Is the association of serum lipase with beta2-microglobulin or C-reactive protein useful for establishing the diagnosis and prognosis of patients with acute pancreatitis?

In the Emergency Department it is mandatory to establish the diagnosis and the prognosis of acute pancreatitis as soon as possible. To evaluate whether the association of serum lipase either with serum beta2-microglobulin or with C-reactive protein allows simultaneously to establish the diagnosis and the prognosis of acute pancreatitis, 96 patients with acute abdomen were studied. Fifty-eight patients had non-pancreatic acute abdomen and the remaining 38 had acute pancreatitis: 23 mild acute pancreatitis, and 15 severe acute pancreatitis. Forty healthy subjects were studied as controls. Lipase, beta2-microglobulin and C-reactive protein were determined in the serum of all subjects, using commercial kits. One patient with acute pancreatitis was not correctly classified when lipase was used to discriminate between patients with non-pancreatic acute abdomen and those with acute pancreatitis. For the discrimination of patients with severe acute pancreatitis from those with the mild form of the disease in the remaining 37 acute pancreatitis patients, beta2-microglobulin had a sensitivity of 53.3 %, specificity of 81.8%, and prognostic accuracy of 70.3 % (27 of the 37 patients correctly classified); 87.5 % of the 96 cases were correctly classified. C-reactive protein showed a lower prognostic accuracy than beta2-microglobulin: sensitivity 86.7%, specificity 45.5%, accuracy 62.2 %; 84.4 % of the cases were correctly classified. Using the polychotomous logistic regression analysis we found the same accuracy in discriminating between patients with acute pancreatitis and those with non-pancreatic acute abdomen (99.0%) but a lower accuracy (54.1%) between patients with severe acute pancreatitis and those with the mild form of the disease. Our study shows that the association of serum lipase with beta2-microglobulin or with C-reactive protein is not useful in simultaneously establishing the diagnosis and prognosis of acute pancreatitis.     

Chronic pancreatitis, acute pancreatitis

MRCP has been recognized as a safe and noninvasive diagnostic method. In the present study we evaluated the usefulness of MRCP in diagnosis of chronic and acute pancreatitis. Two-dimensional fast asymmetric spin-echo (FASE) MRCP was performed in 40 patients with chronic pancreatitis and 13 with acute pancreatitis. In 29 patients (72.5%) with chronic pancreatitis and 9 (66.7%) with acute pancreatitis, main pancreatic duct (MPD) was visualized entirely. MRCP could demonstrate the characteristic findings of chronic pancreatitis such as dilatation and irregularity of MPD in most cases. In acute pancreatitis, MRCP indicated that MPD was normal in diameter, but irregular in configuration compared with that of the control group. MRCP may facilitate the diagnosis of chronic and acute pancreatitis.     

Amylase activity of parotid saliva in acute and chronic pancreatitis

The activity of the alpha-amylase was estimated in the parotid resting saliva of 17 subjects without evidence of pancreatic disease, 17 patients with chronic relapsing pancreatitis in the intervals between acute attacks, and also in 4 patients with acute pancreatitis and 3 patients with an acute attack of chronic relapsing pancreatitis. In the patients with chronic relapsing pancreatitis between attacks the concentration, output and specific activity of the salivary amylase were significantly lowered. The patients with acute pancreatitis exhibited salivary amylase concentrations in the uppper normal to grossly supranormal range, whereas those of the patients with acute attacks of chronic relapsing pancreatitis were distinctly reduced. Unlike the amylase output, the amylase concentration was independent of the rate of salivary flow. Simultaneous infusion of secretin and pancreozymin produced a significant increase in the parotid salivary amylase levels in both the patients without pancreatic disease and in those with chronic relapsing pancreatitis between acute attacks.     

