Clinical Biochemistry 50 (2017) 1275–1280

Contents lists available at ScienceDirect

Clinical Biochemistry
journal homepage: www.elsevier.com/locate/clinbiochem

Review

Lipase or amylase for the diagnosis of acute pancreatitis? T

a,b b,c,⁎
Ola Z. Ismail , Vipin Bhayana
a
Matthew Mailing Centre for Translational Transplant Studies, Lawson Health Research Institute, London, Ontario, Canada
b
Pathology and Laboratory Medicine, London Health Sciences Centre & St. Joseph's Health Care London, London, Ontario, Canada
c
Western University, Department of Pathology and Laboratory Medicine, London, Ontario, Canada

A R T I C L E I N F O A B S T R A C T

Keywords: Acute pancreatitis is a rapid onset of inflammation of the pancreas causing mild to severe life threatening
Acute pancreatitis conditions [1, 2]. In Canada, acute pancreatitis is the 5th most expensive digestive disease in Canada with a
Amylase considerable economic burden on the health care system [3]. The diagnosis of acute pancreatitis is usually based
Lipase on the presence of abdominal pain and elevated levels of serum amylase and/or lipase. Many health care centers
Diagnostic
use either serum amylase, lipase or both to diagnose acute pancreatitis without considering which one could
Biomarkers
provide a better diagnostic accuracy. The aim of this review is to investigate whether serum lipase alone is a
sufficient biomarker for the diagnosis of acute pancreatitis. We have examined various studies looking at the
utilization, sensitivity, specificity and cost associated savings of lipase and amylase in the diagnosis of acute
pancreatitis. When comparing different studies, serum lipase offers a higher sensitivity than serum amylase in
diagnosing acute pancreatitis. Lipase also offers a larger diagnostic window than amylase since it is elevated for a
longer time, thus allowing it to be a useful diagnostic biomarker in early and late stages of acute pancreatitis.
Several recent evidence-based guidelines recommend the use of lipase over amylase. Nevertheless, both lipase
and amylase alone lack the ability to determine the severity and etiology of acute pancreatitis. The co-ordering
of both tests has shown little to no increase in the diagnostic sensitivity and specificity. Thus, unnecessary testing
and laboratory expenditures can be reduced by testing lipase alone.

1. Introduction dysfunction causing injury and inflammatory response. Alcohol abuse

Acute pancreatitis, the inflammatory disorder of the pancreas, is one
of the most frequent gastrointestinal causes of hospital admission. The
annual incidence of acute pancreatitis visits range between 13 and 45
per 100,000 persons in the United States and Canada [4]. Acute pan-
creatitis can either resolve quickly, or cause a systematic inflammatory
response leading to a multi-organ failure and death [5]. Despite im-
provements in the diagnosis of disease and treatment, the mortality rate
of acute pancreatitis remains around 5% [5]. The average length of
hospital stay for acute pancreatitis patients is eight days, with a mean
cost per hospitalization of CAD $8896 [4]. Hence, acute pancreatitis is
an economic burden to patients and the health care system.
2. Etiology and pathophysiology
The most common causes of acute pancreatitis are biliary tract
obstruction by gallstone (up to 40% of cases) and alcohol abuse (up to
35% of cases) [1,6]. Mechanistically, pancreatic duct obstruction by
gallstone leads to the blockage of pancreatic secretion and lysosomal
exerts toxic effect on several types of pancreatic cells, most notably
acinar cells, which results in the generation of toxic metabolite and
activation of signaling pathways promoting the injury of acinar cells
[6]. Other less frequent causes of acute pancreatitis include post en-
doscopic retrograde cholangiopancreatography (ERCP), medication,
infection, hypercalcemia (total serum calcium concentration of >
2.60 mmol/L), hypertriglyceridemia (triglyceride level of > 10 mmol/
L), tumors, vascular abnormalities and abdominal trauma [1]. Genetic
abnormalities such as mutations in the cystic fibrosis transmembrane
conductance regulator allele have been shown to lead to pancreatic
ductal obstruction and recurrent acute pancreatitis [7]. Other muta-
tions in the pancreatic secretory cationic trypsinogen inhibitor gene
have been linked to autosomal dominant hereditary pancreatitis which
manifests as recurrent acute pancreatitis and develops to chronic pan-
creatitis [8].
3. Clinical signs and symptoms
The clinical presentation of acute pancreatitis involves a sudden

⁎
Corresponding author at: London Health Sciences Centre and St. Joseph's Health Care London, 800 Commissioners Road E, Rm. B10-212, London, ON N6C 2R6, Canada.
E-mail address: Vipin.Bhayana@lhsc.on.ca (V. Bhayana).

