[Marked hyperamylasemia--its incidence and clinicopathological observations, especially on postoperative transient hyperamylasemia].
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Amylases↗
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[A case of pancreatic type hyperamylasemia associated with systemic lupus erythematosus--especially about mechanisms and incidence of P-type hyperamylasemia in SLE (author's transl)].
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Adult↗
[Hyperamylasemia after cardiac surgery in children].
OBJECTIVE: To analyze the incidence of hyperamylasemia after cardiac surgery in children, the pathogenic mechanisms and the relationship with morbidity and mortality. PATIENTS AND METHODS: A prospective open study was made in the Intensive Care Unit of a tertiary care pediatric hospital. One hundred thirty-one patients (75 boys and 56 girls), between 7 days and 16 years of age, were studied after cardiac surgery between 1992 and 1994. We determined serum amylase on their admission, at 24 hours, between the 2nd and 5th days, and thereafter according to the clinical evolution. We considered a serum amylase higher than 250 UI/L as hyperamylasemia. We also determined liver enzyme levels (AST, ALT, Gamma-glutamyl transpeptidase, alkaline phosphatase, and direct and total bilirubin) and renal function (urea and creatinine). We studied the relationship between hyperamylasemia and the type of surgery, shock, renal insufficiency, hepatic alterations and mortality. RESULTS: Fourteen patients (10%) showed hyperamylasemia. Mean serum amylase in these patients was 534 +/- 332.6 UI/L (range 252-1426 UI/L). Of the patients were cardiopulmonary bypass was performed, 11.4% presented hyperamylasemia, and 8.5% of the patients without a cardiopulmonary bypass surgery (non-significant difference). Of the children with hyperamylasemia, 42.8% suffered shock during the postoperative period after cardiac surgery and only 15.2% of the rest of the patients (p < 0.05). There were no differences in the incidence of renal insufficiency and liver alterations between children with hyperamylasemia and the rest of the patients. There was no significant difference between the mortality of children with hyperamylasemia (7.1%) and the rest of the children (4.7%; p > 0.05). CONCLUSIONS: Hyperamylasemia is frequent after cardiac surgery in children. Hyperamylasemia is related to shock and the ischemia is probably the most pathogenic factor.
Adolescent↗
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.
Acute Disease↗
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.
Adult↗
Pancreatic hyperamylasemia during acute gastroenteritis: incidence and clinical relevance.
BACKGROUND: Many case reports of acute pancreatitis have been reported but, up to now, pancreatic abnormalities during acute gastroenteritis have not been studied prospectively. OBJECTIVES: To evaluate the incidence and the clinical significance of hyperamylasemia in 507 consecutive adult patients with acute gastroenteritis. METHODS: The clinical significance of hyperamylasemia, related predisposing factors and severity of gastroenteritis were assessed. RESULTS: Hyperamylasemia was detected in 10.2 % of patients studied. Although amylasemia was found over four times the normal values in three cases, the clinical features of acute pancreatitis were recorded in only one case (0.1%). Hyperamylasemia was more likely (17%) where a microorganism could be identified in the stools (p < 0.01). Among patients with positive stool samples, Salmonella spp. and in particular S. enteritidis, was the microorganism most frequently associated with hyperamylasemia [17/84 (20.2 %) and 10/45 (22.2%), respectively], followed by Rotavirus, Clostridium difficile and Campylobacter spp. Patients with hyperamylasemia had more severe gastroenteritis with an increased incidence of fever (80 % vs 50.6 %, O.R. 3.0; P < 0.01), dehydration (18% vs 8.5%; O.R. 2.5; P < 0.05), and a higher mean number of evacuations per day (9.2 vs 7.5; P < 0.05) than those with amylasemia in the normal range. Hyperamylasemia was significantly associated with cholelithiasis, (30.0 % vs 10.7%, O.R. 3.5; P < 0.01) and chronic gastritis or duodenal ulceration (22.0 % vs 10.2%, O.R. 2.4, P < 0.05). CONCLUSIONS: Hyperamylasemia is relatively frequent, and is associated with severe gastroenteritis. However, acute pancreatitis in the setting of acute gastroenteritis, is a rare event.
