Acute Pancreatitis with Normal Serum Lipase

Anish M Shah
1
, Rodney Eddi
2,3
, Shivangi T Kothari
2,3
,
Charbel Maksoud
2,3
, William Scott DiGiacomo
3
, Walid Baddoura
2,3
1
Department of Internal Medicine and
2
Division of Gastroenterology,
Saint Joseph’s Regional Medical Center. Paterson, NJ, USA.
3
Seton Hall University School of Health and Medical Sciences. South Orange, NJ, USA
ABSTRACT
Context Acute pancreatitis is diagnosed on the basis of clinical features, biochemical tests and imaging studies. Normal serum
amylase level has been reported in the setting of acute pancreatitis but normal serum lipase level in acute pancreatitis is extremely
rare. Case report Herein, we present a case series of acute pancreatitis with normal serum lipase levels along with a review of the
topic. Conclusion In appropriate clinical setting, the diagnosis of acute pancreatitis should be entertained even with normal serum
amylase and lipase levels.
INTRODUCTION
Acute pancreatitis is one of the most common causes
for hospitalization in the United States, accounting for
around 220,000 cases per year [1]. Among the new
cases, 80% are interstitial and 20% are necrotizing.
Acute pancreatitis carries an overall mortality of
around 5% and as high as 47% in patients with multi-
organ failure [2]. Necrotizing pancreatitis is
responsible for almost all mortalities attributed to acute
pancreatitis.
Alcohol use, gallstones, hyper-
triglyceridemia,
hypercalcemia,
medications,
endoscopic retrograde cholangiopancreatography and
trauma account for most cases of acute pancreatitis;
however, approximately 20% remain idiopathic [3].
The role of pancreas divisum and sphincter of Oddi
dysfunction is controversial. Clinical manifestations
range from mild epigastric discomfort to critical illness
and death. Occasional cases are only diagnosed at
autopsy. Diagnosis is based on clinical features,
biochemical tests and imaging studies. Guidelines by
the American College of Gastroenterology state that
the diagnosis of acute pancreatitis requires the presence
of the two of the following three criteria: 1)
characteristic abdominal pain; 2) serum amylase and/or
lipase more than 3 times the upper limit of normal; and
3) computed tomography (CT) scan findings
compatible with acute pancreatitis [4]. Serum amylase
and lipase levels threefold or more than normal are
seen in acute pancreatitis and, in the appropriate
clinical setting, used for diagnosis [5]. Normal serum
amylase levels have been reported in some cases of
acute pancreatitis, but serum lipase levels are usually
elevated [6]. Normal serum lipase in the setting of
acute pancreatitis is an extremely rare occurrence. In
our literature review, we found only two case reports of
clinical and radiological evidence of acute pancreatitis
with a normal serum lipase level [7, 8].
We present this case series of acute pancreatitis
(diagnosed on clinical, radiological or autopsy
grounds) with normal serum lipase levels.
CASE REPORTS
Case #1
A 66-year-old Caucasian male was admitted with
fever, malaise, generalized ill-defined abdominal
discomfort and emesis. Past medical history was
significant for diabetes mellitus, hypertension and
coronary artery disease. The patient denied any history
of hepatitis, pancreatitis or alcohol use. On
examination, he was icteric with diffuse abdominal
tenderness. Laboratory tests revealed leukocytosis
(15,500 cells/mm3, reference range: 4,500-11,000
cells/mm3), ketosis, INR 2.2, creatinine 3.0 mg/dL
(reference range: 0.7-1.2 mg/dL), abnormal liver
enzymes (total bilirubin 9.1 mg/dL, reference range;
0.4-2.0 mg/dL; alkaline phosphatase 341 U/L,
reference range; 38-126 U/L; AST 83 U/L, reference
range; 12-42 U/L; ALT 40 U/L, reference range; 14-54
U/L), and normal triglycerides (106 mg/dL, reference
Received December 1st, 2009 - Accepted June 3rd, 1020
Key words Amylases; Lipase; Pancreatitis, Acute Necrotizing
Correspondence Anish M Shah
Department of Internal Medicine, Saint Joseph’s Regional Medical
Center, 703, Main Street, Paterson, NJ, USA 07503
Phone: +1-973.754.2000; Fax: +1-973.754.3376
E-mail: anishshah21@gmail.com
Document URL http://www.joplink.net/prev/201007/21.html

Page 2
JOP. J Pancreas (Online) 2010 Jul 5; 11(4):369-372.
