The role of trypsinogen activation peptide in the early diagnosis of severe acute pancreatitis and the prediction of outcome / 临床外科杂志

Objective To explore the role of trypsinogen activation peptide( TAP)in the early di-agnosis of severe acute pancreatitis( AP)and the prediction of outcome. Methods Eighty-nine cases with pancreatitis were collected containing 45 cases of severe AP and 44 of mild AP. 32 cases of non-AP acute abdominal disease were chosen as control group. Blood of all patients was collected within 6h to measure TAP. ROC curve was used to analyze the results. Results The TAP was different among the three groups (p<0. 01);the TAP of patients with severe AP was the highest. ROC curve indicated that 2. 78 nmol/L was the best cutoff to define AP and non-AP;the sensitivity,specificity and accuracy was 88. 8%,100%and 91. 5%,respectively. 8. 55 nmol/L was used to define severe AP and mild AP;the sensitivity,speci-ficity and accuracy was 92. 9%,95. 2% and 88. 7%,respectively. 11. 20 nmol/L was used to predict the occurrence of complications;the sensitivity,specificity and accuracy was 75. 0%,90. 4% and 82. 2%,re-spectively. Conclusion The TAP can be used to diagnose AP,especially to identify severe AP. The TAP is also beneficial for predicting the outcome of patients with severe AP.

Relationship between Carbachol Hyperstimulation-induced Pancreatic Intracelluar Trypsinogen and NF-кB Activation in Rats in vitro / 华中科技大学学报（医学）（英德文版）

The relationship between intracelluar trypsinogen activation and NF-r,B activation in rat pancreatic acinar cells induced by M3 cholinergic receptor agonist (carbachoi) hyperstimulation was studied. Rat pancreatic acinar cells were isolated, cultured and treated with carbachol, the active pro- tease inhibitor (pefabloc) and NF-кB inhibitor (PDTC) in vitro. Intracelluar trypsin activity was measured by using a fluorogenie substrate. The activity of NF-кB was monitored by using electro- phoretic mobility shift assay. The results showed that after pretreatment with 2 mmol/L pefabloc, the activities of trypsin and NF-кB in pancreatic acinar cells treated with high concertrations of carbachol (10-3 mol/L) in vitro was significantly decreased as compared with control group (P＜0.01). The addi- tion of 10-2mol/L PDTC resulted in a significant decrease of NF-кB activities in pancreatic acinar cells after treated with high concertrations of carbachol (10-3 mol/L) in vitro, but the intracelluar trypsinogen activity was not obviously inhibited (P＞0.05). It was concluded that intracelluar trypsi- nogen activation is likely involved in the regulation of high concertrations of carbachol-induced NF-кB activation in pancreatic acinar cells in vitro. NF-кB activation is likely not necessary for high concertrations of carbachol-induced trypsinogen activation in pancreatic acinar cells in vitro.

Relationship between Carbachol Hyperstimulation-Induced Pancreatic Acinar Cellular Injury and Trypsinogen or NF-κB Activation in Rats in vitro / 华中科技大学学报（医学）（英德文版）

The relationship between M3 cholinergic receptor agonist (carbachol) hyperstimulationinduced pancreatic acinar cellular injury and trypsinogen activation or NF-κB activation in rats was studied in vitro. Rat pancreatic acinar cells were isolated, cultured and treated with carbachol, the active protease inhibitor (pefabloc), and NF-κB inhibitor (PDTC) in vitro. Intracellular trypsin activity was measured by using a fluorogenic substrate. The cellular injury was evaluated by measuring the leakage of LDH from pancreatic acinar cells. The results showed that as compared with control group, 10-3 mol/L carbachol induced a significant increase of the intracellular trypsin activity and the leakage of LDH from pancreatic acinar cells. Pretreatment with 2 mmol/L pefabloc could significantly decrease the activity of trypsin and the leakage of LDH from pancreatic acinar cells (P ＜0.01) following the treatment with a high concentration of carbachol (10-3 mol/L) in vitro. The addition of 10-2 mol/L PDTC didn't result in a significant decrease in the activity of trypsin and the leakage of LDH from pancreatic acinar cells treated with a high concentration of carbachol (10-3 mol/L) in vitro (P＞0.05). It was concluded that intracellular trypsinogen activation is likely involved in pancreatic acinar cellular injury induced by carbachol hyperstimulation in vitro. NF-κB activation may not be involved in pancreatic acinar cellular injury induced by carbachol hyperstimulation in vitro.

Urinary Trypsinogen Activation Peptide (TAP) levels in the patients with acute pancreatitis / 临床外科杂志

Objective To explore the changes of urinary Trypsinogen Activation Peptide (TAP) levels in patients with acute pancreatitis (AP).Methods We observed the association between urinary TAP concentration and severity of acute pancreatitis with competitive enzyme-linked immunosorbent assay(ELISA). Urine samples were collected for TAP concentration at admission,24,48,and 72 h from 57 patients with AP who presented within 48 h of the onset of symptoms and from 11 control patients. Results The median urinary TAP at admission for severe acute pancreatitis(SAP) (98 nmol/L) was signficantly higher than the median for both mild pancreatitis (22 nmol/L,P0.05).The peak median urinary TAP in severe eroup was seen at admission.In the following days,TAP concentrations decreased graduallg.Conclusion Breakthrough activation of trypsinogen in pancreatic interstitial and blood may be the key event in the development of SAP.