Acute Disease↗
The clinical significance of hyperamylasemia in organophosphate poisoning.
OBJECTIVE: Hyperamylasemia with a presumptive diagnosis of acute pancreatitis has been reported following organophosphate poisoning but there are no large-scale studies incorporating more specific diagnostic criteria. METHODS: Retrospective review of the medical records of 159 patients with a diagnosis of organophosphate poisoning over 3 years. Serum amylase, pancreatic amylase, salivary amylase, lipase and cholinesterase levels, and the clinical manifestations were analyzed. RESULTS: Serum amylase data was available for 121 of the 159 study patients. Hyperamylasemia (amylase > or = 360 U/L) was found in 44 patients (36%). Lipase was measured in 28 patients with hyperamylasemia; 9 of 28 had hyperlipasemia (lipase > or = 380 U/L). The finding of hyperamylasemia was closely related to clinical severity and presence of shock. A presumptive diagnosis of painless acute pancreatitis was diagnosed by hyperlipasemia associated with hyperamylasemia, clinical severity, serum LDH, and leukocyte counts. Two patients with presumptive pancreatitis died. Shock, coma, and hypoalbuminemia were the factors predicting fatality. CONCLUSIONS: Hyperamylasemia is frequent in severe organophosphate poisoning. However, hyperamylasemia is not synonymous with acute pancreatitis and pancreatic amylase is not a reliable parameter in the diagnosis of organophosphate-induced pancreatitis due to its low sensitivity and specificity. Lipase assay is indicated in patients with hyperamylasemia for early diagnosis of pancreatitis. Proper image studies and even pathological examination are also needed to confirm the extent of pancreatic injury. With prompt diagnosis and appropriate treatment, a complete recovery can be anticipated unless the patient has otherwise unrelated complications.
Acute Disease↗
Predictive factors for acute pancreatitis and hyperamylasemia after endoscopic papillary balloon dilation.
BACKGROUND: Although endoscopic papillary balloon dilation may result in acute pancreatitis or hyperamylasemia, the risk factors for these complications have not been well documented. Risk factors predictive of acute pancreatitis and hyperamylasemia after endoscopic papillary balloon dilation were retrospectively analyzed. METHODS: In 118 patients who underwent endoscopic papillary balloon dilation for choledocholithiasis, postendoscopic papillary balloon dilation acute pancreatitis and hyperamylasemia (at least 3-fold elevation) were investigated. A multivariate analysis was conducted for 20 potential risk factors related to clinical and procedure characteristics. RESULTS: Bile duct clearance was achieved in 113 patients. Early complications in the form of mild pancreatitis occurred in 7 patients (6%). Multivariate analysis identified history of acute pancreatitis as the only risk factor for postendoscopic papillary balloon dilation pancreatitis. Postendoscopic papillary balloon dilation hyperamylasemia occurred in 30 patients (25%). Multivariate analysis identified 4 independent risk factors for hyperamylasemia: an age of 60 years or less, previous pancreatitis, bile duct diameter 9 mm or less, and difficult bile duct cannulation. CONCLUSIONS: Endoscopic papillary balloon dilation is associated with a relatively low occurrence (6%) of pancreatitis but a high frequency (25%) of hyperamylasemia. The latter may represent pancreatic irritation or latent pancreatic injury. Particular care is necessary when endoscopic papillary balloon dilation is performed in younger patients, those with a history of pancreatitis, patients with a nondilated bile duct, and when cannulation is difficult.
Acute Disease↗
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.
Amylases↗
Is endoscopic balloon dilation for removal of bile duct stones associated with an increased risk for pancreatitis or a higher rate of hyperamylasemia?
