Acute alcohol intoxication: significance of the amylase level

To evaluate the effects of acute alcohol intoxication on serum amylase and isoamylase levels, 58 clinically intoxicated patients with blood alcohol levels greater than 100 mg/dL were studied. Comparisons were made to normal control and a sober chronic alcoholic group. Admitting serum isoamylase levels were determined by cellulose acetate membrane electrophoresis and serum amylase levels measured by the Amylochrome technique. The average blood alcohol level in the intoxicated group was 301 +/- 99 mg/dL. Thirty of the 58 patients had hyperamylasemia (greater than 207 IU). Twenty-five of these 30 patients had hyperamylasemia from nonpancreatic sources (increased salivary isoamylase). Two of the 30 patients had pancreatic hyperamylasemia and three patients had elevated levels of both isoamylases. Neither of the patients with pancreatic hyperamylasemia had clinical evidence of acute pancreatitis. Although nine of the 58 patients had abdominal pain and clinical symptoms suggestive of acute pancreatitis, none of these patients had elevated pancreatic isoamylase. The finding of hyperamylasemia in acutely intoxicated patients is common. This is most frequently due to a rise in the salivary (nonpancreatic) isoamylase. The reliability of the total serum amylase as an indication of pancreatic disease in the intoxicated patient is questioned.     

Elevated serum amylase in patients with chronic pancreatitis: Acute attack or macroamylasemia?

Background and aimAsymptomatic patients with chronic pancreatitis not infrequently have elevated concentrations of amylase, even though detailed examination reveals no indication of an acute exacerbation.MethodsOne hundred and eighty-six consecutive patients with chronic pancreatitis were examined clinically and, if indicated, by ultrasonography and computed tomography. In addition, all patients underwent determination of serum amylase and serum lipase as well as amylase/creatinine clearance, followed as required by a polyethylene glycol test and/or chromatography to demonstrate macroamylase.ResultsTwenty (11%) of the 186 patients had macroamylasemia, and 15 of these 20 had hyperamylasemia. In the remaining five cases the serum amylase levels were within the normal range.ConclusionsPatients with asymptomatic chronic pancreatitis and hyperamylasemia should first be investigated for macroamylasemia, before initiating any costly or complex procedures in the attempt to demonstrate a clinically silent or only mildly symptomatic attack of their disease.     

The Admission Serum Lipase:Amylase Ratio Differentiates Alcoholic from Nonalcoholic Acute Pancreatitis

To determine whether the lipase:amylase ratio differentiates alcoholic from nonalcoholic pancreatitis, we conducted a retrospective review of charts with the diagnosis of acute pancreatitis at the George Washington University Medical Center between January 1988 and July 1990. A total of 446 charts were reviewed. For a patient to be included in the subsequent analysis, the following criteria were met: 1) the patient had typical symptoms of pancreatitis, 2) serum amylase and lipase were analyzed on admission, and 3) a computerized tomographic (CT) scan or ultrasound of the abdomen was obtained within 72 h of admission. Forty-seven charts satisfied the requirements for inclusion in the study. Data collected from the charts included history of alcohol consumption, age, sex, race, admission serum amylase and serum lipase (from this the amylase:lipase ratio was calculated), peak serum amylase and serum lipase, and number of days of abdominal pain before admission. Patients with alcoholic pancreatitis had significantly lower serum amylase levels and significantly higher lipase:amylase ratios than those with nonalcoholic pancreatitis (p < 0.01). There was no difference in the serum lipase between the groups. The higher the lipase:amylase ratio, the greater the specificity of alcohol as the etiology of acute pancreatitis. Only patients with alcoholic acute pancreatitis had lipase:amylase ratios > 5.0 (sensitivity 31%, specificity 100%). Our data point to the clinical utility of the lipase:amylase ratio in differentiating alcoholic from nonalcoholic acute pancreatitis. Prospective studies will be needed to confirm the clinical utility of this ratio.     

Elevated Serum Amylase Activity in the Absence of Clinical Pancreatic or Salivary Gland Disease

Elevated serum amylase activity, in the absence of clinically apparent pancreatic or salivary gland disease, has been observed in many seemingly unrelated conditions. In a search for common etiological factors to account for hyperamylasemia in these conditions, a retrospective analysis was performed. Eighty-four episodes of hyperamylasemia (> 300 I.U./l. Phadebas method) occurring in 75 patients over a one-year period ending in June, 1975 were assigned to one of two groups. Group 1 consisted of 56 (67%) episodes of hyperamylasemia with clinical pancreatitis. Group 2 consisted of 28 (33%) episodes of hyperamylasemia in the absence of clinical pancreatitis. Hypoxemia (pO₂ < 75 mm. Hg.) was found in 9/15 patients in Group 2 who had arterial blood gases measured. To assess the possible relationship between acute hypoxemia and amylase activity, a prospective study was initiated. Patients with known causes of pancreatitis or renal failure were eliminated. Hyperamylasemia was found in 3/8 hypoxemic patients. This raises the possibility that acute hypoxemia alone or in combination with other factors may raise serum amylase activity, possibly through ischemic injury to the pancreas or salivary glands or other amylase containing tissues.     

