogens.
|
|
| 7. |
- Muller, C. A., et al.
(författare)
-
Dexamethasone affects inflammation but not trypsinogen activation in experimental acute pancreatitis
- 2008
-
Ingår i: European Surgical Research. - : S. Karger AG. - 0014-312X .- 1421-9921. ; 40:4, s. 317-324
-
Tidskriftsartikel (refereegranskat)abstract
- Background/Aims: Trypsinogen activation and inflammation are early events in acute pancreatitis. This experimental study aimed to show the effects of dexamethasone on them. Methods: Cerulein and taurocholate pancreatitis were induced in 2 groups of 12 Wistar rats each. Six animals per group were injected with dexamethasone 1 h prior to the induction of acute pancreatitis. Amylase, phospholipase A2, TNF-alpha, IL-6, IL-10, alpha 2-antiplasmin in plasma and trypsinogen activation peptide (TAP) in urine were measured in healthy rats, then 0.5 and 6 h after pancreatitis induction. A severity score based on edema, necrosis and ascites was calculated at 6 h. TNF-alpha, IL-6 and IL-10 were measured 0.5 h after laparotomy in a control sham-operated group of 6 rats. Results: Inflammatory markers increased early in the course of both mild and severe acute pancreatitis and were significantly lowered by dexamethasone. The severity score was higher in taurocholate than in cerulein pancreatitis. It was significantly decreased by dexamethasone only in rats with mild pancreatitis. TAP remained unchanged in mild pancreatitis compared to healthy animals but increased late in the course of taurocholate pancreatitis. Trypsinogen activation was not affected by dexamethasone at all. Conclusion: Inflammation occurred earlier than the increase in urinary TAP in severe pancreatitis in rats. Dexamethasone inhibited inflammation but had no influence on TAP levels in experimental mild and severe acute pancreatitis. Copyright (C) 2008 S. Karger AG, Basel.
|
|
| 8. |
- Regnér, Sara, et al.
(författare)
-
Protease activation, pancreatic leakage, and inflammation in acute pancreatitis: differences between mild and severe cases and changes over the first three days.
- 2008
-
Ingår i: Pancreatology. - : Elsevier BV. - 1424-3903. ; 8:6, s. 600-607
-
Tidskriftsartikel (refereegranskat)abstract
- BACKGROUND/AIMS: The pathophysiology of acute pancreatitis (AP) may be studied using markers of protease activation (active carboxypeptidase B (aCAP), the activation peptide of carboxypeptidase B (CAPAP)), leakage of pancreatic enzymes (trypsinogen-2, procarboxypeptidase B (proCAP), amylase), and inflammation (monocyte chemoattractant protein-1 (MCP-1), CRP). METHODS: This prospective study included 140 cases of AP. Mild (n = 124) and severe (n = 16) cases were compared with respect to serum levels of trypsinogen-2, proCAP, amylase, aCAP, CAPAP (serum/urine), MCP-1 (serum/urine) and CRP on days 1, 2 and 3 from onset of symptoms. All patients with information on all 3 days were included in a time-course analysis (n = 44-55, except amylase: n = 27). RESULTS: High levels in severe versus mild cases were seen for trypsinogen-2, CAPAP in serum and urine, and MCP-1 in serum on days 1-3. No differences were seen for proCAP, amylase and aCAP. MCP-1 in urine was significantly elevated on day 1-2, and CRP on day 2-3. CAPAP and MCP-1 levels peaked early and stayed elevated for 48 h in serum. CONCLUSION: Protease activation and inflammation are early events in AP, with high levels of these markers within 24 h. Protease activation declines after 48 h, whereas inflammation is present for a longer time.
|
|
| 9. |
- Muller, Christophe A., et al.
(författare)
-
Corticosteroid-binding globulin: A possible early predictor of infection in acute necrotizing pancreatitis
- 2007
-
Ingår i: Scandinavian Journal of Gastroenterology. - : Informa UK Limited. - 1502-7708 .- 0036-5521. ; 42:11, s. 1354-1361
-
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%.
|
|
| 10. |
- Lindkvist, Björn, et al.
(författare)
-
Cathepsin B activates human trypsinogen 1 but not proelastase 2 or procarboxypeptidase B
- 2006
-
Ingår i: Pancreatology. - : Elsevier BV. - 1424-3903. ; 6:3, s. 224-231
-
Tidskriftsartikel (refereegranskat)abstract
- Background/Aims: Activation of trypsinogen to trypsin is a crucial step in the development of acute pancreatitis. The cause of this activation is not known although suggested explanations include autoactivation, cathepsin B-mediated activation and activation by mast cell tryptase. The aim of this study was to investigate cathepsin B and tryptase activation of pancreatic zymogens. Methods: Trypsinogen-1, proelastase, and procarboxypeptidase B were purified from human pancreatic juice. Human cathepsin B and beta I- tryptase are commercial products. Activation and degradation of zymogens were measured by activity towards specific substrates for trypsin and pancreatic elastase, ELISAs for procarboxypeptidase B and its activation peptide, and a radioimmunoassay for the trypsinogen activation peptide. Results: Cathepsin B caused activation of trypsinogen-1 with a trypsin yield of about 30% of that produced by enterokinase. Proelastase and procarboxypeptidase B was not activated by cathepsin B. None of the zymogens were inactivated by cathepsin B. Neither monomeric nor tetrameric tryptase could activate any of the examined zymogens. Conclusion: Cathepsin B is a competent activator of trypsinogen-1, although not as efficient as enterokinase. If cathepsin B is to play a role in protease activation in acute pancreatitis, this most probably occurs by activation of trypsinogen.
|
|