http://dx.doi.org/10.1016/j.clinbiochem.2017.07.003
Received 25 April 2017; Received in revised form 14 July 2017; Accepted 15 July 2017
Available online 16 July 2017
0009-9120/ © 2017 The Canadian Society of Clinical Chemists. Published by Elsevier Inc. All rights reserved.
O.Z. Ismail, V. Bhayana
onset of abdominal pain in the upper left quadrant that radiates to the
back with nausea and vomiting [5,6]. Patients could also present fever,
hypotension, tachycardia, abdominal distension, and/or jaundice. Since
the clinical presentation of acute pancreatitis varies, a clinical classifi-
cation system is used to assist in managing patients according to their
disease severity. The most currently used classification system in
guidelines and clinical diagnosis is the Revised Atlanta Classification
[9]. This classifies the disease into two phases, early and late, with
various severity index; mild, moderate and severe [9]. Mild acute
pancreatitis is the most common form with no organ failure, local
complications (such as necrosis and pseudocyst formation) or sys-
tematic complications [6,9,10]. Moderately severe acute pancreatitis is
indicated by transient organ failure (lasting < 48 h) and/or local or
systematic complications. Severe acute pancreatitis is classified by
persistent single or multiple organ(s) failure (lasting for > 48 h). The
revised Atlanta Classification diagnosis of acute pancreatitis entails the
presence of at least two of three criteria; abdominal pain, serum lipase
or amylase activity at least three times the upper limit of normal, or
characteristic radiological findings by contrast-enhanced CT, transab-
dominal ultrasonography or MRI [6,9]. Both abdominal pain and ele-
vated lipase or amylase serve as the first steps in diagnosing acute
pancreatitis, with less reliance on radiological findings that increase
medical costs. Predicting the course of acute pancreatitis is often dif-
ficult; thus it is necessary to start immediate basic treatment at its first
signs. This often includes fluid resuscitation, oxygen supplementation,
analgesia, and nutritional support [6]. In gallstone-associated acute
pancreatitis patients, a cholecystectomy is generally performed [5].
4. Current diagnostic biomarkers for acute pancreatitis
An important part of acute pancreatitis' diagnosis and treatment is
the assessment of pancreatic enzymes, specifically serum amylase and
lipase.
4.1. Total and pancreatic amylase
Amylase is synthesized mostly by pancreatic acinar cells and sali-
vary glands, and in negligible level by adipose tissue, the gonads, fal-
lopian tubes and intestinal tract and skeletal muscles [1,11,12]. Hu-
mans only have one specific isoenzyme, the α-amylase, with different
isoforms specific to the pancreatic or salivary gland. The use of specific
monoclonal antibodies allows for the detection of specific pancreatic α-
amylase in a serum test rather than total amylase level [13,14]. The
measurement of pancreatic amylase has improved the sensitivity and
specificity in the diagnosis of acute pancreatitis [15,16]. However, due
to the increased cost associated with measuring pancreatic amylase and
inconvenience when it comes to different instrumental platforms, the
measurement of pancreatic amylase has been largely disregarded while
the measurement of total amylase continues to be widely used in clin-
ical laboratory [14,17,18]. Most of amylase is reabsorbed by the renal
proximal tubules where the liver is responsible for breaking down most
of the amylase with very little excreted through renal system [19,20].
Renal clearance of amylase refers to the rate of glomerular filtration
and tubular reabsorption of amylase and is usually elevated in acute
pancreatitis [21].
The serum amylase concentration usually reflects the balance be-
tween the rate of amylase synthesis and removal. In the case of acute
pancreatitis, the rise in serum amylase level to at least three times the
upper limit of normal occurs rapidly in the blood, with peaks at three to
six hours following the onset of symptoms, a half-life of ten to twelve
hours and persistent elevation for three to five days.
Hyperamylasemia could occur due to other pancreatic diseases,
such as pancreatic obstruction and pancreatic cancer [1]. High amylase
levels could also occur as a result of several malignant conditions, such
as breast, colon, lung, and ovarian cancers [1]. The loss of bowel in-
tegrity, in conditions such as ulcers, intestinal perforation, perforated
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Clinical Biochemistry 50 (2017) 1275–1280
duodenal ulcer or ischemia and appendicitis, could lead to hyper-
amylasemia due to the reabsorption of amylase from the intestinal
lumen [11,17]. In addition, decreased metabolic clearance of amylase
as indicated by decrease renal filtration and reabsorption, causes an
increase in serum amylase level [20,21]. This has been seen in condi-
tions such as renal failure or macroamylasemia. Macroamylasemia is
referred to the large complex formed between amylase and im-
munoglobulins (usually IgA), which usually leads to a decrease in renal
function and prolong the presence of amylase in serum and subse-
quently an abnormal increase in the level of serum amylase [1,22].
Other non-pancreatic conditions causing elevated amylase include
cystic fibrosis, burns, hepatitis, cirrhosis, acidosis, pregnancy, gyneco-
logical disorder, peritonitis, chronic alcoholism, acute aortic dissection,
head injury and various drugs and infectious diseases [1]. Salivary
diseases involving salivary glands could also increase the level of total
amylase in serum by more than three folds, causing the need for more
specific pancreas enzymes in order to determine the diagnosis of acute
pancreatitis.
4.2. Lipase
Serum lipase is another pancreatic enzyme that is mainly produced
by acinar cells and is at 100 times greater concentration than other
isoforms of hepatic, endothelial and lipoprotein lipase [1]. In acute
pancreatitis, the increased permeability of cells producing serum lipases
allows the release of enzymes to circulate at a high level. Hence, the
elevation of serum lipase arises within three to six hours of onset
symptoms, peaks within 24 h, and has a persistent elevation of up to
two weeks [1]. This gives lipase a larger diagnostic window in com-
parison to amylase. In addition, lipase has a higher specificity than
amylase since it is mainly produced by pancreas. When the lipase test
was first introduced in the 1930′s [13], it was difficult to measure and
consequently had limited use due to interferences by lipoprotein lipase,
intestinal lipase, hepatic lipase and carboxylesterase. However, the use
of reagent systems that are specific for pancreatic lipase and addition of
bile salts, colipase and calcium as cofactor has improved the specificity
and sensitivity of the lipase test [5,13]. The specificity of the lipase test
is still not perfect due to several cases of non-pancreatic related ele-
vations in lipase with normal amylase levels and no abdominal dis-
comfort. These cases are usually present in patients with renal in-
sufficiency and high alcohol intake [5]. Similar to amylase, elevated
serum lipases with abdominal discomfort could be due to other non-
pancreatic diseases, such as trauma, appendicitis, diabetic ketoacidosis,
inflammatory bowel disease, intestinal obstruction or infraction, fat
embolism, liver, renal failure, and hypertriglyceridemia [1]. Other
cases associated with abdominal pain were due to acute cholecystitis or
esophagitis and non-pancreatic malignant tumors secreting lipolytic
enzymes. In addition, numerous drugs and infections attribute to the
non-pancreatic increase in lipase levels.
4.3. Limitation of the amylase and lipase tests
Despite the use of amylase or lipase to diagnose acute pancreatitis,
there are several cases where symptoms and radiologic evidences point
to acute pancreatitis with normal levels of lipase and amylase. In some
of these cases, normal levels of amylase and lipase were found in
gallstone and alcohol induced acute pancreatitis, and even in severe
necrotizing acute pancreatitis [23]. Another cases have showed a
normal level of lipase and amylase in acute pancreatitis patients with
hypertriglyceridemia [6,23,24]. These normal levels could be related to
the timing of patients' presentation to the emergency department where
a very early or late presentations might give normal level results.
Various studies suggested that an initial negative result of lipase and
amylase tests is unlikely to yield a positive result, especially when the
patient is presented to the emergency department within < 4 to 5 h of
onset abdominal pain [25]. These cases highlight the importance of
