Hyperamylasemia after cardiac surgery. Incidence, significance, and management

The significance of hyperamylasemia and its relationship to pancreatitis after cardiac surgery is controversial. Three hundred consecutive patients undergoing cardiopulmonary bypass were prospectively studied to determine the incidence and significance of postoperative hyperamylasemia. Ninety-six of three hundred patients (32%) developed hyperamylasemia. Fifty-six patients (19%) were classified as having isolated hyperamylasemia because they were asymptomatic and had normal serum lipase. Thirty-two patients (10.7%) had subclinical pancreatitis defined as elevation of serum amylase and lipase or pancreatic isoamylase. Many of these patients had mild gastrointestinal symptoms that were self-limited. Eight patients (2.7%) had overt pancreatitis documented by clinical findings, biochemical abnormalities, and computed tomography (CT) scan or autopsy. Isoamylase analysis demonstrated that isolated hyperamylasemia usually originated from nonpancreatic sources. However, hyperamylasemia occurring in conjunction with abdominal signs and symptoms or elevated serum lipase was almost always pancreatic in origin. Patients with hyperamylasemia had a significantly higher mortality rate (seven of 96 patients, 7.5%) than those with normal serum amylase (two of 204 patients, 0.9%) (p less than 0.01) even when the amylase was nonpancreatic in origin (five of 56 patients, 9%). The reason that nonpancreatic hyperamylasemia is associated with increased postoperative mortality is not established but may represent a variety of metabolic aberrations or tissue injuries. It is concluded that 1) hyperamylasemia after cardiopulmonary bypass is a marker of potential clinical importance, and 2) pancreatitis in this setting is more common than previously recognized and is a potentially lethal complications. Successful treatment depends on early diagnosis and aggressive treatment.     

Foregut mucosal defects: an etiology of hyperamylasemia

To evaluate a preliminary correlation of hyperamylasemia to upper gastrointestinal bleeding, total serum amylase and serum isoamylase profiles were determined in 50 patients with upper gastrointestinal bleeding. Etiologies of the bleeding were determined in 46 patients including gastritis or duodenitis in 25, gastric ulcers in 12, duodenal ulcers in 3, Mallory-Weiss tears in 3, gastric carcinoma in 2, and esophageal varices in 1. Gastritis or duodenitis was seen incidentally in 14 more patients. Hyperamylasemia was seen in 38 patients, most commonly being due to a rise of both nonpancreatic and pancreatic isoamylases (18 patients). In 13 patients it was due to an elevation of nonpancreatic amylase alone, and in 7 patients secondary to elevated pancreatic isoamylase alone. Acute pancreatitis raises only the pancreatic component and cannot explain the hyperamylasemia in most of these patients. Hyperamylasemia did not correlate to etiology of the bleeding; gastritis or duodenitis present in the majority of these patients appears to be the unifying factor. Since both nonpancreatic and pancreatic amylases are present in the duodenum and the stomach with pyloric reflux, reabsorption of intraluminal amylase across damaged mucosa is postulated as a mechanism to explain the observed isoamylase patterns. The possibility of decreased amylase clearance as an explanation is unlikely. An alternative central nervous system mechanism might be invoked. It is concluded that hyperamylasemia is a complex event which the use of isoamylase analysis is beginning to elucidate. The hyperamylasemia seen commonly in patients presenting with upper gastrointestinal bleeding does not imply the presence of acute pancreatitis.     