Trypsin activity

A normal serum amylase level is found in up to 32% of patients with acute alcoholic pancreatitis. This underlines the need for more sensitive diagnostic tests in this frequent cause of pancreatitis. Animal and human studies have shown that chronic alcohol consumption leads to important modifications in trypsinogen metabolism. The present work has prospectively analyzed admission serum trypsin activity with a new biochemical test and usual markers such as amylase, lipase, and immunoreactive trypsin in 32 attacks of acute pancreatitis. Seventeen were due to alcohol and 15 to other causes, including 11 with gallstone pancreatitis. High trypsin activity (median: 235 units/liter; range: 165–853) was found in all patients with acute alcoholic pancreatitis even when the amylase level was normal on admission (3/17: 18%). Trypsin activity did not differ between nonalcoholic pancreatitis (N=15): 84 units/liter (42–98), alcoholic controls (N=15): 77 units/liter (40–122), and healthy controls (N=62): 81 units/liter (15–143). The difference was not related to the severity of disease or circulating α₂-macroglobulin, α₁-protease inhibitor, or immunoreactive trypsinogen levels. Lipase/amylase ratio was less discriminant than trypsin activity between alcoholic and nonalcoholic diseases. We conclude that serum trypsin activity seems specific to acute alcoholic pancreatitis and should be included in new prospective studies assessing biochemical testing of alcohol-related pancreatic diseases.     

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.     

Serum amylase isozymes in patients with chronic pancreatitis with hyperamylasemia

In order to clarify the relationship between hyperamylasemia and clinical states in chronic pancreatitis, serum amylase isozymes were studied in 39 cases of chronic pancreatitis including 13 cases of alcoholic pancreatitis. Hyperamylasemia in chronic pancreatitis is generally due to high pancreatic type isoamylase (P-amylase) activity in acute exacerbation, sometimes accompanied by a transient elevation in salivary type isoamylase (S-amylase). On remission, however, hyperamylasemia due to high S-amylase activity has been found. These were cases of advanced alcoholic pancreatitis, which exhibited a characteristic pattern of low serum P-amylase and high serum S-amylase activities while the clearance ratio (Cam/Ccr) was normal despite high S-amylase activity. It should be noted that hyperamylasemia in chronic pancreatitis may be caused by high S-amylase activity in addition to high P-amylase activity, especially in alcoholic pancreatitis.     

Pancreatic enlargement in alcoholic pancreatitis: prevalence and natural history.

We determined the prevalence and natural history of pancreatic enlargement by abdominal ultrasonography or computed tomography in 72 patients with alcoholic pancreatitis. Pancreatic enlargement was observed in 54 patients (75%); it was diffuse in 28 (52%) and focal in 26 (48%). The focal enlargement was frequently cystic (50%), while the diffuse enlargement was only occasionally cystic (7%). Sequential imaging of the pancreas in 29 patients demonstrated partial to total resolution of pancreatic enlargement in greater than 50% during 6 months of follow-up. Determination of serum amylase and p-isoamylase activity was neither sensitive nor specific for pancreatic enlargement in alcoholic pancreatitis.     

Atypical eating disorder masquerading as recurrent acute pancreatitis: the value of multiple pancreatic serological markers.

A 28-year-old woman with nausea, vomiting, and abdominal pain had been hospitalized elsewhere on 13 separate occasions over the year before this admission for similar episodes thought to be secondary to acute pancreatitis. She had undergone repeated work-ups including endoscopic retrograde cholangiopancreatography, computed tomographic scan, and exploratory laparotomy. There was a discrepancy between her unremarkable physical examination and extremely elevated amylase (3,210 U/L) which suggested nonpancreatic hyperamylasemia; normal serum pancreatic isoamylase, trypsinogen, and lipase confirmed this suspicion. The patient was noted to have self-induced vomiting in the hospital which she admitted was frequent behavior. her psychiatric disturbance was characterized as an atypical eating disorder. This case illustrates that hyperamylasemia in association with abdominal pain, nausea, and vomiting may not be secondary to pancreatitis and that use of a second serum marker (such as trypsinogen, lipase, or isoamylase) helps to establish a definitive diagnosis.     