Evaluation of the clinical usefulness of APACHE II and SAPS systems in the initial prognostic classification of acute pancreatitis: a multicenter study

The clinical usefulness of the APACHE II and SAPS systems in the early prognostic classification of patients with acute pancreatitis has been evaluated in a prospective multicenter study. We aimed to identify early those patients with acute pancreatitis who should be monitored closely to expedite the detection and treatment of complications. One hundred eighty-two patients with acute pancreatitis were included; 28 were classified as severe, having developed at least one major complication of the disease. The scores obtained through the APACHE II and SAPS systems in these severe cases were significantly higher than the scores in the mild cases of acute pancreatitis (p < 0.001). The sensitivity of these systems in the prognostic classification of acute pancreatitis was 70.4% for APACHE II and 66.7% for SAPS, and the specificity was 79.1% for both. When applying APACHE II and SAPS systems in the early phase of acute pancreatitis, the possibility of misdiagnosing the severity exists, thus limiting the application of these systems in the initial assessment of prognostic classification. In conclusion, APACHE II and SAPS systems are of limited clinical utility in the early prognostic evaluation of acute pancreatitis because of their low positive predictive value.     

Results and consequences of frequent quality control of quantitative clinical 1H-MR-spectroscopy

BACKGROUND: The cut-off point of serum C-reactive protein to differentiate the mild from the severe form of acute pancreatitis is still debated; data concerning the C-reactive protein pattern in assessing the severity of acute biliary pancreatitis are lacking. AIM: To define the best cut-off point in differentiating the severe from the mild form of acute biliary pancreatitis. PATIENTS: Fifty patients with acute biliary pancreatitis: 34 patients with mild pancreatitis and 16 with the severe form of the disease were studied. METHODS: Serum C-reactive protein concentrations were assessed in all patients upon admission and for the following 5 days. RESULTS: No significant difference in serum C-reactive protein levels was found in the first 2 days in patients with mild pancreatitis compared to those with the severe form of the disease. Using a cut-off point of 11 mg/dl, the sensitivity of serum C-reactive protein in assessing the severity of acute pancreatitis during the first two days of the study was 9% and 57%, the specificity, 93% and 81%, and the accuracy 71% and 74%, respectively. CONCLUSIONS: Serum determination of C-reactive protein in the first 48 hours of the disease is not a reliable marker of the severity of acute biliary pancreatitis.     

Postoperative changes in the coagulation and fibrinolytic systems in endoluminal stent-graft treatment of thoracic aortic aneurysms

Length of stay (LOS) predictions in acute pancreatitis could be used to stratify patients with severe acute pancreatitis, make treatment and resource allocation decisions, and for quality assurance. Artificial neural networks have been used to predict LOS in other conditions but not acute pancreatitis. The hypothesis of this study was that a neural network could predict LOS in patients with acute pancreatitis. The medical records of 195 patients admitted with acute pancreatitis were reviewed. A backpropagation neural network was developed to predict LOS >7 days. The network was trained on 156 randomly selected cases and tested on the remaining 39 cases. The neural network had the highest sensitivity (75%) for predicting LOS >7 days. Ranson criteria had the highest specificity (94%) for making this prediction. All methods incorrectly predicted LOS in two patients with severe acute pancreatitis who died early in their hospital course. An artificial neural network can predict LOS >7 days. The network and traditional prognostic indices were least accurate for predicting LOS in patients with severe acute pancreatitis who died early in their hospital course. The neural network has the advantage of making this prediction using admission data.     

Clinical value of pancreatitis-associated protein in acute pancreatitis

OBJECTIVES: Pancreatitis-associated protein (PAP) is a secretory protein that is overexpressed by the pancreas during acute pancreatitis. This study was carried out to assess the clinical value of PAP in acute pancreatitis, particularly its ability to indicate the severity of the disease. METHODS: Twenty-one healthy subjects, 58 patients with acute pancreatitis, and 20 patients with nonpancreatic acute abdomen were studied. In addition to serum PAP concentration, serum concentrations of amylase, lipase, and C-reactive protein (CRP) were measured at admission and, in patients with acute pancreatitis, during the following 5 days. RESULTS: On admission, serum PAP concentrations were abnormally high in 46 of the 58 patients with acute pancreatitis (79%); serum amylase, in 57 patients (98%); serum lipase, in all patients (100%); and serum CRP, in 40 patients (69%). During the subsequent days of the study, PAP and CRP tended to increase, whereas amylase and lipase decreased. No significant differences in PAP or amylase and lipase concentrations were found between patients with mild pancreatitis and those with severe pancreatitis during the entire study period, whereas from the third day to the sixth day, CRP concentrations were significantly higher in patients with severe pancreatitis than in those with mild pancreatitis. Among the 20 patients with nonpancreatic acute abdomen, PAP concentrations were abnormally high in 10 (50%), whereas amylase concentrations were abnormally high in five (25%), and lipase concentrations were high in two (10%). CONCLUSIONS: Our results indicate that the clinical value of PAP in acute pancreatitis is quite limited and, in particular, that PAP is not a useful marker for determining the severity of the disease.     

