Objective To study the basic and clinical achievements in diagnosis and therapy of hereditary pancreatitis. Methods Related literatures of recent years were reviewed. Results Hereditary pancreatitis was a rare type of pancreatitis, with an estimated penetrance of 80%, and was believed to be caused by a mutation in the cationic trypsinogen gene. Patients with hereditary pancreatitis had a high frequency of pancreatic cancer.Conclusion The progress has been made on hereditary pancreatitis and has given us many useful suggestions for a better understanding about this difficult medical problem.
Objective To investigate the significance of urinary trypsinogen-2 dipstick test and the ratio of urinary amylase to urinary creatinine for the diagnosis of acute pancreatitis(AP).Methods A total of 57 consecutive patients who were suspected as AP presenting with abdominal pain at the emergency department experienced the test of serum and urinary amylase, urinary creatinine assay, urinary trypsinogen-2 dipstick and ultrasonography. Results There were 18 patients diagnosed as acute pancreatitis, the serum amylase assay had a sensitivity of 88.9 percent (cutoff value, 300 U per liter) and a specificity of 87.2 percent, the sensitivity and specificity of the urinary amylase assay and the ratio of urinary amylase to urinary creatinine were 88.9 (cutoff value, 2000 U per liter), 94.4 (cutoff value, 120 U per mmol Cr), 84.6 and 89.7 percent, respectively. The sensitivity and specificity of the urinary trypsinogen-2 test strip were 94.4 and 92.3 percent. The sensitivity of the ultrasonography were 88.9 percent. Conclusion Urinary trypsinogen-2 dipstick test is a good index for the diagnosis of AP. The ratio of urinary amylase to urinary creatinine is also a useful index and may be better than urinary amylase for the diagnosis of AP.
【Abstract】Objective To investigate the production and possible significance of plasma trypsinogen activation peptides (TAP) in rat experimental acute pancreatitis. Methods Ninety SD rats were randomly allocated to five groups: group EP with retrograde ductal infusion of 3%sodium taurocholate; group NP with retrograde ductal infusion of 5%sodium taurocholate; group TP with retrograde ductal infusion of 3%sodium taurocholate and ulinastatin(UTI) intravenous infusion half an hour later; group CP with 0.9% NS retrograde ductal infusion; group OP with sham operation. Animals in each group were killed 3h,6h and 24h after infusion. Plasma TAP was determined by EIA.The histological severity of the pancreas were assessed by Schmidt method. Results The pancreatic pathological changes in group NP was significantly severe than in group EP. At 3h and 6h after infusion, plasma TAP concentration of group NP (4.798±0.169)nmol/L and (3.999±0.299)nmol/L were significant higher than that of group EP(2.416±0.148)nmol/L and (3.356±0.211)nmol/L. At 6h after infusion plasma TAP concentration of group TP 〔(1.611±0.113)nmol/L〕 was significant lower than that of group EP(3.356±0.211)nmol/L. The difference of plasma TAP concentration between group EP and group NP appeared prior to the difference of the histopathological changes of pancreas between two groups. Conclusion Plasma TAP concentration is connected with the severity of sodium taurocholate-induced rat pancreatitis. Plasma TAP concentration may be used as a marker for early assessment of the severity of this experimental acute pancreatitis.
Objective To explore the secretion law of high mobility group box 1（HMGB1）in rat pancreatic acinar cells induced by trypsin activation peptide（TAP）and release of HMGB1 affected by ethyl pyruvate（EP）. Methods The experiment was performed in 12 SD rats. The pancreatic acinar cells of rats were taken out and then separated into three groups：control group， TAP group， and EP group. TAP was added into TAP group and EP group（keep TAP at a final concentration of 3 nmol/L）， respectively， but EP was added into EP group only （keep EP at a final concentration of 28 mmol/L）. The expressions of HMGB1 mRNA and protein were detected by using real-time quantitative reverse transcription polymerase chain reaction（RT-PCR）or Western blot at 3 h， 6 h， 12 h， and 24 h time point， respectively. The relationship between HMGB1 and TAP action time was explored by rank correlation. Results Compared with control group， the expressions of HMGB1 mRNA and protein were increased with prolongation of the TAP action in TAP group and EP group（P＜0.05）. Compared with TAP group， the expressions of HMGB1 mRNA and protein were decreased in EP group（P＜0.05）. The expressions of HMGB1 mRNA and protein were increased with prolongation of the TAP action（P＜0.05）， and were highest at 12 h time point（P＜0.01）in TAP group. There were positive correlation between the expressions of HMGB1 mRNA and protein and TAP action time（rs=0.971， P＜0.01；rs=0.966， P＜0.01）.Conclusions TAP can induce the release of HMGB1 in pancreatic acinar cells. There is positive relationship between TAP in early stage and HMGB1 in later period of acute pancreatitis. EP can inhibit the release of HMGB1.