Correlation of serum amylase levels with pancreatic pathology and pancreatitis etiology

Fifty-one patients, 35 men and 16 women, with acute pancreatitis were studied prospectively with early computed tomography (CT). Etiological factors for acute pancreatitis were alcohol abuse (n = 28), gallstones (n = 14), pancreas cancer (n = 3) and miscellaneous (n = 6). Admission serum amylase levels ranged between 68-5,856 U/L with a mean of 1,090 +/- 1,369 U/L. The mean serum amylase level was significantly different between patients with alcoholic pancreatitis (439 +/- 302 U/L) and gallstone pancreatitis (2,480 +/- 1,575) (p less than 0.001). The initial pancreatic CT findings and corresponding mean serum amylase levels were in CT grade A (pancreas normal) 1,499 +/- 1,569 U/L (n = 11), in CT grade B (pancreatic enlargement with inflammation confined to pancreas) 1,144 +/- 1,542 U/L (n = 18), in CT grade C (inflammatory extension into one peripancreatic space) 722 +/- 962 U/L (n = 13) and in CT grade D (inflammatory extension into two or more peripancreatic spaces) 590 +/- 369 U/L (n = 9). However, on separating the etiology subgroups, there was no increase or decrease in the serum amylase level with increasing pancreatic inflammatory involvement. Pancreatic complications (pseudocyst, abscess, necrosis) requiring surgical intervention developed only in patients with CT grades C and D. We conclude that within the etiologic subgroups there is no correlation between the initial serum amylase level and the extent of pancreatic involvement visualized by CT. These findings provide a pathological basis for the clinical observation that the initial serum amylase level cannot predict the outcome in acute pancreatitis.     

Lipase/amylase ratio. A new index that distinguishes acute episodes of alcoholic from nonalcoholic acute pancreatitis.

Because of observations that patients with acute episodes of alcoholic pancreatitis had high serum lipase levels whereas patients with gall stone pancreatitis had high serum amylase levels, a prospective study was undertaken to determine whether the ratio of serum lipase to serum amylase, a newly computed ratio, would discriminate between acute episodes of alcoholic and nonalcoholic pancreatitis. In phase one, 30 consecutive patients with acute pancreatitis were entered into the study and divided into groups A and B. Patients with renal failure were excluded from the study. Group A consisted of 20 patients in whom the etiology of pancreatitis was alcohol. Group B consisted of 10 patients whose pancreatitis was nonalcoholic in etiology (predominantly gallstones). Serum lipase values in group A ranged 492 to 25,706 U/L (median, 3433 U/L) and in group B from 711 to 31,153 U/L (median, 1260 U/L). These differences were not significant statistically. Serum amylase values in group A ranged from 104 to 2985 U/L (median, 331 U/L) and in group B from 423 to 13,000 (median, 1187 U/L). Although these figures were statistically different (P less than 0.005), there was a considerable degree of overlap in the values between the two groups. The lipase/amylase ratio calculated from the blood sample obtained at presentation appeared to be a promising discriminatory index. The lipase/amylase ratio was calculated by using the amylase and lipase levels expressed as multiples of the upper limit of normal in each case. The lipase/amylase ratios in the alcoholic group ranged from 2.2 to 14.8, whereas the lipase/amylase ratio in nonalcoholic pancreatitis ranged from 0.31 to 1.93. These differences were statistically significant (P less than 0.005). A lipase/amylase ratio of greater than 2 was indicative of an alcoholic etiology, and a ratio of less than 2 suggested that the pancreatitis was nonalcoholic in nature. In phase two, this lipase/amylase ratio of 2 was applied prospectively to an unselected population of 21 consecutive patients with acute pancreatitis. Thirteen patients had a lipase/amylase ratio of greater than 2; in 11 of them, the etiology of the pancreatitis was alcohol. Eight patients had a lipase/amylase ratio of less than 2; of them, only 1 patient had an alcoholic etiology for the pancreatitis. These differences were statistically significant (P less than 0.05).(ABSTRACT TRUNCATED AT 400 WORDS)     

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.     