BACKGROUND AND STUDY AIMS: We studied the rate of pancreatitis and asymptomatic hyperamylasemia after endoscopic balloon dilation (EBD) and endoscopic sphincterotomy (EST) for removal of bile duct stones. PATIENTS AND METHODS: Patients with bile duct stones of all sizes were randomly allocated to undergo EBD (8-mm dilation balloon) or EST. Pancreatitis was defined as epigastric pain combined with at least a threefold rise in serum amylase at 24 hours after the endoscopic retrograde cholangiopancreatography (ERCP). Asymptomatic hyperamylasemia was defined as a threefold rise in serum amylase without epigastric pain. RESULTS: There were 180 patients (67 men, 113 women; mean age 67, SD 16.2) available for analysis. Complete stone removal after a single ERCP was achieved in 82 (88%) of 93 EBD patients and in 81 (93%) of 87 EST patients (P = 0.38). Mechanical lithotripsy was used more frequently in the EBD group (31% vs. 13%, P = 0.005). Early complications occurred in 16 EBD patients (17%) and in 19 EST patients (22%) (P = 0.46). Pancreatitis was observed in seven patients in each group (8%). Logistic regression identified no significant predictors for the occurrence of pancreatitis. Asymptomatic hyperamylasemia occurred in 21 EBD patients (23%) vs seven EST patients (8%) (P = 0.008). Logistic regression identified EBD as the only significant predictor for asymptomatic hyperamylasemia: odds ratio 2.9 (95% confidence interval (CI) 1.1 to 7.3, R2 = 0.02). CONCLUSIONS: We did not observe a difference in the rate of pancreatitis between EBD and EST. Asymptomatic hyperamylasemia was observed more frequently after EBD. Although asymptomatic hyperamylasemia is not a clinical entity, this finding may indicate that EBD causes more irritation of the pancreas than EST.
Aged↗
Hyperamylasemia in inflammatory bowel disease.
We determined the prevalance and significance of hyperamylasemia in 180 patients with idiopathic inflammatory bowel disease (IBD) (83 with ulcerative colitis, and 97 with Crohn's disease). Serum total amylase and pancreatic and salivary isoamylase activity were measured in all patients. In all patients with hyperamylasemia, we measured isoamylase activity by cellulose acetate electrophoresis and lipase activity, assayed for the presence of macroamylase, and carried out pancreatic ultrasound examination and barium studies of the upper gastrointestinal tract. Eight of 97 patients with Crohn's disease (8%) had hyperamylasemia; 4 of them had an elevated pancreatic isoamylase and 2 a raised lipase activity. All patients with hyperamylasemia had normal ultrasonographic scans of the pancreas and no evidence of duodenal involvement on barium meal. None had macroamylasemia. We found no relationship of hyperamylasemia to disease site, activity, and duration or therapy and no patient developed clinical evidence of pancreatitis. We conclude that a small but important number of patients with Crohn's disease have hyperamylasemia not associated with overt pancreatitis. In the absence of appropriate indications, it requires no investigation.
Amylases↗
Hyperamylasemia in acute carbon monoxide poisoning.
Of patients with acute carbon monoxide poisoning admitted to the Trauma Intensive Care Unit of the Osaka University Hospital 39.5% (17/43) manifested hyperamylasemia. Iszyme studies in 16 such patients revealed 87.5% to be of the salivary type. Two patients presented with hyperamylasemia of the pancreatic-salivary type. There was no pancreatic type hyperamylasemia among these patients, negating the possible involvement of the pancreas in hyperamylasemia from carbon monoxide poisoning. There was a statistically significant difference in amylase levels between the arterial and the external jugular venous blood, indicating the salivary gland as the organ mainly responsible for hyperamylasemia in carbon monoxide poisoning. Amylase levels coincided well with the level of consciousness and the base excess. The amylase levels correlated significantly with beta-glucuronidase levels, suggesting the hyperpermeability of cell membranes of the salivary gland as the chief factor in hyperamylasemia secondary to acute carbon monoxide poisoning.
Adolescent↗
Evaluation of a rapid urine amylase test using post-ERCP hyperamylasemia as a model.