O.Z. Ismail, V. Bhayana
clinical judgment and radiological examination in diagnosing acute
pancreatitis with normal amylase and lipase levels. Nevertheless, most
clinicians will usually rely on clinical presentation and elevated levels
of serum amylase and/or lipase to diagnose acute pancreatitis.
In clinical practice, both lipase and/or amylase tests lack the ability
to determine the severity and etiology of pancreatitis. In terms of se-
verity determination, recent studies showed that combining lipase with
other tests, such as serum c-reactive protein and procalcitonin, could
help in determining the severity of the illness following diagnosis
[26–29]. In pediatric patients, a lipase level of equal to or more than
seven times the Upper Limit of Reference Interval (ULR) has been
shown to be an early indicator for severe acute pancreatitis [30]. The
sensitivity of lipase in predicting severe pediatric acute pancreatitis
ranges between 72% and 85%, but the specificity is much lower at a
range between 41% and 56% [30,31]. Another retrospective study
showed that combining serum calcium and lipase together improved
the specificity of predicting severe pediatric acute pancreatitis [30,32].
Lipase might offer a competitive edge over amylase in determining the
severity of acute pancreatitis, though these results should be interpreted
with caution.
Measuring both lipase and amylase to determine the etiology of
acute pancreatitis has been a highly debated subject [33]. The first
prospective study of 20 patients concluded that a ratio of lipase to
amylase serum level greater than two is indicative of alcoholic acute
pancreatitis [34]. Several retrospective studies found that a lipase to
amylase ratio of more than five is indicative of alcoholic pancreatitis
(sensitivity 31%, specificity 100%) [35–37]. In another study, the lipase
to amylase ratio was found to have a greater sensitivity (96%) for di-
agnosing obstructive biliary acute pancreatitis than individual tests of
alanine transaminase, aspartate transaminase, lipase or amylase [38].
In contrast, the ratio of lipase to amylase in other studies did not cor-
relate with the cause of acute pancreatitis [33,39–42]. The sensitivity,
specificity, accuracy, and positive and negative predictive values of li-
pase to amylase ratios were ineffective in determining the etiology of
acute pancreatitis [42–45].The effectiveness of the ratio of lipase to
amylase in determining the etiology remains questionable. Never-
theless, elevated serum amylase or lipase with high levels of aspartate
aminotransferase, alanine aminotransferase and alkaline phosphatase
has been associated with biliary obstruction; a cause of acute pan-
creatitis [36,46,47].
4.4. Evidence-based guideline recommendations
In clinical biochemistry laboratories, guidelines and recommenda-
tions published by international organizations or scientific societies are
helpful to determine which laboratory test should be used for the di-
agnosis of acute pancreatitis. Many international guidelines, such as
that of the International Association of Pancreatology, recommend the
use of lipase or amylase for acute pancreatitis diagnosis, with pre-
ference towards serum lipase [48]. The earliest guideline to recommend
the use of lipase only for the diagnosis of acute pancreatitis was by the
United Kingdom Working Group, in 2005, since lipase has a longer half-
life than amylase and it is only released from the pancreas [49]. Simi-
larly, the Japanese guideline has always relied on elevated levels of
serum lipase in the diagnosis of acute pancreatitis, where the mea-
surement of pancreatic amylase is only recommended if the measure-
ment of lipase is difficult to perform [50]. Interestingly, the Italian
Society of Clinical Biochemistry and Clinical Molecular Biology re-
commended the use of pancreatic serum amylase than total serum
amylase due to its fast detection of pancreatic injury [51]. However,
their recent guideline prefers lipase over amylase in the detection of
acute pancreatitis [52]. The practice guidelines released by the Amer-
ican College of Gastroenterology suggest that both serum amylase and
lipase could be used for the diagnosis of acute pancreatitis, with pre-
ference to lipase test [53]. In 2016, the Canadian Practice Guidelines
concluded that the serum lipase test should only be performed in
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Clinical Biochemistry 50 (2017) 1275–1280
patients suspected of acute pancreatitis, and that a threefold increase is
required to make a diagnosis [54]. In summary, various guidelines have
shifted their preference to lipase test instead of amylase in order to
diagnose acute pancreatitis.
4.5. Comparing amylase and lipase
Many clinicians co-ordered both amylase and lipase to increase the
accuracy in diagnosing a patient with acute abdominal pain [1]. When
comparing amylase to lipase we will consider which test has a better
sensitivity and specificity and whether co-ordering provides a more
accurate diagnosis.
Literatures review by Beauregard et al. indicated that several pro-
spective and retrospective studies did not find any significant diagnostic
advantage of lipase over amylase in term of specificity, sensitivity and
accuracy [55]. Hence, we can confidently replace amylase testing with
lipase. In an early prospective study, where different diagnostic cut-off
points to diagnose acute pancreatitis were used, no difference was
found between serum amylase and lipase in terms of diagnostic accu-
racy as measured by the area under the Receiver Operating Curve
(ROC) [56]. On the other hand, a study of patients admitted with acute
abdominal pain indicated that serum lipase offered a better diagnostic
efficiency than amylase (94% versus 91%) [57], despite the tests having
similar degrees of specificity and sensitivity. Given that the level of li-
pase stays elevated for a longer time than that of amylase, a prospective
study looking at the level of amylase and lipase during the first day in
comparison to the third day of presentation of acute abdominal pain
revealed that serum lipase has a better degree of sensitivity and spe-
cificity for diagnosing acute pancreatitis during both early and late
stages of the disease [58]. A cut-off of three folds of the upper limit of
reference has improved the diagnostic criteria for acute pancreatitis by
increasing the sensitivity and specificity of both amylase and lipase
tests [1,2,59–62]. Several retrospective and cohort studies, summarized
in Table 1, have indicated that lipase is much more sensitive than
amylase and should replace amylase or co-ordering of both amylase and
lipase test when diagnosing acute pancreatitis. Moreover, amylase has
been shown to have a lower sensitivity that is influenced by the cause of
acute pancreatitis and the timing of the test due to its short half-life
[1,60–62]. When considering all the published studies on this topic, the
sensitivity of lipase and amylase tests in diagnosing acute pancreatitis
ranges between 64% to 100% and 45% to 87%, respectively. The spe-
cificities for lipase and amylase tests are similar and in the range of 92%
to 99%. Hence, lipase might offer a better diagnostic utility when it
comes to diagnosing acute pancreatitis.
There are several cases where the lipase test is often preferred over
the amylase test. In the case of hyperlipidemic acute pancreatitis, lipase
offers a better diagnostic accuracy of 91.8% than amylase (40.3%)
[64,65]. Patients with new or repeated alcoholic pancreatitis tend to
have normal amylase levels and only lipase would appear to be elevated
[66] [67]. Additionally, patients' prolong wait time for admission into
the hospital after the onset of symptoms, in which blood samples are
taken later than 24 h of onset of symptoms, usually show high levels of
lipase and normal levels of amylase [1]. The latter has accounted for up
to 19–32% of normal amylase level in acute pancreatitis cases [68,69].
This suggests that lipase is a much better diagnostic test than amylase.
4.6. Cost of amylase and lipase
An important aspect in clinical biochemistry laboratories is the cost
associated with running laboratory tests. Several studies have examined
the impact of utilizing serum lipase test only to diagnose acute pan-
creatitis in terms of cost saving advantages for laboratories and the
health care system (summarized in Table 2). In a pre- and post-cohort
study done in an emergency department setting involving educational
intervention for hospital staff (staff doctors, residents, nurses) to reduce
the co-ordering of lipase and amylase, the level of co-ordering was
O.Z. Ismail, V. Bhayana Clinical Biochemistry 50 (2017) 1275–1280