Oxidative stress: an important phenomenon with pathogenetic significance in the progression of acute pancreatitis

BACKGROUND: Reactive oxygen species and related oxidative damage have been implicated in the initiation of acute pancreatitis. Changes in these parameters during disease progression merit further investigation. AIMS: To evaluate changes and the clinical relevance of superoxide radicals, endogenous antioxidants, and lipid peroxidation during the course of acute pancreatitis. PATIENTS AND METHODS: Superoxide radicals (measured as lucigenin amplified chemiluminescence), ascorbic acid, dehydroascorbic acid, alpha tocopherol, and lipid peroxidation (measured as thiobarbiturate reactive substances) were analysed in blood samples from 56 healthy subjects, 30 patients with mild acute pancreatitis, and 23 patients with severe acute pancreatitis. The association with grades of disease severity was analysed. Measurements were repeated one and two weeks after onset of pancreatitis. RESULTS: In the blood from patients with acute pancreatitis, there were increased levels of the superoxide radical as well as lipid peroxides. There was notable depletion of ascorbic acid and an increased fraction of dehydroascorbic acid. Changes in alpha tocopherol were not great except in one case with poor prognosis. Differences between severe and mild acute pancreatitis were significant (p < 0.01). Variable but significant correlations with disease severity scores were found for most of these markers. The normalisation of these indexes postdated clinical recovery one or two weeks after onset of disease. CONCLUSIONS: Heightened oxidative stress appears early in the course of acute pancreatitis and lasts longer than the clinical manifestations. The dependence of disease severity on the imbalance between oxidants and natural defences suggests that oxidative stress may have a pivotal role in the progression of pancreatitis and may provide a target for treatment.     

Seizure control after stimulation of the vagus nerve: clinical outcome measures

Our objective was to determine whether pleural effusion is a predictor of severity in acute pancreatitis and, if so, whether it is an independent predictor. One hundred ninety-six consecutive cases of acute pancreatitis from October 1, 1994, to September 30, 1995, were reviewed. Medical records were analyzed for evidence of pleural effusion by chest radiograph and severe acute pancreatitis by identification of pancreatic necrosis or organ system dysfunction. Data were analyzed to determine if identification of pleural effusion provided an early sign of severity. Among 135 patients who underwent chest radiography, pleural effusion was seen in 16 of 19 (84.2%) with severe pancreatitis and 10 of 116 (8.6%) of patients with mild pancreatitis (p < 0.001). Pleural effusion was noted in severe pancreatitis prior to clinical or computed tomography evidence of severity in only 20% of cases. Pleural effusion is strongly associated with severity in acute pancreatitis but provides independent information on severity in only a minority of cases.     

Mucinous cystadenoma of the pancreas as a cause of acute pancreatitis

Acute pancreatitis is only rarely the first presentation of a cystic neoplasm of the pancreas. Mucinous cystadenomas have not been reported to be a cause of acute pancreatitis; however, we present two cases of mucinous cystadenoma of the pancreas which have caused acute pancreatitis. Both patients (female) presented acute abdominal pain, with serum amylase elevation and ultrasound scan (US) and computed tomography (CT) evidence of moderate pancreatitis, which resolved with medical treatment; fluid collection in the distal pancreas had been misinterpreted as a pseudocyst. There was no history of alcohol abuse or gallstone disease. After distal pancreatectomy the diagnosis of mucinous cystadenoma was confirmed; in one case a large pseudocyst was associated with this diagnosis. Pre-operative differential diagnosis between inflammatory and neoplastic cysts is difficult, especially when the patient's first presentation is due to an episode of acute pancreatitis. A neoplastic cyst should be considered when acute pancreatitis attacks occur in non-alcoholic women, who do not have gallstone disease.     

What place for endoscopic sphincterotomy in treatment of acute pancreatitis?