OBJECTIVE: The initial diagnosis of acute pancreatitis is often based on clinical criteria together with elevations of serum amylase and lipase. A reliable bedside urine test could facilitate the early diagnosis of pancreatitis. We evaluated a rapid urine amylase test (Rapignost) by using post-ERCP hyperamylasemia as a human model of acute development of hyperamylasemia suggestive of pancreatitis. METHODS: Seventy-five patients undergoing ERCP were prospectively evaluated. Patients with renal insufficiency, hyperlipidemia, or hyperglycemia were excluded. Before ERCP, patients had serum amylase and lipase measured, and urine amylase tested with the Rapignost test strip. At 4 and 16-24 h post-ERCP, a serum and urine (test strip) amylase were measured again; the adequacy of urine collection was verified by measuring a 2-h creatinine clearance. Patients were clinically assessed for the development of clinical pancreatitis. The concordance of the strip result with post-ERCP hyperamylasemia was assessed. RESULTS: The sensitivity of the test strip for the detection of hyperamylasemia was greatest at 16-24 h post-ERCP (78%). Specificity was uniformally high (100% specificity at 16-24 h post-procedure). The test strip was positive in all cases of clinical pancreatitis. Of three cases of clinically evident ERCP-induced pancreatitis, only one was urine test strip positive by 4 h post-procedure. CONCLUSIONS: Using post-ERCP hyperamylasemia as a model, the Rapignost rapid urine amylase test strip was only marginally sensitive but highly specific for hyperamylasemia. The urine test strip was positive in all cases of clinical pancreatitis and may be a useful bedside test for the diagnosis of acute pancreatitis.
Adolescent↗
Hyperamylasemia in patients with the acquired immunodeficiency syndrome.
Marked elevations of serum amylase, unexplained despite extensive evaluation in patients with acquired immunodeficiency syndrome (AIDS), prompted this retrospective review of 85 patients to determine the prevalence of hyperamylasemia and identify any associated demographic and etiologic factors. Of 39 patients who had amylase determinations, 54% had hyperamylasemia (2/3 pancreatic, 1/3 salivary) and 31% had pancreatitis. Biliary tract disease, alcohol intake, and opportunistic infections were similar in hyperamylasemic and normoamylasemic subjects. Non-Caucasian race, intravenous drug abuse, renal dysfunction, alkaline phosphatase elevation, and pentamidine use were more prevalent in patients with hyperamylasemia (p less than 0.001, p less than 0.001, p less than 0.01, p less than 0.05, and p less than 0.05, respectively). However, by stepwise deletion multiple regression analysis, only non-Caucasian race, pentamidine use, and Mycobacterium avium-intracellulare infection were significant, independent predictors of hyperamylasemia (R2 = 0.65). Followed over time, in a historical prospective manner, case fatality rates (66.6% and 61.1%) and median survival times (101 and 84 days) were similar in the hyperamylasemic and normoamylasemic groups. We conclude that, although pancreatitis occurs frequently in AIDS, hyperamylasemia is often of salivary origin and clinical outcome is unaffected. Certain demographic factors are strongly associated with hyperamylasemia in AIDS patients, but multiple, concurrent, etiologic factors are probably operative in these patients.
Acquired Immunodeficiency Syndrome↗
Hyperamylasemia following cardiopulmonary bypass.
In order to study the occurrence of postbypass hyperamylasemia, 75 patients undergoing cardiopulmonary bypass (CPB) were studied from March 1989 to January 1990. There were 49 males and 26 females. Among them, 27 had congenital heart disease, 30 had valvular disease, and 18 had coronary artery disease. There were 27 patients with at least one elevated serum amylase sample after operation. Thus, the overall incidence of hyperamylasemia was 36%. As compared with the preoperative data (1.3%), there was a statistically significant difference in the occurrence of hyperamylasemia (p less than 0.05). Three patients had overt clinical pancreatitis postoperatively. There was no positive correlation between the serum amylase level and the occurrence of pancreatitis (p greater than 0.05). Forty-two cases had a significant elevation of the amylase creatinine clearance ratio (ACCR) after CPB. However, there was no significant difference between the groups with pulsatile and nonpulsatile CPB (p greater than 0.05). Three patients (4%) died in our series. The causes of death were heart failure in two and fulminant pancreatitis associated with low cardiac output in one. Although our experience in dealing with pancreatitis improved survival, mortality was still high (33.3%) in our series. Nevertheless, there was no apparent correlation between mortality and postbypass hyperamylasemia (p greater than 0.05). Logistic regression analysis was used to analyze the risk factors of the occurrence of hyperamylasemia, and the analysis revealed that patients with coronary artery disease were susceptible to postbypass hyperamylasemia. Our studies indicate that the use of total serum amylase or ACCR to monitor for the occurrence of pancreatitis in postbypass patients is inadequate.(ABSTRACT TRUNCATED AT 250 WORDS)
Amylases↗
Hyperamylasemia after cardiopulmonary bypass: pancreatic cellular injury or impaired renal excretion of amylase?