Table 1
Summary of various studies comparing lipase against amylase (URL - Upper Limit of Reference interval, AP - Acute Pancreatitis).

Design and reference Participant Threshold Results Conclusion

(patients with abdominal pain/AP)
Serum lipase Serum amylase

Prospective study 384 /60 Two times URL Diagnostic accuracy and efficiency No difference between amylase and lipase in
[56] is > 95% for both diagnosing AP
Retrospective study 306/48 Serum lipase: > 208 U/ 92% Sensitivity 93% Sensitivity Both tests are associated with AP, but serum
[57] L 87% Specificity 87% Specificity lipase is better than amylase
Serum amylase: > 110 94% Diagnostic 91% Diagnostic
U/L accuracy accuracy
Prospective study 328/51 Serum lipase: Day 1: Day 1 Serum lipase is better at diagnosing early and
[58] > 208 U/L (Day1) 64% Sensitivity 45% Sensitivity late AP
> 216 U/L (Day 3) 97% Specificity 97% Specificity
Serum amylase: Day 3 Day 3
> 176 U/L (Day 1) 55% Sensitivity 35% Sensitivity
> 126 U/L (Day 3) 84% Specificity 92% Specificity
Retrospective study 17,531/320 Serum lipase > 208 U/ 90.3% Sensitivity 78.7% Sensitivity Serum lipase is more accurate marker for AP
[63] *49 had elevated lipase only L 93.6% Specificity 92.6% Specificity
Serum amylase > 114
U/L
Cohort study [2] 1,520/44 Three times URL 64% Sensitivity 50% Sensitivity Serum lipase is preferable to use in
97% Specificity 99% Specificity comparison to amylase alone or both tests
Retrospective study 3451/34 Three or more times 95.5% Sensitivity 63.6% Sensitivity Both enzymes have good accuracy but lipase
[59] *33 patients had elevated amylase URL 99.2% Specificity 99.4% Specificity is more sensitive than amylase
only and 50 had elevated lipase only
Cohort study [60] 151/117 Three times URL 96.6% Sensitivity 78.6% Sensitivity Lipase is more sensitive in diagnosing AP and
*6 patients with gallstone-induced 99.4 Specificity 99.1% Specificity using it alone would present a substantial cost
and 5 patients with alcohol-induced saving on health care system
AP had elevated lipase only
Prospective study 476/154 Three times URL 91% Sensitivity 62% Sensitivity Lipase is more sensitive than amylase and
[61] *58 patients had a normal amylase 92% Specificity 93% Specificity should replace amylase in diagnosis of AP
level
Cohort study [62] 50/42 Three times URL 100% Sensitivity 78.6% Sensitivity Lipase is a better choice than amylase in
*8 patients had elevated lipase only diagnosis of AP