The role of serum isoamylase and lipase determinations in clinical practice

To determine the clinical utility of routine determination of serum isoamylase (pancreatic/salivary) and/or lipase activity, sera were tested from 109 consecutive patients with elevated total serum amylase. Without knowledge of the isoamylase and lipase results, an assessment was made of the confidence with which the attending medical staff had made or excluded a diagnosis of acute pancreatitis. The attending staff had considered acute pancreatitis to be probable in 78, possible in 12 and unlikely in 19 patients. The confidence of the clinical diagnosis of acute pancreatitis was directly related to the degree of elevation of the serum total amylase: (mean IU/l +/- s.e.m.) probable pancreatitis 1807 +/- 313, possible pancreatitis 680 +/- 74, pancreatitis unlikely 493 +/- 50. Pancreatic isoamylase was elevated in 97% of patients with probable pancreatitis, 92% with possible pancreatitis and 68% in whom pancreatitis had been considered unlikely. Lipase elevations generally parallelled these results. Although gall-stones were usually sought among patients with probable pancreatitis, they were rarely sought in patients in the other categories. In conclusion, amylase isoenzyme or lipase determinations add little information in cases of clinically suspected acute pancreatitis with marked hyperamylasemia. The tests may have a role in the evaluation of patients with clinically unexplained hyperamylasemia by defining more precisely the origin of the amylase.     

Hyperamylasemia after cardiopulmonary bypass

Postpump pancreatitis has been described to occur in patients undergoing cardiac surgery with cardiopulmonary bypass. Twenty patients were prospectively analyzed with sera drawn for total serum amylase, pancreatic isoamylase, and nonpancreatic isoamylase levels. Six of 19 patients were found to be hyperamylasemic postoperatively, the majority of which were not due to pancreatic isoamylasemia . No patient had clinical pancreatitis. These findings suggest that elevations of serum amylase is common after cardiopulmonary bypass and is not indicative of pancreatitis.     

Postoperative hyperamylasemia in patients undergoing abdominal surgery: the relationship between serum and peritoneal amylase levels]

This study was undertaken to investigate the incidence of postoperative hyperamylasemia and amylase levels of intraperitoneal drainage in 106 patients undergoing major abdominal surgery. The results were as follows: 1. Postoperative hyperamylasemia was found in 36.8% of all patients, with higher incidence of hyperamylasemia being in accordance with greater surgical intervention to the pancreas. 2. The isoamylase pattern of postoperative hyperamylasemia was dominant in the salivary type. 3. The levels of such serum pancreatic enzymes as lipase, trypsin and elastase 1 were higher in the pancreatic-type group than in the salivary-type group, particularly with the elastase 1 levels being statistically higher in the former. 4. Increases in peritoneal amylase activity were found in those cases of greater surgical intervention to the pancreas, postoperative hyperamylasemia and higher serum pancreatic isoamylase levels. 5. Diagnosis of postoperative pancreatitis was confirmed in one case by clinical and laboratory findings and CT examination. It might be concluded that postoperative high peritoneal amylase levels suggest occurrence or possible occurrence of postoperative pancreatitis.     

Diagnostic value of serum elastase 1 in pancreatic disease

We studied serum elastase 1 concentrations in patients with pancreatic disease to assess its diagnostic value and compare its sensitivity and specificity with that of amylase and pancreatic isoamylase. Markedly raised concentrations of elastase 1 were found in all twenty-nine patients with acute pancreatitis (amylase was elevated in all but three and pancreatic isoamylase in all but one). Serial measurements of the three enzymes in acute pancreatitis showed that elastase remained elevated longer than amylase and pancreatic isoamylase. The majority of chronic pancreatitis patients studied during a painful relapse (16 out of 21, 76 per cent) had elastase concentrations above the upper normal limit. Amylase and pancreatic isoamylase were elevated in 11 (52 per cent) and in 13 (62 per cent), respectively. Most patients with chronic pancreatitis studied during clinical remission (39 out of 43) had serum elastase levels either within (n = 24) or below (n = 15) the control range. The latter had severe exocrine pancreatic insufficiency and steatorrhoea. In carcinoma of the pancrease, 20 out of 32 (63 per cent) had abnormal serum elastase concentrations; 16 were higher and 4 lower than the control range. Amylase was abnormal in 10 (31 per cent) (8 high, 2 low), and pancreatic isoamylase was abnormal in 16 (50 per cent) (11 high, 5 low). In 46 control patients with non-pancreatic abdominal pain, serum elastase concentrations were not significantly different from those in healthy controls. Elastase was slightly raised in two, whereas amylase and pancreatic isoamylase were elevated in seven and eight, respectively. We conclude that serum elastase 1 is a highly sensitive and specific indicator of pancreatic disease.     

