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Reply to: Benign Pancreatic Hyperenzymemia or Gullo’s Syndrome

Luca Frulloni*, Franca Patrizi, Laura Bernardoni, Giorgio Cavallini

Department of Surgical and Gastroenterological Sciences, University of Verona. Verona, Italy

*Corresponding Author:
Luca Frulloni
Cattedra di Gastroenterologia
Dipartimento di Scienze Chirurgiche e
Policlinico GB Rossi
Piazzale LA Scuro
10 37134 Verona
Phone +39-045.807.4437
Fax +39-045.820.5584
E-mail: [email protected]

Received: December 13th, 2005

Visit for more related articles at JOP. Journal of the Pancreas


Hyperamylasemia; Lipase; Pancreas


Dear Sir,

We thank Dr. Gullo for his comment on our paper recently published [1].

First of all, we would again like to emphasize that an increase of serum pancreatic enzyme (amylase and/or lipase) in asymptomatic patients may be a laboratory finding without clinical significance or a manifestation of extra-pancreatic diseases, but it may also be related to pancreatic damage. Our clinical experience together with some previously published papers [2, 3, 4] and an in-progress work by our group suggest that, in a variable percentage of cases, asymptomatic hyperamylasemia and/or hyperlipasemia may be the first biochemical sign of pancreatic involvement by an inflammatory or neoplastic process. Probably, this is not so common as has recently been reported (more than 50% of cases) [2], but pancreatic disease can be found in a significant percentage of cases. For example, long standing hyperamylasemia (up to 7 years) is often present in patients affected by intraductal papillary mucinous neoplasms [5, 6], probably secondary to partial or complete occlusion of the main or secondary pancreatic ducts by mucin.

Secondly, pancreatic steatosis, namely the presence of lipid droplets in the acinar cells of the pancreas, has been observed both in animals [2, 7, 8, 9, 10, 11] and in humans [12, 13, 14, 15]. The pathogenesis of pancreatic steatosis has not been defined, but malnutrition [7, 10, 12] and alcohol abuse [7, 12, 13] have been implicated in the pathogenesis. We postulated that dyslipidemia may also be a cause of intra-acinar accumulation of lipids (similarly to hepatic steatosis). Therefore, pancreatic steatosis in “some” patients with pancreatic hyperenzymemia and dyslipidemia may alter intracellular exocytosis. Our preliminary results in an ongoing study seem to confirm that the content of lipids in the pancreas quantified by MR in “some” patients with hypercholesterolemia and/or hypertriglycerid hypertriglyceridemia and serum pancreatic hyperenzymemia is higher than in normal controls.

Finally, Dr. Gullo asked why we detect only an increase of serum pancreatic amylase and not other serum pancreatic enzymes. Currently, in clinical practice, we determine only serum pancreatic amylase instead of lipase, and, as stressed in the paper, we may observe an increase in both serum pancreatic enzymes. However, in some cases only hyperamylasemia or hyperlipasemia may be observed and we do not have an answer for this. We can only observe that a serum increase of only one hepatic enzyme may be documented in hepatic steatosis [16].

In conclusion, we agree that sporadic pancreatic hyperenzymemia may be a benign syndrome without clinical significance, but in clinical practice we should consider that it may represent a biochemical sign of disease, including pancreatic disease.


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