reduced by 2% [70]. Once the amylase test entry was removed from the
order list, the percentage of co-ordering dropped by 77%, resulting in
cost savings of $135,000 US per year [70,71]. In Canada, we have ex-
amined the volume of amylase and lipase tests ordered for 12 months in
the three London, Ontario hospitals that are associated with the London
Health Sciences Center. There were 28,807 amylase and lipase tests
performed with 9758 tests for amylase. The total cost of amylase and
lipase is about $14,000 CAD per year, with $6000 CAD for the cost of
amylase tests alone. Even though amylase is not as frequently ordered
as lipase at the London Health Sciences Center (about 34% of total
tests), eliminating the amylase test from the order list could bring sig-
nificant cost savings to the laboratory and health care system.
5. Conclusion
Over the years, lipase test has become a much more sensitive and
specific biomarker in diagnosing acute pancreatitis. Lipase offers a
larger diagnostic window when compared to amylase. Clinical evi-
dence, meta-analysis and various evidence-based guidelines have
recommended the use of lipase as the only diagnostic marker in an
effort to eliminate unnecessary expenditures of co-ordering both lipase
and amylase tests. Unfortunately, there is no international consensus on
eliminating amylase from the laboratory testing. Since clinical guide-
lines clearly discourage the use of both amylase and lipase, the next step
in laboratory medicine should focus on eliminating the practice of or-
dering both amylase and lipase to diagnose acute pancreatitis in the
health care sector. For a clinical biochemistry laboratory to successfully
implement the use of lipase only, a careful cost-benefit, cost-effective-
ness and, most importantly, cost-utility analysis of eliminating amylase
test should be considered. Another area of consideration is the fre-
quency of ordering lipase and/or amylase for monitoring the progress
of acute pancreatitis and whether therapeutic intervention is successful
in resolving pancreatitis and further preventing the progression into
organ dysfunction. Determining the appropriate rejection rule for re-
ordering lipase and/or amylase will minimize unnecessary repeat of
tests, provide cost saving advantages, and influence clinician-requesting
behaviour [72]. These strategies in general may help in advancing the
current practices in laboratories to provide more efficient, effective and

Table 2
Summary of studies exploring the cost implication associated with eliminating amylase test.