Hyperamylasemia and acute pancreatitis after pancreatoduodenectomy: Two different entities

BackgroundSerum amylase activity greater than the institutional upper limit of normal (hyperamylasemia) on postoperative day 0-2 has been suggested as a criterion to define postoperative acute pancreatitis after pancreatoduodenectomy, but robust evidence supporting this definition is lacking.BackgroundTo assess the clinical impact of hyperamylasemia after pancreatoduodenectomy and to define postoperative acute pancreatitis.MethodsData of 1,235 consecutive patients who had undergone pancreatoduodenectomy between January 2010 and December 2014 were extracted from a prospective database and analyzed. Postoperative acute pancreatitis was defined based on the computed tomography severity index. Logistic regression modeling was used to calculate the postoperative acute pancreatitis rate of the entire study population.ResultsHyperamylasemia on postoperative day 1 was found in 52% of patients after pancreatoduodenectomy. Patients with hyperamylasemia on postoperative day 1 had statistically significantly greater morbidity and mortality than patients with a normal serum amylase activity on postoperative day 1 with the rates of postoperative pancreatic fistula of 14.5% vs 2.1%, and 90-day mortality of 6.6% vs 2.2%, respectively. Of the 364 patients who underwent postoperative computed tomography, 103 (28%) had radiologic signs of acute pancreatitis, thus defining them as having postoperative acute pancreatitis by our definition. Logistic regression modeling showed a 14.7% rate of postoperative acute pancreatitis for the entire patient cohort and 29.2% for patients with hyperamylasemia on postoperative day 1. Outcomes of patients with postoperative acute pancreatitis defined based on the computed tomography severity index showed a rate of postoperative pancreatic fistula of 32.4% and a 90-day mortality rate of 11.8%, which were worse than those of patients with hyperamylasemia on postoperative day 1 alone.ConclusionHyperamylasemia on postoperative day 1 is a frequent finding after pancreatoduodenectomy, but hyperamylasemia on postoperative day 1 alone is not synonymous with postoperative acute pancreatitis because only 29.2% of such patients have acute pancreatitis based on computed tomography findings. Postoperative acute pancreatitis is a dangerous complication after pancreatoduodenectomy, but its prevalence, according to the gold standard of CT, is not as high as reported previously. Our data suggest that hyperamylasemia on postoperative day 1 and postoperative acute pancreatitis are 2 different entities.     

Hyperamylasemia and subclinical pancreatitis after cardiac surgery

Hyperamylasemia after cardiac surgery is common but typically causes no clinical concern because it consists mainly of the salivary isoenzyme. In this study we evaluated the incidence, source, and time course of postoperative hyperamylasemia with special attention to the possibility of subclinical pancreatitis. In 88 patients prospectively tested for serum amylase and lipase concentrations, elastase 1 activity, and amylase isoenzyme characteristics, 57 (64%) showed hyperamylasemia during the early postoperative period. In most cases early hyperamylasemia was not of pancreatic origin, but two patients were diagnosed with subclinical pancreatitis. Among the last 23 patients, 5 of 10 patients with early hyperamylasemia exceeding 1000 IU/L showed late hyperamylasemia on the seventh postoperative day, when it represented mainly the pancreatic isoenzyme. Lipase concentrations and elastase 1 activities were elevated in these cases. Late hyperamylasemia following cardiac surgery may be of pancreatic origin and indicative of subclinical pancreatitis, even if early hyperamylasemia was of salivary origin.     

