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.     

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.     

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.     

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.     

A correlation between clinical pancreatitis and isoenzyme patterns of amylase

Fifty-seven patients admitted with the clinical diagnosis of acute pancreatitis had isoamylase analysis on their sera to determine the source of their hyperamylasemia. Our objective was to correlate the isoamylase pattern with our clinical observations. Thirty-nine of 57 patients (68%) had pancreatic hyperamylasemia as expected, but 18 of 57 patients (32%) had normal levels of pancreatic amylase. The hyperamylasemia in the latter group was due either to nonpancreatic hyperamylasemia (16 of 57) of macroamylasemia (2 of 57). Consequently, hyperamylasemia associated with abdominal pain, nausea, and vomiting led to the incorrect diagnosis of acute pancreatitis in 32% of the patients. The measurement of isoamylase profiles can be done rapidly and inexpensively. Knowledge that hyperamylasemia is nonpancreatic in origin may have an important influence on treatment, hospitalization, and the extent of laboratory and radiologic investigation.     

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.     

Evaluation of amylase and lipase in the diagnosis of acute pancreatitis

Background : The diagnosis of acute pancreatitis relies heavily on a raised amylase. Methods : In the present study patients were prospectively categorized, without knowledge of pancreatic enzyme levels, into acute pancreatitis (AP; n = 51), disease controls (n = 35), indeterminate as to pancreatitis (n = 189) or exclusions (non‐pancreatitis diseases where amylase may be elevated; n = 53). Results : Enzyme levels were analysed by receiver operator characteristics (ROC) curves, with specificity > 80%. Day 1 serum lipase gave the greatest diagnostic accuracy (area under ROC curve = 0.128; P = 0.041 vs serum amylase). At the calculated diagnostic threshold of 208 U/L, lipase gave a sensitivity of 67% and a specificity of 97%. Other diagnostic thresholds (day 1) were: serum total amylase, 176 U/L (ROC 0.104, sensitivity 45%, specificity 97%), urinary total amylase, 550 U/L (ROC 0.108, sensitivity 62%, specificity 97%) and serum pancreatic isoamylase, 41 U/L (ROC 0.107, sensitivity 63%, specificity 85%). At delayed diagnosis (3 days) no enzyme was superior to lipase. The combination of lipase and amylase did not increase diagnostic accuracy. Conclusion : Serum lipase is recommended for diagnosis of AP, both early and late in the disease. Although highly specific when elevated, all pancreatic enzymes have low sensitivity for diagnosis.     

Cholangio-venous reflux as a cause of recurrent hyperamylasemia in choledochal dilatation with anomalous pancreaticobiliary ductal union: an experimental study

Cylindrical choledochal dilatation, associated with anomalous pancreaticobiliary ductal union, causes recurrent episodes of right hypochondrial pain, vomiting, and fever. The symptoms are very often accompanied by hyperamylasemia, which is generally considered to be due to acute pancreatitis. However, our clinical experience and experimental studies have led us to the conclusion that pancreatitis is not the sole cause of hyperamylasemia. In this paper we report our further investigations of the cause of the hyperamylasemia. In 22 mongrel adult dogs, intracholedochal infusion was performed under a continuous hydrostatic pressure of 20 cm H2O for 2 hours. Solutions of amylase from three different sources and a lipase were used in the range of concentrations found clinically in the bile within a cylindrical choledochal dilatation. In the 3 groups, hyperamylasemia was proven by quantitative estimation of serum amylase level and/or by the changes in specific amylase isozymes. Lipase was also shown to transfer into the blood stream. In an additional experiment on 5 dogs, only the extrahepatic biliary tree, including the gallbladder, was infused with a solution of amylase from Bacillus subtilis. This produced no increase in the serum amylase. Our experiments suggest that amylase passes from the hepatocholedochal system into the blood stream. This phenomenon has long been known as cholangiovenous reflux.     

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.     

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.     

The role of oxygen-derived free radicals in the pathogenesis of acute pancreatitis.

Acute pancreatitis may be initiated in the ex vivo, perfused canine pancreas preparation by a variety of stimuli. These include oleic acid infusion (FFA), partial duct obstruction with secretin stimulation (POSS), and a 2-hour period of ischemia (ISCH). In each model, pancreatitis is characterized by weight gain, edema, and hyperamylasemia. Oxygen-derived free radicals such as superoxide, hydrogen peroxide, and the hydroxyl radical are highly reactive toxic substances that are normally produced in small amounts during oxidative metabolism. Ordinarily, these substances are detoxified by endogenous intracellular enzymes called free radical scavengers (FRS), such as superoxide dismutase (SOD) and catalase (CAT). These studies were undertaken to evaluate the possible role of oxygen-derived free radicals in the initiation of acute pancreatitis in the isolated canine model. All preparations were perfused for 4 hours with autologous blood. Controls (N = 6): these glands remained normal in appearance, gained minimal weight (6 +/- 1 g), and serum amylase remained normal (less than 1000 u/dl). FFA pancreatitis, FFA alone (N = 6): these glands became edematous, gained weight (113.5 +/- 27.0 g), and developed hyperamylasemia (2087 +/- 387 u/dl). FFA + FRS (N = 6), SOD (50 mg) and CAT (50 mg) were added to the perfusate at time zero: these glands became only minimally edematous, gained less weight (31.8 +/- 10.1 g, p less than 0.05), and amylase remained normal (p less than 0.05). POSS pancreatitis, POSS alone (N = 8): these glands became edematous, gained weight (38.6 +/- 4.6 g), and developed marked hyperamylasemia (9522 +/- 3226 u/dl). POSS + FRS (N = 6): these glands did not develop edema, gained less weight (15.1 +/- 2.6 g, p less than 0.05), and serum amylase only increased to 1815 +/- 343 u/dl, (p less than 0.05). ISCH pancreatitis, ISCH alone (N = 6): these glands became edematous, gained weight (75.8 +/- 25 g), and developed hyperamylasemia (1679 +/- 439 u/dl). ISCH + FRS (N = 6): these glands did not develop edema, gained only 18.3 +/- 9.0 g (p less than 0.005), and serum amylase remained normal (p less than 0.05). These studies demonstrate that, in this canine preparation, acute pancreatitis is significantly ameliorated by oxygen-free radical scavengers. Since this was true whether the pancreatitis was produced by FFA infusion, POSS, or ischemia, it suggests that oxygen-derived free radicals may mediate a common essential step in the pathogenesis of all forms of pancreatitis.     