STUDY AIM: A prospective study was undertaken in order to evaluate the effects of endoscopic sphincterotomy on the evolution of biliary and idiopathic acute pancreatitis. PATIENTS AND METHODS: Among 320 patients with acute pancreatitis observed from 1986 to 1996, 118 were excluded from the study for etiological reasons and 137 were included for an endoscopic sphincterotomy within 72 hours from their admission. There were nine technical failures and 128 endoscopic sphincterotomies were performed. Sixty-five eligible patients were not included for logistic problems or patients' refusal; they can be considered as a "control group". RESULTS: The mortality rate of endoscopic sphincterotomy was 0 and the morbidity rate 2.1%. The mortality rate of acute pancreatitis was 3.1% in the sphincterotomy group vs 7.6% in the control group (P = 0.1) (NS) and the morbidity rate 25% versus 32% (P > or = 0.1) (NS). CONCLUSION: These results suggest that endoscopic sphincterotomy could be beneficial in acute biliary or idiopathic pancreatitis but they are not statistically significant. Endoscopic sphincterotomy does not increase the severity of acute pancreatitis and can be considered particularly in cases of gallstone pancreatitis but it should be performed less than 48 hours after the onset of acute pancreatitis.     

Role of endogenous and exogenous cholecystokinin in experimental acute pancreatitis induced in rats by the duodenal loop technique

The role of endogenous cholecystokinin (CCK) release and exogenous CCK-8 administration in the development and progression of acute pancreatitis and in the early recovery phase of acute pancreatitis were investigated in rats with closed duodenal loop (CDL)-induced pancreatitis. The subcutaneous injection of CCK-8 (2 micrograms/kg) stimulated a physiological level of pancreatic enzyme secretion in normal control rats, but did not lead to any biochemical or histological evidence of acute pancreatitis. A higher dose of CCK-8 (8 micrograms/kg), however, did produce both biochemical and histological evidence of acute pancreatitis in the normal control rats. When 2 micrograms/kg of CCK-8 was injected subcutaneously in rats 6 and 12 h after the creation of the CDL, neither the biochemical nor the histological findings of acute pancreatitis showed any progression compared with the changes in controls given no CCK-8. Serum CCK levels, measured by radio-immunoassay, increased significantly from mean levels of 5.39 pg/ml (+/- 0.95 SD) before creation of the CDL to 42.06 pg/ml (+/- 2.27 SD) 6 h after, and 41.95 pg/ml (+/- 1.88 SD) 12 h after its creation (P < 0.01). The difference between serum CCK levels at 6 and 12 h was not statistically significant. Following the release of the loop, serum CCK levels decreased gradually, especially in rats in which the loop was released 6 h after being created. Although no marked biochemical and histological changes of acute pancreatitis were observed following the administration of 2 micrograms/kg of CCK-8 to rats upon release of the loop 6 h and 12 h after its creation, a higher dose of CCK-8 (8 micrograms/kg) in these rats adversely affected both the biochemical and histological findings of acute pancreatitis. Based on these findings, it was concluded that neither endogenous CCK release, as a result of the CDL, nor physiological stimulation of the pancreas by exogenous CCK-8 administration, caused progression from edematous to hemorrhagic acute pancreatitis, and neither CCK treatment had any adverse effect on the early recovery phase of CDL-induced acute pancreatitis. A pharmacological dose of CCK, however, exacerbated the acute pancreatitis, even in the early recovery stage.     

Acute pancreatitis: conservative therapy)

Conservative treatment of acute pancreatitis is symptomatic and depends on the severity of the disease. For treatment of mild pancreatitis, fasting and intravenous application of fluids and analgetics is usually sufficient. Patients with severe pancreatitis should be monitored in an Intensive Care Unit and may require antibiotics. For treatment of acute pancreatitis, a large number of interventions has been suggested. They include nasogastric tubes, drugs which reduce pancreatic and gastric secretion, and treatments which inhibit activated proteases. Controlled studies have shown that most of these measures are ineffective. The value of early ERCP in acute pancreatitis is still under debate. ERCP appears to be helpful in biliary pancreatitis, especially if choledocholithiasis is present. Surgery should be reserved to those patients who do not respond to conservative treatment.     