Alcohol-induced salivary hyperamylasemia

The effects of alcohol intoxication on serum amylase levels were tested in both normal subjects and chronic alcoholics. Paired samples of ethanol levels and isoamylase levels in the normal subjects (n = 11) showed a rise in both total serum amylase (P less than 0.01) and nonpancreatic isoamylase (P less than 0.05) after drinking. Unpaired cohort groups of sober chronic alcoholics at a rehabilitation facility (n = 46) and intoxicated chronic alcoholics in an emergency room (n = 58) were also compared. Average blood alcohol levels in the intoxicated controls were 93 mg% compared to a level of 301 mg% in the intoxicated chronic alcoholic. Intoxication superimposed on chronic alcoholism caused a moderate rise in the total serum amylase (NS) and a significant elevation of the nonpancreatic isoamylase (P less than 0.01). Sober chronic alcoholics had a significantly greater average total serum amylase (P less than 0.001) and nonpancreatic isoamylase (P less than 0.01) than the normal controls. No difference in the average pancreatic isoamylase levels was seen in any group. These data suggest a biphasic response to alcohol on the serum amylase level. Acute and chronic changes appear to operate independently. The cause for these effects is speculative. Isoamylase analysis is needed in the alcoholic population to sort out the meaning of hyperamylasemia.     

Postoperative hyperamylasemia (POH) and acute pancreatitis after pancreatoduodenectomy (POAP): State of the art and systematic review

BackgroundPostoperative hyperamylasemia is a frequent finding after pancreatoduodenectomy, but its incidence and clinical implications have not yet been analyzed systematically. The aim of this review is to reappraise the concept of postoperative hyperamylasemia with postoperative acute pancreatitis, including its definition, interpretation, and correlation.MethodsOnline databases were used to search all available relevant literature published through June 2019. The following search terms were used: “pancreaticoduodenectomy,” “amylase,” and “pancreatitis.” Surgical series reporting data on postoperative hyperamylasemia or postoperative acute pancreatitis were selected and screened.ResultsAmong 379 screened studies, 39 papers were included and comprised data from a total of 9,220 patients. Postoperative hyperamylasemia was rarely defined in most of these series, and serum amylase values were measured at different cutoff levels and reported on different postoperative days. The actual levels of serum amylase activity and the representative cutoff levels required to reach a diagnosis of postoperative acute pancreatitis were markedly greater on the first postoperative days and tended to decrease over time. Most studies analyzing postoperative hyperamylasemia focused on its correlation with postoperative pancreatic fistula and other postoperative morbidities. The incidence of postoperative acute pancreatitis varied markedly between studies, with its definition completely lacking in 40% of the analyzed papers. A soft pancreatic parenchyma, a small pancreatic duct, and pathology differing from cancer or chronic pancreatitis were all predisposing factors to the development of postoperative hyperamylasemia.ConclusionPostoperative hyperamylasemia has been proposed as the biochemical expression of pancreatic parenchymal injury related to localized ischemia and inflammation of the pancreatic stump. Such phenomena, analogous to those associated with acute pancreatitis, could perhaps be renamed as postoperative acute pancreatitis from a clinical standpoint. Patients with postoperative acute pancreatitis experienced an increased rate of all postoperative complications, particularly postoperative pancreatic fistula. Taken together, the discrepancies among previous studies of postoperative hyperamylasemia and postoperative acute pancreatitis outlined in the present review may provide a basis for stronger evidence necessary for the development of universally accepted definitions for postoperative hyperamylasemia and postoperative acute pancreatitis.     

Postoperative hyperamylasemia, pancreatitis, and primary hyperparathyroidism

One hundred patients with biochemically proved primary hyperparathyroidism had serum amylase estimations before and after cervical or mediastinal exploration. After operation the patients were monitored for the development of abdominal symptoms suggestive of pancreatitis. Although hyperamylasemia occurred in four patients after operation, clinical acute pancreatitis did not arise. Amylase fractionation confirmed the presence of excessive salivary isoamylase in all four patients. Operation on patients with marginally elevated serum creatinine concentrations, those receiving furosemide, and those undergoing concomitant thyroid operation appeared to increase the likelihood of salivary-based hyperamylasemia; this finding suggested an altered renal handling of amylase in the immediate postoperative period. The results of this prospective study and reviewed reports of additional patients undergoing parathyroidectomy indicate that this operation is unlikely to be complicated by postoperative pancreatitis. The probable risk of both pancreatitis and hyperamylasemia would appear to be no more than that with other nonabdominal surgical procedures.     