JOP. Journal of the Pancreas - http://www.joplink.net - Vol. 11, No. 4 - July 2010. [ISSN 1590-8577]
370
range: 0-160 mg/dL). Serum amylase and lipase levels
were 33 U/L (reference range: 36-128 U/L) and 15 U/L
(reference range: 8-57 U/L), respectively. Ultrasound
of the abdomen revealed a common bile duct diameter
of 1.3 cm, cholelithiasis, ascites, an edematous
pancreas and a diffusely echogenic liver. Abdominal
CT scan with intravenous contrast confirmed the
ultrasonographic findings showing ascites, diffuse
pancreatitis and gallbladder distension with stones
(Figure 1). Patient was hemodynamically unstable for
surgical intervention. The hospital course was
complicated by septic shock, worsening azotemia, and
respiratory failure requiring fluids, vasopressors,
broad-spectrum
antibiotics,
percutaneous
cholecystostomy, mechanical ventilation and dialysis.
The patient’s condition deteriorated over 3 weeks
ending with his demise. Serum amylase and lipase
levels throughout the hospitalization remained normal.
Autopsy revealed severe acute necrotizing pancreatitis
with centrilobular hemorrhagic necrosis of the liver and
cholestasis.
Case #2
A 37-year-old African-American female was admitted
with complaints of epigastric pain and emesis for one
day. She denied any change in bowel habits, fever,
cough or hematemesis; however she did admit to
alcohol ingestion two days prior to admission. She
related a history of moderate alcohol consumption and
an episode of pancreatitis three years prior. There was
epigastric tenderness on physical examination.
Laboratory tests showed WBC 9,800 cells/mm3,
normal liver enzymes (AST 22 U/L; ALT 16 U/L;
alkaline phosphatase 55 U/L; total bilirubin 0.6
mg/dL), normal serum triglyceride level (54 mg/dL);
amylase and lipase were 95 U/L and 31 U/L,
respectively. CT scan of the abdomen with intravenous
contrast showed swelling of the head and body of the
pancreas with peripancreatic inflammatory changes
consistent with acute pancreatitis (Figure 2).
Abdominal ultrasound revealed a common bile duct
diameter of 3 mm, no gallbladder wall thickening or
gallstones. The patient was treated with intravenous
fluids and analgesics. Amylase and lipase levels
remained normal throughout the admission. Three days
after admission, she was discharged home with
complete resolution of symptoms.
Case #3
A 59-year-old African-American man was admitted
with abdominal pain of three-day duration, associated
with emesis and hiccups. Past medical history was
significant for diabetes mellitus. He admitted to alcohol
use once to twice a month. On examination, there was
mild epigastric tenderness. Laboratory studies showed
leukocytosis (15,700 cells/mm3); hematocrit was
45.4% (reference range: 36.0-46.0%), serum creatinine
was 1.4 mg/dL; transaminases were mildly elevated
(AST 89 U/L, ALT 65 U/L); alkaline phosphatase and
bilirubin were normal. Amylase and lipase were 108
U/L and 35 U/L, respectively. CT scan of the abdomen
with intravenous contrast showed stranding around the
head of the pancreas suggestive of acute pancreatitis.
Ultrasound of the abdomen showed a common bile
duct diameter of 9 mm, no gallstones, and
heterogeneous pancreatic head consistent with
pancreatitis versus a mass lesion. MRI of the abdomen
with contrast showed prominent inflammatory changes
surrounding the pancreas, with no necrosis or
pseudocyst formation (Figure 3). The hepatitis profile
was negative. Patient was treated with intravenous
Figure 2. CT scan of the abdomen with contrast (Case #2).
Figure 1. CT scan of the abdomen with contrast (Case #1).
Figure 3. MRI of the abdomen with contrast (Case #3).

Page 3
JOP. J Pancreas (Online) 2010 Jul 5; 11(4):369-372.
JOP. Journal of the Pancreas - http://www.joplink.net - Vol. 11, No. 4 - July 2010. [ISSN 1590-8577]
371
fluids, insulin and antiemetics. Repeated measurements
of amylase and lipase were normal. Patient had an
uneventful recovery and was discharged home on day
6.