Design and reference Costs Volume of test Results

Cohort study (UK) [2] Amylase costs £1.94

Cohort study (UK) [60]
Prospective study (US) [71]
Lipase costs £2.50
1383 request for 62 days
costing £6136 for both tests
• Testing lipase only will result in cost saving
Single amylase or lipase cost about
£0.69 each
2979 requests costing
£2949.21
• Measuring lipase would save health care system an estimate of
£893.70 per year
Cost of both measured together were
£0.99.
Patients charged $35 for either lipase
or amylase
618 co-ordered both lipase and
amylase
• Amylase test was removed from common order sets in the
electronic medical record
• Reduced the co-ordering of lipase and amylase to 294
• Overall saving of $135,000 per year
1278
O.Z. Ismail, V. Bhayana
patient-centered services.
Acknowledgments
None.
References
[1] G. Lippi, M. Valentino, G. Cervellin, Laboratory diagnosis of acute pancreatitis: in
search of the holy grail, Crit. Rev. Clin. Lab. Sci. 49 (1) (2012) 18–31.
[2] P.A. Sutton, D.J. Humes, G. Purcell, J.K. Smith, F. Whiting, T. Wright, L. Morgan,
D.N. Lobo, The role of routine assays of serum amylase and lipase for the diagnosis
of acute abdominal pain, Ann. R. Coll. Surg. Engl. 91 (5) (2009) 381–384.
[3] C.D.H. Foundation, Statistics - pancreatitis. http://www.cdhf.ca/en/statistics (2009
2017).
[4] C.W. Teshima, R.J. Bridges, R.N. Fedorak, Canadian digestive health foundation
public impact series 5: pancreatitis in Canada. Incidence, prevalence, and direct and
indirect economic impact, Can. J. Gastroenterol. 26 (8) (2012) 544–545.
[5] J.D. Quinlan, Acute pancreatitis, Am. Fam. Physician 90 (9) (2014) 632–639.
[6] P.G. Lankisch, M. Apte, P.A. Banks, Acute pancreatitis, Lancet 386 (9988) (2015)
85–96.
[7] R. Pezzilli, A.M. Morselli-Labate, V. Mantovani, E. Romboli, P. Selva, M. Migliori,
R. Corinaldesi, L. Gullo, Mutations of the CFTR gene in pancreatic disease, Pancreas
27 (4) (2003) 332–336.
[8] D.C. Whitcomb, M.C. Gorry, R.A. Preston, W. Furey, M.J. Sossenheimer,
C.D. Ulrich, S.P. Martin, L.K. Gates Jr., S.T. Amann, P.P. Toskes, R. Liddle,
K. McGrath, G. Uomo, J.C. Post, G.D. Ehrlich, Hereditary pancreatitis is caused by a
mutation in the cationic trypsinogen gene, Nat. Genet. 14 (2) (1996) 141–145.
[9] P.A. Banks, T.L. Bollen, C. Dervenis, H.G. Gooszen, C.D. Johnson, M.G. Sarr,
G.G. Tsiotos, S.S. Vege, A.P.C.W. Group, Classification of acute pancreatitis—2012:
revision of the Atlanta classification and definitions by international consensus, Gut
62 (1) (2013) 102–111.
[10] S.J. Harper, S. Cheslyn-Curtis, Acute pancreatitis, Ann. Clin. Biochem. 48 (Pt 1)
(2011) 23–37.
[11] C. Pieper-Bigelow, A. Strocchi, M.D. Levitt, Where does serum amylase come from
and where does it go? Gastroenterol. Clin. N. Am. 19 (4) (1990) 793–810.
[12] M. Crook, Hyperamylasaemia: don't forget undiagnosed carcinoma, Ann. Clin.
Biochem. 51 (Pt 1) (2014) 5–7.
[13] N.W. Tietz, Support of the diagnosis of pancreatitis by enzyme tests—old problems,
new techniques, Clin. Chim. Acta 257 (1) (1997) 85–98.
[14] N.W. Tietz, A. Burlina, W. Gerhardt, W. Junge, P. Malfertheiner, T. Murai, M. Otte,
W. Stein, M. Gerber, G. Klein, et al., Multicenter evaluation of a specific pancreatic
isoamylase assay based on a double monoclonal-antibody technique, Clin. Chem. 34
(10) (1988) 2096–2102.
[15] M.Y. Moridani, I.L. Bromberg, Lipase and pancreatic amylase versus total amylase
as biomarkers of pancreatitis: an analytical investigation, Clin. Biochem. 36 (1)
(2003) 31–33.
[16] R.W. Yang, Z.X. Shao, Y.Y. Chen, Z. Yin, W.J. Wang, Lipase and pancreatic amylase
activities in diagnosis of acute pancreatitis in patients with hyperamylasemia,
Hepatobiliary Pancreat. Dis. Int. 4 (4) (2005) 600–603.
[17] D. Yadav, N. Agarwal, C.S. Pitchumoni, A critical evaluation of laboratory tests in
acute pancreatitis, Am. J. Gastroenterol. 97 (6) (2002) 1309–1318.
[18] D. Yadav, B. Ng, M. Saul, E.D. Kennard, Relationship of serum pancreatic enzyme
testing trends with the diagnosis of acute pancreatitis, Pancreas 40 (3) (2011)
383–389.
[19] R.J. Vissers, R.B. Abu-Laban, D.F. McHugh, Amylase and lipase in the emergency
department evaluation of acute pancreatitis, J. Emerg. Med. 17 (6) (1999)
1027–1037.
[20] P.A. Clavien, S. Burgan, A.R. Moossa, Serum enzymes and other laboratory tests in
acute pancreatitis, Br J Surg 76 (12) (1989) 1234–1243.
[21] P.A. Banks, S. Sidi, M.L. Gelman, K.H. Lee, A.L. Warshaw, Amylase-creatinine
clearance ratios and serum amylase isoenzymes in moderate renal insufficiency, J.
Clin. Gastroenterol. 1 (4) (1979) 331–335.
[22] J.E. Berk, H. Kizu, P. Wilding, R.L. Searcy, Macroamylasemia: a newly recognized
cause for elevated serum amylase activity, N. Engl. J. Med. 277 (18) (1967)
941–946.
[23] A.M. Shah, R. Eddi, S.T. Kothari, C. Maksoud, W.S. DiGiacomo, W. Baddoura, Acute
pancreatitis with normal serum lipase: a case series, JOP 11 (4) (2010) 369–372.