Susceptibility of the pancreas to ischemic injury in shock.

The pancreas, like the kidney, is highly vulnerable to ischemic necrosis. This form of pancreatic injury may express itself as prolonged hyperamylasemia with only minimal signs or symptoms of inflammation, or may produce severe pancreatitis followed by abscesses and death. Autopsy examination of patients dying after oligemic shock showed a 9% incidence of major pancreatic injury if there was not concomitant acute renal tubular necrosis (ATN), but a 50% incidence in those with ATN. Similarly, among patients dying after non-oligemic shock, 12% of those without ATN had major pancreatic injury but 35% with ATN also had pancreatic ischemic injury. Among 13 selected patients examined prospectively after being in shock, pancreatic injury was indicated by hyperamylasemia, hyperlipasemia, elevated amylase/creatinine clearance ratio, and elevated circulating isoamylases specifically of pancreatic origin. Four of the 13 had clinical manifestations of pancreatitis. Not only must shock be added to this list of causes of pancreatitis, but pancreatic ischemia due to hypoperfusion may also be the critical factor which causes the progression from edema to necrosis in other forms of pancreatitis, including those associated with alcohol and biliary disease.     

Acute pancreatitis after cardiopulmonary bypass

We have described a spectrum of pancreatic surgery after cardiopulmonary bypass. At one end is a subclinical lesion which was manifested only by elevations in serum isoamylase levels (27 percent of patients) and increased ribonuclease levels (13 percent of patients) in asymptomatic patients followed after cardiac surgery. At the other end is a severe and often lethal necrotizing pancreatitis. Acute necrotizing pancreatitis was found at autopsy in 25 percent of 138 patients who died after cardiac surgery, and it correlated strongly with low output, acute tubular necrosis, and infarction of the liver, spleen, or bowel. It was the principal cause of death in 4 percent of these patients. In addition, 24 percent of 38 nonsurgical patients who died from cardiac failure and hypoperfusion had acute pancreatitis at autopsy, whereas acute pancreatitis was not observed in 55 nonsurgical patients who died without a significant period of low output. Acute pancreatitis was recognized postoperatively in 12 patients (0.2 percent). Three had mild pancreatitis, and all responded well to conservative therapy. In nine patients, fulminant necrotizing pancreatitis developed. Their courses were characterized by significant early postoperative hemodynamic compromise, abdominal distention, ileus, fever, and episodes of late vascular instability associated with hypocalcemia. The diagnosis of pancreatitis was usually missed because of the absence of pain, tenderness and hyperamylasemia. The diagnosis was confirmed at laparotomy in eight patients and at autopsy in one. The only two survivors among the nine with severe cases had aggressive mobilization, debridement, and wide drainage of the necrotic pancreas. We suggest that a mild subclinical injury to the pancreas may occur as a consequence of cardiopulmonary bypass and may progress to severe ischemic necrosis if hypoperfusion follows in the postoperative period, the presentation of necrotizing pancreatitis may be atypical in the cardiac surgical patient and should be considered if nonspecific abdominal symptoms are present, and aggressive debridement and drainage may be the optimal treatment for aggressive forms of this disease.     

Puzzling persistent hyperamylasemia, probably neither pancreatic nor pathologic

Increased serum amylase levels most commonly signify pancreatic disease. One hundred seventeen consecutive patients were studied because their serum amylase levels were abnormally high for periods ranging from 3 to 48 weeks. In each case, extensive clinical and radiologic evaluation had failed to reveal a reason for the abnormality. The amylase isoenzymes of their sera were separated by polyacrylamide gel electrophoresis, and the fractions were measured by a saccharogenic assay. The findings in the 117 patients showed that 79 percent had non-pancreatic causes for their hyperamylasemia. The biggest single group (64 percent) had a normal distribution of isoamylases, albeit at unusually high concentrations. This phenomenon, which has not been defined previously, is probably a variant of normal in which the homeostatic balance between production and metabolism is set at a high level. Macroamylasemia accounted for 6 percent of the cases and salivary hyperamylasemia for only 9 percent. Three patients had the characteristic isoamylase pattern ("old amylase") associated with pancreatic pseudocysts. Isoamylase fractionation is a cheap, efficient, and effective means of ruling out a pancreatic cause for hyperamylasemia. It is probable that in the majority of cases of persistent hyperamylasemia without obvious clinical cause there will be no disease at all.     