BACKGROUND: Postoperative hyperamylasemia and even acute pancreatitis are associated with coronary artery bypass grafting (CABG). The mechanism of hyperamylasemia and pancreatic acinar cell damage was studied in 20 patients undergoing CABG. METHODS: Serial blood and urine samples at eight time points before, during, and 24 hours after the CABG were collected. Salivary and pancreatic isoamylases, the fractional clearance of isoamylases (i.e., relative to creatinine clearance), pancreatic phospholipase A2 (a specific serum marker of pancreatic acinar cell injury), and cystatin C (a sensitive marker of glomerular filtration rate) were measured. RESULTS: Mild serum hyperamylasemia (300 to 1000 units/L) was found in 11 of 20 (55%) and severe (> 1000 units/L) in 6 of 20 (30%) patients with no signs of clinical acute pancreatitis. Hyperamylasemia occurred from 6 to 24 hours after the CABG and was mainly caused by pancreatic isoamylase. Serum pancreatic phospholipase A2 concentration remained unchanged, which excludes acinar cell damage. Although renal glomerular filtration was normal during CABG as measured by serum cystatin C and creatinine clearance, the fractional clearance of isoamylases decreased. CONCLUSIONS: The decreased rate of excretion into urine, rather than pancreatic cellular damage, is the major source of hyperamylasemia after CABG.
Amylases↗
Is hyperamylasemia after cardiac surgery due to cardiopulmonary bypass?
Although hyperamylasemia has been reported in a large proportion of patients undergoing cardiac surgery with cardiopulmonary bypass, its clinical significance and pathogenetic mechanisms remain poorly understood. The study was designed to investigate whether avoidance of cardiopulmonary bypass would limit amylase elevation. Serum levels of amylase and lipase were measured preoperatively as well as 24 and 48 hours postoperatively in 58 patients undergoing elective coronary artery bypass grafting. Three surgical approaches were used: cardiopulmonary bypass (n = 32) and off-pump through a median sternotomy (n = 14) or a left minithoracotomy (n = 12). There was no hospital mortality or postoperative abdominal complications. Transient hyperamylasemia occurred in 14 patients: 7 (22%), 5 (36%), and 2 (17%) in the respective groups. The increase in amylase levels was similar among the groups. However, no lipase elevation was detected in any patient. There was no clear correlation between hyperamylasemia and increased creatinine levels. Perioperative plasma calcium levels were normal in patients who had hyperamylasemia. Our results indicate that hyperamylasemia after bypass surgery is not related to the use of cardiopulmonary bypass or the mode of surgical access.
Aged↗
Hyperamylasemia in diabetic ketoacidosis: sources and significance.
The origins and clinical significance of hyperamylasemia during diabetic ketoacidosis are unclear. We have therefore correlated important clinical and laboratory indices of diabetic ketoacidosis with sequential determinations of serum and urine amylase concentrations, amylase/creatinine clearance ratios, and specific amylase isozyme types. Hyperamylasemia occurred in 79% of our patients with diabetic ketoacidosis, often after admission to the hospital. Among these patients, 48% had pancreatic-type, 36% salivary-type, and 16% mixed-type (pancreatic and salivary) hyperamylasemia. There were no correlations between the presence, degree, or isozyme type of hyperamylasemia and most laboratory or clinical characteristics, including gastrointestinal symptoms. Patients with pancreatic-type hyperamylasemia tended to have higher amylase/creatinine clearance ratios, but it was not possible to unequivocably diagnose acute pancreatitis during diabetic ketoacidosis with current routine clinical or laboratory procedures.
Adult↗