[24] K. Ko, L. Tello, J. Salt, Acute pancreatitis with normal amylase and lipase, Best of
Gastroenterology, 2011.
[25] A. Agrawal, M. Parikh, K. Thella, S. Jasdanwala, ED dilemma: acute pancreatitis
with normal lipase and amylase; a series of 8 cases, Am. J. Emerg. Med. (2016).
[26] S.M. Staubli, D. Oertli, C.A. Nebiker, Laboratory markers predicting severity of
acute pancreatitis, Crit. Rev. Clin. Lab. Sci. 52 (6) (2015) 273–283.
[27] C. Dervenis, C.D. Johnson, C. Bassi, E. Bradley, C.W. Imrie, M.J. McMahon,
I. Modlin, Diagnosis, objective assessment of severity, and management of acute
pancreatitis. Santorini consensus conference, Int. J. Pancreatol. 25 (3) (1999)
195–210.
[28] C. Wilson, A. Heads, A. Shenkin, C.W. Imrie, C-reactive protein, antiproteases and
complement factors as objective markers of severity in acute pancreatitis, Br. J.
Surg. 76 (2) (1989) 177–181.
[29] B.M. Rau, E.A. Kemppainen, A.A. Gumbs, M.W. Büchler, K. Wegscheider, C. Bassi,
P.A. Puolakkainen, H.G. Beger, Early assessment of pancreatic infections and
1279
Clinical Biochemistry 50 (2017) 1275–1280
overall prognosis in severe acute pancreatitis by procalcitonin (PCT): a prospective
international multicenter study, Ann. Surg. 245 (5) (2007) 745–754.
[30] M.J. Coffey, S. Nightingale, C.Y. Ooi, Serum lipase as an early predictor of severity
in pediatric acute pancreatitis, J. Pediatr. Gastroenterol. Nutr. 56 (6) (2013)
602–608.
[31] A. Fabre, O. Boulogne, J. Gaudart, E. Mas, J.P. Olives, J. Sarles, Evaluation of serum
lipase as predictor of severity of acute pancreatitis in children, J. Pediatr.
Gastroenterol. Nutr. 58 (4) (2014) 41–42.
[32] M.J. Bierma, M.J. Coffey, S. Nightingale, P.F. Van Rheenen, C.Y. Ooi, Predicting
severe acute pancreatitis in children based on serum lipase and calcium: a multi-
centre retrospective cohort study, Pancreatology 16 (4) (2016) 529–534.
[33] R. Pezzilli, R. De Giorgio, Etiology of acute pancreatitis: beware of the lipase/
amylase ratio!, Gastroenterology 128 (7) (2005) 2179–2180.
[34] V.V. Gumaste, P.B. Dave, D. Weissman, J. Messer, Lipase/amylase ratio. A new
index that distinguishes acute episodes of alcoholic from nonalcoholic acute pan-
creatitis, Gastroenterology 101 (5) (1991) 1361–1366.
[35] S.M. Tenner, W. Steinberg, The admission serum lipase:amylase ratio differentiates
alcoholic from nonalcoholic acute pancreatitis, Am. J. Gastroenterol. 87 (12)
(1992) 1755–1758.
[36] D. Stimac, M. Rubinić, T. Lenac, D. Kovac, A. Vcev, D. Miletic, Biochemical para-
meters in the early differentiation of the etiology of acute pancreatitis, Am. J.
Gastroenterol. 91 (11) (1996) 2355–2359.
[37] R.C. Pacheco, L.C. Oliveira, Lipase/amylase ratio in biliary acute pancreatitis and
alcoholic acute/acutized chronic pancreatitis, Arq. Gastroenterol. 44 (1) (2007)
35–38.
[38] S.C. Kazmierczak, P.G. Catrou, F. Van Lente, Enzymatic markers of gallstone-in-
duced pancreatitis identified by ROC curve analysis, discriminant analysis, logistic
regression, likelihood ratios, and information theory, Clin. Chem. 41 (4) (1995)
523–531.
[39] R. Pezzilli, P. Billi, M. Miglioli, L. Gullo, Serum amylase and lipase concentrations
and lipase/amylase ratio in assessment of etiology and severity of acute pancrea-
titis, Dig. Dis. Sci. 38 (7) (1993) 1265–1269.
[40] M. Jaakkola, P. Sillanaukee, K. Löf, T. Koivula, I. Nordback, Blood tests for detec-
tion of alcoholic cause of acute pancreatitis, Lancet 348 (8909) (1994) 1328–1329.
[41] E. Ansari, D.A. Talenti, J.A. Scopelliti, J.M. Saadat, B.D. Zehr, Serum lipase and
amylase ratio in acute alcoholic and nonalcoholic pancreatitis by using Dupont ACA
discrete clinical analyzer, Dig. Dis. Sci. 41 (9) (1996) 1823–1827.
[42] P.G. Lankisch, M. Petersen, Lipase/amylase ratio: not helpful in the early etiological
differentiation of acute pancreatitis, Z. Gastroenterol. 32 (1) (1994) 8.
[43] D.C. Sadowski, J.K. Todd, L.R. Sutherland, Biochemical models as early predictors
of the etiology of acute pancreatitis, Dig. Dis. Sci. 38 (4) (1993) 637–643.
[44] L.G. King, C.B. Seelig, J.E. Ranney, The lipase to amylase ratio in acute pancreatitis,
Am. J. Gastroenterol. 90 (1) (1995) 67–69.
[45] R. Pezzilli, P. Billi, B. Barakat, F. Miglio, Lipase-amylase ratio does not determine
the etiology of acute pancreatitis. Another myth bites the dust, J. Clin.
Gastroenterol. 26 (2) (1998) 34–38.
[46] K. Dholakia, C.S. Pitchumoni, N. Agarwal, How often are liver function tests normal
in acute biliary pancreatitis? J. Clin. Gastroenterol. 38 (1) (2004) 81–83.
[47] M.J. McMahon, I.R. Pickford, Biochemical prediction of gallstones early in an attack
of acute pancreatitis, Lancet 2 (8142) (1979) 541–543.
[48] W.G.I.A.A.P. Guidelines, IAP/APA evidence-based guidelines for the management
of acute pancreatitis, Pancreatology 13 (4) (2013) 1–15.
[49] Working Party of the British Society of Gastroenterology, Association of Surgeons of