Isoamylase levels in bone marrow transplant patients are affected by total body irradiation and not by graft-versus-host disease

Abstract. The mean total serum amylase levels in patients was 3.2 ± 0.5 μkat/l (± SE) before total body irradiation (TBI) prior to bone marrow transplantation of which 50% was due to pancreatic isoamylase and 50% salivary isoamylase. Total serum amylase increased to a maximum of 100.3 ± 12.3 μkat/l on the first dayafter TB Iandmostofthis increase was due to an increase in salivary isoamylase (90.0 ± 12.1 μkat/l). In association with this, all patients had clinical symptoms of parotitis. An increase in pancreatic isoamylase was found in 27% of the patients; however, none of them had clinical symptoms of pancreatitis. Serum amylase levels returned to normal within 5 days after TBI but then decreased to subnormal values, remaining below the normal range for 3 weeks. Pancreatic isoamylase returned to pre-irradiation levels 1.5 months after TBI, while salivary isoamylase remained low for the rest of the observation time. TBI of 7.5 Gyat 26 cGy/min gave significantly lower salivary amylase at 2 days after TBI compared with 10 Gy at 4 cGy/min: 32 ± 4 versus 76 ± 13 μkat/l ( P < 0.05). At 2.5 and 6 months after TBI significantly higher total amylase levels were recorded for patients treated with 7.5 Gy of TBI compared with 10 Gy: 2.5 ± 0.4 and 2.7 ± 0.3 versus 2.0 ± 0.5 and 0.8 ± 0.3 μkat/1, respectively ( P < 0.01, P < 0.05, respectively). Acute or chronic GVHD did not affect acinar cells in this investigation.     

Macroamylasemia and other chronic nonspecific hyperamylasemias: Chemical oddities or clinical entities?

Seventeen patients with chronic hyperamylasemia were studied using standard clinical and laboratory parameters, amylase/creatinine clearance ratios, and polyacrylamide gel electrophoresis of serum amylases. These patients, none of whom had evidence of pancreatic disease or other specific source for the elevated serum amylase, fell into three groups: (1) Normal serum isoamylase profile and normal amylase clearance (6 patients). We postulate that the generalized hyperamylasemia may be due to reduced extrarenal catabolism of amylase, a previously undescribed phenomenon. (2) Macroamylasemia and very low amylase clearance (9 patients). Seven of the nine patients had recurrent epigastric pain. Evidence for an autoimmune basis is discussed. (3) Salivary-type hyperamylasemia and low amylase clearance (2 patients). This entity may really be macroamylasemia in which the macroamylase complex dissociated during analysis. Chronic hyperamylasemia is often not of pancreatic origin. The assumption that the pancreas is at fault, especially if there is abdominal pain, may cause morbidity due to gross overtreatment.     

Pancreatic complications following orthotopic liver transplantation

During fiscal year 1986, 40 out of 196 patients (21%) developed hyperamylasemia following orthotopic liver transplantation. The placement of a retropancreatic aortohepatic arterial interposition graft was associated with hyperamylasemia (p < 0.025). Eight patients (20%) developed clinically significant acute pancreatitis and its sequelae; abscesses and pseudocysts each in 2. Pancreatitis was attributable to the retropancreatic arterial graft in 4, viral infection in 2 and obstruction of the pancreatic duct in 1 patient. All 4 patients with arterial graft-related pancreatitis exhibited poor graft function immediately postoperatively, of whom 2 required retransplantation - both of which failed to function. Five patients died (63%); 2 from primary graft non-function, 2 due to sepsis and 1 from systemic cytomegalovirus infection. We conclude that acute pancreatitis after liver transplantation is a life-threatening complication which is often associated with graft non-function.     