Detection of painless pancreatitis by computed tomography in patients with post-endoscopic retrograde cholangiopancreatography hyperamylasemia

ObjectivesPost-endoscopic retrograde cholangiopancreatography (ERCP) pancreatitis is diagnosed on the basis of pancreatic pain and hyperamylasemia. However, because the diagnosis of abdominal pain is not objective, there may be some cases of painless pancreatitis among patients with post-ERCP hyperamylasemia (PEH). We reviewed the computed tomography (CT) findings of PEH cases to determine the incidence of painless pancreatitis.MethodsBetween July, 2005 and December, 2011, CT was performed in 91 patients with hyperamylasemia 18 h after ERCP. We reviewed the CT findings and graded the severity of pancreatitis according to the Balthazar grading system. Grades C, D, and E were defined as pancreatitis.ResultsThirty-four patients (37%) had pancreatitis according to the CT findings. There was a significant difference in the serum amylase levels between the positive- and negative-CT finding groups (1306 ± 833 vs. 786 ± 315 IU/L, respectively; p = 0.0012). Receiver operating characteristic curve analysis showed that the amylase cut-off value for discriminating between the 2 groups was 795 IU/L (6.36 times the upper normal limit).ConclusionsThirty-seven percent of PEH patients had painless pancreatitis. CT is useful to determine pancreatitis in patients taking analgesics, steroids, or anti-immunological drugs and those with diabetes mellitus and 18-h serum amylase levels of >6 times the normal upper limit.     

Underestimation of acute pancreatitis: patients with only a small increase in amylase/lipase levels can also have or develop severe acute pancreatitis

BACKGROUND: In most treatment studies on acute pancreatitis, pancreatologists base their diagnosis on amylase/lipase levels more than three times above the upper limit of normal (>3n) and thus exclude patients with smaller enzyme level increases. The recommendations derived from the results of treatment studies do not take into account such patients. Non-pancreatologists frequently believe that only patients with high enzyme levels have a serious prognosis. AIMS: To question the assumption that high enzyme levels indicate severe, and conversely low enzyme levels indicate mild, acute pancreatitis. PATIENTS/METHODS: This retrospective study includes 284 consecutive patients with a first attack of acute pancreatitis. The cause was biliary in 114 (40%) patients, alcoholism in 83 (29%), other in 21 (7%), and unknown in 66 (23%). Patients were divided into two groups according to their serum enzyme levels (amylase: 3n, n = 196; lipase: 3n, n = 233). Renal impairment, indication for dialysis and artificial ventilation, development of pseudocysts, necessity for surgery, and mortality were taken as parameters of severity. RESULTS: The incidence of severity was the same for both the 3n groups. CONCLUSIONS: The severity of acute pancreatitis is independent of the elevation in serum amylase/lipase level (3n) on admission. Patients with only a slight increase can also have or develop severe acute pancreatitis. Patients with 相似文献   

Pancreatic Hyperamylasemia and Hyperlipasemia in Association with Cytomegalovirus Infection Following Unrelated Cord Blood Transplantation for Acute Myelogenous Leukemia

Cytomegalovirus (CMV)-associated pancreatitis is rare after allogeneic hematopoietic stem cell transplantation (SCT). We describe a patient who developed pancreatic hyperamylasemia and hyperlipasemia in association with CMV infection after cord blood transplantation (CBT). A 31-year-old man with acute myelogenous leukemia underwent CBT. A neutrophil count consistently greater than 500/microL was achieved on day +21. Positive results for CMV antigenemia on days +35 and +67 prompted 2 courses of preemptive therapy with ganciclovir or foscarnet. The CMV antigenemia value again became positive on day +134. On day +141, serum amylase and lipase activities markedly increased to 1221 IU/L and 894 IU/L, respectively. The patient had no abdominal symptoms. Ultrasonography and computed tomography results showed no abnormalities of the pancreas. A diagnosis of possible pancreatitis was made. After the initiation of foscarnet therapy, the CMV antigenemia results soon became negative, and serum amylase and lipase activities returned to normal. Therefore, CMV infection was considered to play a major role in the development of pancreatic hyperamylasemia and hyperlipasemia in our patient. The present report indicates that CMV infection should be included in the differential diagnosis for patients with pancreatic hyperamylasemia after SCT.     

The Lipase to Amylase Ratio in Acute Pancreatitis

Objectives : The ratio of serum lipase to serum amylase has been proposed to distinguish acute episodes of alcoholic from nonalcoholic pancreatitis. We evaluated the efficacy of this test in a community hospital setting. Methods : Charts of all patients discharged with a diagnosis of acute pancreatitis over 19 months were retrospectively reviewed. Patients were excluded if their cre-atinine was greater than 3.0 mg/dl, if the amylase and lipase were not measured within 72 h of the onset of symptoms, or if the cause of pancreatitis was not known by the time of discharge. Results : Of the 56 patients, 31 had alcoholic pancreatitis. The lipase to amylase ratio did not differ significantly between patients with alcoholic and nonalcoholic pancreatitis. Median amylase and lipase were significantly higher in nonalcoholic pancreatitis; however, the wide ranges of both meant that neither amylase nor lipase accurately determined the cause of pancreatitis. Conclusion : The lipase to amylase ratio does not appear to be sufficiently sensitive or specific to distinguish alcoholic from nonalcoholic acute pancreatitis.     