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.     

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.     

Amylase clearance in differentiating acute pancreatitis from peptic ulcer with hyperamylasemia.

Thirty-four patients with abdominal pain, tenderness, and hyperamylasemia suggesting acute pancreatitis were studied prospectively to elucidate the relationship between peptic ulcer disease and pancreatitis. Confirming evidence of pancreatitis and/or ulcer was obtained either at laparotomy of by upper gastrointestinal roentgenograms. The presence or absence of pancreatitis was substantiated by measurement of the amylase/creatinine clearance ratio, which is significantly higher (p less than 0.001) in patients with acute pancreatitis (9.3 plus or minus 0.9), than in patients without pancreatitis (3.1 plus or minus 0.2). Nine of the 34 patients were found to have gastric or duodenal ulcers. However, seven of the nine, despite an elevated serum amylase, had no sign of pancreatitis at surgery, on radiological examination, or by elevation of the amylase/creatinine clearance ratio (3.1 plus or minus 0.4). It is suggested that hyperamylasemia associated with peptic ulcer disease is most often not indicative of acute pancreatitis and that treatment is most appropriately directed at the ulcer.     

Fictitious pancreatitis in choledochal cyst

The classical presentation of choledocal cyst has been regarded as a triad of abdominal pain, jaundice and a palpable abdominal mass; unusual presentations include rupture of the choledocal cyst with bile peritonitis, pancreatitis and bleeding esophageal varices. We are reporting 3 children presenting clinically as recurrent acute pancreatitis with elevated serum amylase and found to have type I choledocal cyst. Despite elevated serum amylase there was no evidence of pancreatic inflammation at laparotomy. High amylase concentration was found in fluid contained within the cyst. This was probably responsible for the elevated serum amylase and also the inflammatory reaction seen in the wall of the choledocal cyst. These cases support the hypothesis that pancreatic reflux into the bile ducts is the etiological factor in the development of choledocal cyst. Our 3 cases were treated by cyst excision and have remained asymptomatic. The presence of hyperamylasemia should not delay appropriate surgical management. The treatment of choice is cyst excision, since it will eliminate factors contributing to the development of cholangitis and hyperamylasemia.     

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 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.     

Sulindac-induced acute pancreatitis mimicking gallstone pancreatitis

Two patients with sulindac-induced acute pancreatitis presented clinically with abdominal pain, right upper-quadrant tenderness, markedly increased serum amylase values, and hyperbilirubinemia, findings initially suggestive of gallstone pancreatitis. Ultrasound examinations were negative for gallstones. One patient was inadvertently treated two years later with sulindac with recurrence of abdominal pain, marked hyperamylasemia, and jaundice. Clinical resolution was rapid with each episode following discontinuation of sulindac.     

Acute pancreatitis and normoamylasemia. Not an uncommon combination.

A consecutive series of 352 attacks of acute pancreatitis (AP) was studied prospectively in 318 patients. AP was ascertained by contrast-enhanced CT scan in all but four cases in which diagnosis was made at operation or autopsy. Sixty-seven of these cases (19%) had normal serum amylase levels on admission (i.e., less than 160 IU/L, a limit that includes 99% of control values), a figure considerably higher than generally admitted. When compared to AP with elevated serum amylase, normoamylasemic pancreatitis was characterized by the following: (1) the prevalence of alcoholic etiology (58% vs. 33%, respectively, p less than 0.01), (2) a greater number of previous attacks in alcoholic pancreatitis (0.7 vs. 0.4, p less than 0.01); and (3) a longer duration of symptoms before admission (2.4 vs. 1.5 days, p less than 0.005). In contrast AP did not appear to differ significantly in terms of CT findings, Ranson's score, and clinical course, when comparing normo- and hyperamylasemic patients, although there was a tendency for normoamylasemic patients to follow milder courses. Serum lipase was measured in 65 of these normoamylasemic cases and was found to be elevated in 44 (68%), thus increasing diagnostic sensitivity from 81% when amylase alone is used to 94% for both enzymes. A peritoneal tab was obtained in 44 cases: amylase concentration in the first liter of dialysate was greater than 160 IU/L in 24 cases (55%), and lipase was greater than 250 U/L in 31 cases (70%). Twelve of these 44 cases had low peritoneal fluid and plasma concentrations for both enzymes. Thus little gain in diagnostic sensitivity was obtained when adding peritoneal values (96%) to serum determinations. AP is not invariably associated with elevated serum amylase. Multiple factors may contribute to the absence of hyperamylasemia on admission, including a return to normal enzyme levels before hospitalization or the inability of inflamed pancreases to produce amylase. Approximately two thirds of cases with normal amylasemia were properly identified by serum lipase determinations. AP does not appear to behave differently when serum amylase is normal or elevated, and should therefore be submitted to similar therapeutic regimens in both conditions.