Acute pancreatitis due to pyritinol: an immune-mediated phenomenon

A 23-year-old man experiencing three episodes of acute pancreatitis of undetermined etiology is described. Repeated questioning revealed that all three events had occurred after intake of the drug pyritinol. Controlled rechallenge with a single dose of the drug led to a fourth episode of acute pancreatitis. Skin testing was negative, but lymphocyte stimulation tests and double fluorescence analysis detected pyritinol-activated CD4 and CD8 lymphocytes. Together with the clinical observation that the intervals between drug intake and start of symptoms of acute pancreatitis became shorter with repeated exposure, the data are consistent with an immune-mediated origin of the pancreatitis. Pyritinol has to be added to the list of drugs capable of inducing acute pancreatitis.     

Phenformin-associated pancreatitis

Although phenformin has been previously reported to be associated with acute pancreatitis, little emphasis of this association has been made in the literature. We report the case of a 70-year-old diabetic man who developed acute hemorrhagic pancreatitis and severe lactic acidosis while taking phenformin. The patient was not taking any other medications, nor did he have any of the known metabolic conditions associated with pancreatitis. We review the four previously published cases of patients who developed acute pancreatitis while taking phenformin. Three of those patients also developed lactic acidosis, a well-known complication of phenformin therapy. Although phenformin has been reported to increase the serum amylase activity and to alter the content of the pancreatic secretions in response to various stimuli, the manner in which the drug might cause acute pancreatitis remains completely unknown.     

Dynamic activity of bladder neck and external sphincter in ejaculation

Macroamylasemia and acute pancreatitis are both associated with a high serum amylase. The former is an incidental laboratory finding and seems to have no apparent clinical significance or specificity. On the other hand, acute pancreatitis is a serious illness demanding recognition and treatment. Persistently normal pancreatic scans convincingly exclude acute pancreatitis and should alert one to the possible presence of macroamylasemia.     

Acute pancreatitis associated with the use of lisinopril

OBJECTIVE: To report a case of acute pancreatitis associated with lisinopril use. CASE SUMMARY: A 67-year-old man with no past history of pancreatitis or its associated risk factors developed acute pancreatitis after taking lisinopril for two years. To date, the use of angiotensin-converting enzyme (ACE) inhibitors and development of pancreatitis has been described in the literature with captopril, enalapril maleate, and one case temporally related to lisinopril use. CONCLUSIONS: The use of ACE inhibitors as first-line agents in controlling hypertension and congestive heart failure has increased. In addition to monitoring for efficacy and commonly reported adverse effects, clinicians need to be aware that acute pancreatitis may occur with all ACE inhibitors.     

Fibrotic stricture of the extrapancreatic biliary tract: a new complication of acute pancreatitis. Two cases

Two cases of fibrotic stricture of the extrapancreatic common bile duct were observed 3 and 5.5 months after severe acute alcoholic pancreatitis. The diagnosis was made by endoscopic retrograde cholangiography in both cases. Although colonic or ureteric stenosis have been reported after acute pancreatitis, this is the first report of extrapancreatic biliary stricture occurring after acute pancreatitis. The strictures could have arisen by either an enzymatic or ischemic mechanism. Outcome was favorable after surgical hepaticojejunostomy.     

Thoracoscopic surgery using voice controlled robot for spontaneous pneumothorax

Although there is abundant literature on the association of L-asparaginase and acute pancreatitis in patients undergoing chemotherapy, few studies have investigated the usefulness of pancreatic enzyme measurement in the early diagnosis of L-asparaginase-induced acute pancreatitis. We measured levels of serum pancreatic enzymes before, during, and after L-asparaginase therapy in nine children with acute lymphocytic leukaemia or non-Hodgkin lymphoma. Serum levels of amylase, pancreatic isoamylase, and lipase did not change between the 1st and 30th day of L-asparaginase administration. However, the serum trypsin and elastase- levels, 10 and 20 days after beginning L-asparaginase therapy, were significantly higher than those prior to therapy. CONCLUSION: L-asparaginase may induce subclinical pancreatitis and the estimation of serum trypsin and elastase-1 may be useful in the early diagnosis of L-asparaginase-induced acute pancreatitis.