Case Presentation: A 52-year-old female presented with epigastric abdominal pain started two days ago. Her past medical history was significant for Hepatitis C. She denied a history of acute pancreatitis.
Her initial laboratory tests, including basic metabolic panel, complete blood counts, and liver function tests were all in normal range except for lactic acid of 4.1 mmol/L (Reference range: 0.7 to 2.1 mmol/L). Her lipase was 33 U/L (Unit/Liter) (Reference range: 23-300 U/L) and her amylase was 37 U/L (Reference range: 50-130 u/l).

A contrast-enhanced computerized tomogram of the abdomen suggested acute severe interstitial pancreatitis (Figure 1). Further tests, including lipid profiles, Ultrasound of the abdomen and MRCP, were nonsignificant. The IgG subclass 4 was 0.5 mg/dL (Reference range: 4.0-86.0 mg/dL) and her HIV screening was negative.

However, her lactate was persistently elevated. It was still at 6.4 mmol/L on the hospital day 7. Her renal and hepatic function remained normal. However, her lipase levels were below the normal range (Figure.2).

Repeat CT of the abdomen on the hospital day 7 revealed a new 7.7x 6.3x 6.7 cm complex collection in the subhepatic region compatible with an extrapancreatic acute necrotic collection (Figure 3).

She was hemodynamically stable and tolerating the diet very well. She was discharged home. A follow- up CT of the abdomen and pelvis showed a residual 2.1×1.9 cm complex fluid collection 5 months later.

Discussion: Our patient had severe acute pancreatitis with persistent organ dysfunction. Her lactate was persistently elevated, which indicated poor tissue perfusion and/or intravascular volume depletion. She was also found to have a large pseudocyst formation on the hospital day seven. However, throughout her hospital course, her serum amylase and lipase levels remained in the normal or low range. She presented early in her clinical courses (within the first 72 hours since symptoms started). Because abnormally elevated lipase persists for weeks, one can safely conclude the phase of disease course should not be the cause of her normal lipase on presentation.

Acute pancreatitis with normal lipase is the rare entity. There are only a few case reports of such presentation. No plausible pathophysiology could explain this rare entity. However, acute pancreatitis could be the rare manifestation of pancreatic cancer (PC). In a nationwide, population-based, matched cohort study in Denmark, researchers found that within the first 2 years of follow-up, patients with acute pancreatitis had a nearly 20-fold increased risk for pancreatic cancer compared with the comparison population (adjusted hazard ratio, 19.5). Diffuse pancreatic inflammation might have masked the presence of an underlying lesion in the pancreas or a small-sized tumor may preclude an early diagnosis of cancer.

Recently, low serum lipase levels were identified as a significant and independent predictor for pancreatic cancer. At the advanced stage of pancreatic cancer, similar to the case of chronic pancreatitis, an organ insufficiency may predominate, resulting in a low production of pancreatic enzymes and low serum enzyme activities. Our patient had extreme low lipase of 10 U/L, which warrants a close follow up for pancreatic cancer.

Conclusions: With the high prevalence of acute pancreatitis, clinicians should stay alert for such diagnosis in appropriate clinical settings, even with normal serum amylase and lipase levels, and be diligent for possible underlying pancreatic cancer.