DISCUSSION
The pathogenesis of acute pancreatitis includes
increased conversion of trypsinogen to trypsin, which
leads to pancreatic injury and an inflammatory
response [3]. Additionally, amylase and lipase are
released from pancreatic acinar cells. Serum
trypsinogen activation peptide and trypsinogen-2 are
more specific early markers for pancreatitis but are
expensive and not readily available [9, 10]. Serum
amylase and lipase are also found in other organs like
salivary glands and extrapancreatic abdominal organs.
Following the initial onset of acute pancreatitis, serum
amylase level increases rapidly over 3 to 6 hours, with
a half-life of 10-12 hours; it remains elevated for 3 to 5
days [6] and is excreted by the kidneys. Serum lipase
level increases in 3 to 6 hours, peaks in 24 hours and
remains elevated for one to two weeks [7]. Serum
lipase, unlike amylase, is reabsorbed by the kidney
tubules and hence remains elevated for prolonged
period which may be helpful in late presenting patients
[11]. Several studies have reported a negative
predictive value of serum lipase in diagnosing acute
pancreatitis to be between 94 and 100 percent [7, 10].
Serum amylase can be normal in acute on chronic
pancreatitis, hypertriglyceridemia-induced pancreatitis
or in late presentations [6]. However, a normal blood
lipase level in acute pancreatitis is a rare event; to our
knowledge only two cases have been reported in the
English literature. Cartier et al. reported acute
pancreatitis diagnosed on CT scan with normal lipase
levels in a patient presenting with abdominal pain and
vomiting for 24 hours [7]. Mayersak et al. reported a
case of pancreatitis diagnosed on CT scan in a post-
operative patient with normal serum amylase, lipase
and urinary amylase [8].
Our three patients presented with complaints of
abdominal pain and emesis. Two of the patients had
diabetes mellitus; the third had history of pancreatitis
in the distant past. Two had elevated WBC count on
presentation. One had pancreatitis of the head, the
second of the head and body while the third had diffuse
pancreatitis. Two patients had gallstone pancreatitis;
the other was alcohol-induced. One had severe
necrotizing pancreatitis with systemic complications
and death; the other two had an uneventful recovery.
CT scan diagnosed acute pancreatitis in all cases.
Patient #2 did not have any more episodes of acute
pancreatitis on one-year follow-up while patient #3 was
diagnosed with pancreatic head cancer a few months
later. Thus, acute pancreatitis may be the first
manifestation of a pancreatic cancer. The normal
enzyme levels in the first patient may be due to late
presentation of the patient and/or pancreatic necrosis
leading to decrease in the levels of amylase and lipase.
Helical contrast-enhanced CT scan is considered the
‘gold standard’ for diagnosis and evaluation of patients
with acute pancreatitis [12]. Although some experts
criticize the use of early imaging in the presence of
other supporting evidence of pancreatitis, it may be
helpful in establishing the diagnosis when biochemical
markers are not compatible with the clinical suspicion.
Additionally, it may identify other pathology and/or
complications. Ultrasound has a limited role in
diagnosing acute pancreatitis. Bowel gas due to ileus
makes visualization of the pancreas difficult, but it may
help identify gallstones and choledocholithiasis.
MRI/magnetic resonance cholangiopancreatography
(MRCP) is more expensive, requires more patient
cooperation and takes longer, but it is as sensitive as
CT scan to detect acute pancreatitis and its
complications, and can be used in patients allergic to
iodinated contrast media [13]. Endoscopic Ultrasound
(EUS) can detect small stones in the common bile duct
and is the most accurate test to identify cholelithiasis as
cause of acute pancreatitis. It is especially useful when
standard imaging modalities do not detect cholelithiasis
or microlithiasis. Endoscopic retrograde cholangio-
pancreatography (ERCP) along with endoscopic
sphincterotomy helps in extraction of common bile
duct stones and drain infected bile in acute pancreatitis
[14]. EUS has a sensitivity of 91% for detecting
choledocholithiasis as compared with 50% with
transabdominal ultrasound [15].
Acute pancreatitis can have a variable presentation. It
may be mild, self-limiting or can be severe, fulminant
type. The treatment of mild type is supportive while
severe form needs close monitoring in intensive care
unit with surgical and/or radiological intervention [15].