Great Britain and Ireland, Pancreatic Society of Great Britain and Ireland,
A.o.U.G.I.S.o.G.B.a. Ireland, UK guidelines for the management of acute pancrea-
titis, Gut 54 (3) (2005) 1–9.
[50] M. Yokoe, T. Takada, T. Mayumi, M. Yoshida, S. Isaji, K. Wada, T. Itoi, N. Sata,
T. Gabata, H. Igarashi, K. Kataoka, M. Hirota, M. Kadoya, N. Kitamura, Y. Kimura,
S. Kiriyama, K. Shirai, T. Hattori, K. Takeda, Y. Takeyama, M. Hirota, M. Sekimoto,
S. Shikata, S. Arata, K. Hirata, Japanese guidelines for the management of acute
pancreatitis: Japanese guidelines 2015, J. Hepatobiliary Pancreat. Sci. 22 (6)
(2015) 405–432.
[51] M. Panteghini, F. Ceriotti, F. Pagani, S. Secchiero, M. Zaninotto, C. Franzini,
I.S.o.C.B.a.C.M.B.S.W.G.o. Enzymes, Recommendations for the routine use of pan-
creatic amylase measurement instead of total amylase for the diagnosis and mon-
itoring of pancreatic pathology, Clin. Chem. Lab. Med. 40 (2) (2002) 97–100.
[52] R. Pezzilli, A. Zerbi, V. Di Carlo, C. Bassi, G.F. Delle Fave, W.G.o.t.I.A.f.t.S.o.t.P.o.A.
Pancreatitis, Practical guidelines for acute pancreatitis, Pancreatology 10 (5) (2010)
523–535.
[53] S. Tenner, J. Baillie, J. DeWitt, S.S. Vege, G. American College of, American college
of gastroenterology guideline: management of acute pancreatitis, Am J
Gastroenterol 108 (9) (2013) 1400–1415 (1416).
[54] J.A. Greenberg, J. Hsu, M. Bawazeer, J. Marshall, J.O. Friedrich, A. Nathens,
N. Coburn, G.R. May, E. Pearsall, R.S. McLeod, Clinical practice guideline: man-
agement of acute pancreatitis, Can. J. Surg. 59 (2) (2016) 128–140.
[55] J.M. Beauregard, J.A. Lyon, C. Slovis, Using the literature to evaluate diagnostic
tests: amylase or lipase for diagnosing acute pancreatitis? J. Med. Libr. Assoc. 95 (2)
(2007) 121–126.
[56] P. Clavé, S. Guillaumes, I. Blanco, N. Nabau, J. Mercé, A. Farré, L. Marruecos,
F. Lluís, Amylase, lipase, pancreatic isoamylase, and phospholipase a in diagnosis of
acute pancreatitis, Clin. Chem. 41 (8) (1995) 1129–1134.
[57] C.W. Chase, D.E. Barker, W.L. Russell, R.P. Burns, Serum amylase and lipase in the
evaluation of acute abdominal pain, Am. Surg. 62 (12) (1996) 1028–1033.
[58] J. Treacy, A. Williams, R. Bais, K. Willson, C. Worthley, J. Reece, J. Bessell,
D. Thomas, Evaluation of amylase and lipase in the diagnosis of acute pancreatitis,
ANZ J. Surg. 71 (10) (2001) 577–582.
O.Z. Ismail, V. Bhayana
[59] J.W.Y. Chang, C.H. Chung, Diagnosing acute pancreatitis: amylase or lipase? Hong
Kong J. Emerg. Med. 18 (2011) 20–24.
[60] D. Gomez, A. Addison, A. De Rosa, A. Brooks, I.C. Cameron, Retrospective study of
patients with acute pancreatitis: is serum amylase still required? BMJ Open 2 (5)
(2012).
[61] S. Hofmeyr, C. Meyer, B.L. Warren, Serum Lipase should be the laboratory test of
choice for suspected acute pancreatitis, S. Afr. J. Surg. 52 (3) (2014) 72–75.
[62] H.S. Batra, A. Kumar, T.K. Saha, P. Misra, V. Ambade, Comparative study of serum
amylase and lipase in acute pancreatitis patients, Indian J. Clin. Biochem. 30 (2)
(2015) 230–233.
[63] R.C. Smith, J. Southwell-Keely, D. Chesher, Should serum pancreatic lipase replace
serum amylase as a biomarker of acute pancreatitis? ANZ J. Surg. 75 (6) (2005)
399–404.
[64] G. Yin, X. Cang, G. Yu, G. Hu, J. Ni, J. Xiong, Y. Hu, M. Xing, C. Chen, Y. Huang,
M. Tang, Y. Zhao, G. Cheng, R. Wan, S. Wang, X. Wang, Different clinical pre-
sentations of hyperlipidemic acute pancreatitis: a retrospective study, Pancreas 44
(7) (2015) 1105–1110.
[65] W. Tsuang, U. Navaneethan, L. Ruiz, J.B. Palascak, A. Gelrud, Hypertriglyceridemic
pancreatitis: presentation and management, Am. J. Gastroenterol. 104 (4) (2009)
1280
Clinical Biochemistry 50 (2017) 1275–1280
984–991.
[66] S.L. Orebaugh, Normal amylase levels in the presentation of acute pancreatitis, Am.
J. Emerg. Med. 12 (1) (1994) 21–24.
[67] S.J. Spechler, J.W. Dalton, A.H. Robbins, S.G. Gerzof, J.S. Stern, W.C. Johnson,
D.C. Nabseth, E.M. Schimmel, Prevalence of normal serum amylase levels in pa-
tients with acute alcoholic pancreatitis, Dig. Dis. Sci. 28 (10) (1983) 865–869.
[68] W.R.P.S.P.O.D.J.W. Matull, Biochemical markers of acute pancreatitis, J. Clin.
Pathol. 59 (2006) 340–344.
[69] P.A. Clavien, J. Robert, P. Meyer, F. Borst, H. Hauser, F. Herrmann, V. Dunand,
A. Rohner, Acute pancreatitis and normoamylasemia. Not an uncommon combi-
nation, Ann. Surg. 210 (5) (1989) 614–620.
[70] K.A. Volz, D.C. McGillicuddy, G.L. Horowitz, R.E. Wolfe, N. Joyce, L.D. Sanchez,
Eliminating amylase testing from the evaluation of pancreatitis in the emergency
department, West J Emerg Med 11 (4) (2010) 344–347.
[71] J.S. Barbieri, J.M. Riggio, R. Jaffe, Reducing co-ordering of amylase and lipase
testing at an academic medical center: a quality improvement project, Am. J. Med.
Qual. 31 (3) (2016) 286–287.
[72] S. Ferraro, F. Braga, M. Panteghini, Laboratory medicine in the new healthcare
environment, Clin. Chem. Lab. Med. 54 (4) (2016) 523–533.