Undetected Fatal Acute Pancreatitis: Why is the Disease so Frequently Overlooked?

An analysis of postmortem investigations between 1980 and 1985 revealed 43 patients with acute pancreatitis. In 13 (30.2%) of them, the diagnosis was first established at autopsy. In eight of the latter patients, the diagnosis could have been present on admission. The etiology was alcoholism in three patients, hypothermia in one, biliary tract disease in one, and unknown in three patients. In five patients, acute pancreatitis developed after gastric, pancreatic, or biliary tract surgery. Abdominal pain was present in only one patient. Amylase levels had been estimated in 11 patients, but the level was in the diagnostic range (greater than or equal to 3 times of upper normal level) in only four. Consequently, ultrasound examination was performed in only two of the latter four patients, but failed to show the pancreas because of intestinal gas. To diagnose acute pancreatitis at an earlier stage and to improve therapy and prognosis, we recommend that serum amylase levels be measured and ultrasound examination be performed. If the results are inconclusive, this should be followed by computed tomography for all abdominal emergency cases and for patients who have undergone cardiopulmonary or upper abdominal surgery, especially when the patients deteriorate or fail to improve postoperatively.     

Serum amylase measured four hours after endoscopic sphincterotomy is a reliable predictor of postprocedure pancreatitis

OBJECTIVE: Acute pancreatitis is a common complication after endoscopic sphincterotomy (ES) and endoscopic retrograde cholangiopancreatography (ERCP). The aim of this study was to detect the time when the peak of serum amylase was predictive for pancreatitis or severe hyperamylasemia, to plan a prolonged follow-up in the hospital and for outpatients. METHODS: In a prospective series of 409 consecutive patients undergoing ES, serum amylase activity was measured immediately before the procedure and 2, 4, 8, and 24 h thereafter; the data obtained at 2, 4, and 8 h were compared with those at 24 h and with the outcome. Sensitivity for long-lasting severe hyperamylasemia (more than five times the upper normal limit) and pancreatitis were also defined for all sampling times. RESULTS: At 24 h after ES, amylase was still more than five times the upper normal limit in 26 patients, 19 of whom had mild/moderate acute pancreatitis. There was a significant difference (p < 0.01 at all sampling times) between the 26 patients with 24-h severe hyperamylasemia and those with lower levels. The sensitivity of amylase measurement in detecting pancreatitis or long-lasting severe hyperamylasemia was highest at 8 h. However, the 4-h assessment appears to be a reliable predictor in practice, as more than two-thirds of cases of pancreatitis (all but one with computed tomography-confirmed pancreatitis) occurred among patients whose 4-h amylasemia was higher than five times the upper normal limit. CONCLUSIONS: Serum amylase assessment 4 h after ES minimizes the likelihood of underestimating the risk of postprocedure pancreatitis. It is therefore a reliable, cost-effective follow-up, particularly in outpatients.     

静脉滴注丹参注射液预防ERCP术后高淀粉酶血症及急性胰腺炎的临床研究

目的探讨丹参注射液预防内镜逆行胰胆管造影(ERCP)术后高淀粉酶血症及胰腺炎的临床疗效。方法将100例胆总管结石需行ERCP术患者,随机分为观察组50例和对照组50例,两组患者ERCP术后给予常规鼻胆引流、抗感染、抑制胰酶分泌等治疗,观察组于ERCP术前及术后1 d,给予丹参注射液250 mL,2次/d,静脉滴注。分别于术前、术后3 h、24 h检测两组患者的血淀粉酶、脂肪酶水平、术后24 h CRP。统计术后高淀粉酶血症、胰腺炎发生率。结果两组患者术后3 h、24 h血淀粉酶明显高于术前,但观察组术后3 h、24 h血淀粉酶低于对照组同期水平(P0.05);观察组患者高淀粉酶血症发生率为42%(21/50),术后胰腺炎发生率为0%(0/50),对照组高淀粉酶血症发生率为80%(40/50),术后胰腺炎发生率为8%(4/50)。结论丹参注射液对ERCP术后高淀粉酶血症、胰腺炎有一定的预防作用。