The treatment of acute pancreatitis consists of fluid
resuscitation, pain management, and nutritional
support. Oral feeding can be started within 24-72 hours
of disease onset in mild pancreatitis. Prophylactic
antibiotic use is not recommended in patients with
acute pancreatitis. Carbapenem antibiotic should be
given in patients with pancreatic necrosis with organ
failure as well as septic appearing patients.
Debridement of the infected necrotic pancreas is the
treatment of choice. This could be done surgically but
lately direct endoscopic necrosectomy through an
opening in the stomach is being used [2].
In conclusion, we suggest that in the appropriate
clinical setting, diagnosis of acute pancreatitis should
be entertained even with normal amylase and lipase
levels, and further investigated utilizing appropriate
imaging modalities.
Conflict of interest The authors have no potential
conflict of interest
References
1. DeFrances CJ, Hall MJ, Podgornik MN. Advance Data From
Vital and Health Statistics. No. 359. 2003 National Hospital
Discharge Survey. Centers for Disease Control and Prevention.
Atlanta, GA 30333, USA. National Center for Health Statistics,
2005.

Page 4
JOP. J Pancreas (Online) 2010 Jul 5; 11(4):369-372.
JOP. Journal of the Pancreas - http://www.joplink.net - Vol. 11, No. 4 - July 2010. [ISSN 1590-8577]
372
2. Talukdar R, Vege SS. Recent developments in acute pancreatitis.
Clin Gastroenterol Hepatol 2009; 7(11 Suppl):S3-9. [PMID
19896095]
3. Whitcomb DC. Value of genetic testing in management of
pancreatitis. Gut 2004; 53:1710-7. [PMID 15479696]
4. Banks PA, Freeman ML, Practice Parameters Committee of the
American College of Gastroenterology. Practice guidelines in acute
pancreatitis. Am J Gastroenterol 2006;101:2379-400. [PMID
17032204]
5. Cotton PB, Lehman G, Vennes J, Geenen JE, Russell RC,
Meyers WC, et al. Endoscopic sphincterotomy complications and
their management: an attempt at consensus. Gastrointest Endosc
1991; 37:383-93. [PMID 2070995]
6. Clavien PA, Robert J, Meyer P, Borst F, Hauser H, Herrmann F,
et al. Acute pancreatitis and normoamylasemia. Not an uncommon
combination. Ann Surg 1989; 210:614-20. [PMID 2479346]
7. Cartier T, Sogni P, Perruche F, Meyniard O, Claessens YE,
Dhainaut JF, Der Sahakian G. Normal lipase serum level in acute
pancreatitis: a case report. Emerg Med J 2006; 23:701-2. [PMID
16921084]
8. Mayersak JS, Viviano CJ, Babiarz JW. Computed axial
tomography pancreatitis: an atypical asymptomatic postoperative
disease without serum or urinary enzyme evaluation. Wis Med J
1997; 96:25-8. [PMID 9128430]
9. Kylänpää-Bäck M, Kemppainen E, Puolakkainen P, Hedström J,
Haapiainen R, Perhoniemi V, et al. Reliable screening for acute
pancreatitis with rapid urine trypsinogen-2 test strip. Br J Surg 2000;
87:49-52. [PMID 10606910]
10. Al-Bahrani AZ, Ammori BJ. Clinical laboratory assessment of
acute pancreatitis. Clin Chim Acta 2005; 362:26-48. [PMID
16024009]
11. Sternby B, O'Brien JF, Zinsmeister AR, DiMagno EP. What is
the best biochemical test to diagnose acute pancreatitis? A
prospective clinical study. Mayo Clin Proc 1996; 71:1138-44. [PMID
8945483]
12. Fernández-del Castillo C, Rattner DW, Warshaw AL. Acute
pancreatitis. Lancet 1993; 342:475-9. [PMID 8102434]
13. Maher MM, Lucey BC, Gervais DA, Mueller PR. Acute
pancreatitis: the role of imaging and interventional radiology.
Cardiovasc Intervent Radiol 2004; 27:208-25. [PMID 15024494]
14. Whitcomb DC. Clinical practice. Acute pancreatitis. N Engl J
Med 2006; 354:2142-50. [PMID 16707751]
15. Koo BC, Chinogureyi A, Shaw AS. Imaging acute pancreatitis.
Br J Radiol 2010; 83:104-112. [PMID 20139261]

There are no products listed under this category.