Serum elastase I levels in pancreatic disease

The radioimmunoassay for human elastase I used in this study is accurate, sensitive, and specific, which we have confirmed. The assay can be done within 4 hours, which is important for clinical purposes. A total of 103 subjects were examined, and levels of 99 to 370 ng/dl (mean 200) in normal human sera were determined. The serum elastase levels in acute, acute relapsing, and chronic relapsing pancreatitis were significantly higher than normal. Although serial determinations returned to normal within 5 days after the onset of the attack, they decreased gradually and remained high on the 7th, 10th, and 11th days in patients who still had residual signs of pancreatitis. The values in patients with chronic pancreatitis and various other diseases were normal. The values in patients with acute pancreatitis were significantly higher than in those with hyperamylasemia of non-pancreatic origin. Twelve of 19 patients with pancreatic cancer had abnormal serum elastase levels; this was especially true in patients with cancer of the pancreatic head. We believe that the measurement of serum elastase levels by radioimmunoassay will become a useful diagnostic method for pancreatic disease in the future.     

The Nature and Significance of Hyperamylasemia Following Operation

Total serum amylase activity was found to be significantly elevated postoperatively in 11 (10%) of 110 patients undergoing various surgical procedures. Isoamylase analysis revealed that the rise was chiefly in the pancreatic-type isoamylase in seven of the 11 patients showing postoperative serum amylase elevations; in the other four patients, the elevation occurred principally in the salivary-type isoamylase. These data demonstrate that postoperative hyperamylasemia occurs surprisingly often and that serum amylase activity may rise even when the surgical procedure is extra-abdominal. Moreover, elevation of serum amylase activity after surgery is not necessarily an indication of pancreatitis and may reflect instead a rise in salivary-type isoamylase.     

SHOULD SERUM PANCREATIC LIPASE REPLACE SERUM AMYLASE AS A BIOMARKER OF ACUTE PANCREATITIS?

BACKGROUND: Serum pancreatic lipase may improve the diagnosis of pancreatitis compared to serum amylase. Both enzymes have been measured simultaneously at our hospital allowing for a comparison of their diagnostic accuracy. METHODS: Seventeen thousand five hundred and thirty-one measurements of either serum amylase and or serum pancreatic lipase were made on 10 931 patients treated at a metropolitan teaching hospital between January 2001 and May 2003. Of these, 8937 were initially treated in the Emergency Department. These results were collected in a database, which was linked by the patients' medical record number to the radiology and medical records. Patients with either an elevated lipase value or a discharge diagnosis of acute pancreatitis had their radiological diagnosis reviewed along with their biochemistry and histology record. The diagnosis of acute pancreatitis was made if there was radiological evidence of peripancreatic inflammation. RESULTS: One thousand eight hundred and twenty-five patients had either elevated serum amylase and or serum pancreatic lipase. The medical records coded for pancreatitis in a further 55 whose enzymes were not elevated. Three hundred and twenty of these had radiological evidence of acute pancreatitis. Receiver operator characteristic analysis of the initial sample from patients received in the Emergency Department showed improved diagnostic accuracy for serum pancreatic lipase (area under the curve (AUC) 0.948) compared with serum amylase (AUC, 0.906, P < 0.05). A clinically useful cut-off point would be at the diagnostic threshold; 208 U/L (normal <190 U/L) for serum pancreatic lipase and 114 U/L (normal 27-100 U/L) for serum amylase where the sensitivity was 90.3 cf., 76.8% and the specificity was 93 cf., 92.6%. 18.8% of the acute pancreatitis patients did not have elevated serum amylase while only 2.9% did not have elevated serum pancreatic lipase on the first emergency department measurement. CONCLUSION: It is concluded that serum pancreatic lipase is a more accurate biomarker of acute pancreatitis than serum amylase.