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Hemolyzed specimens from patients with acute pancreatitis.

Q We occasionally receive specimens on patients experiencing acute pancreatitis. They are typically very lipemic and significantly hemolyzed. I understand the lipemia (we airfuge/ultrafuge them to remove the lipemia). But I wonder about the reason for the hemolysis. It appears to be "fresh" hemolysis--bright red not brownish--and it seems to persist until the patient's elevated lipase begins to abate. The hemolysis results in significantly elevated potassiums, of course. We have tried doing bedside whole-blood potassiums, and the results are better [lower] than the plasma potassiums we get on our main chemistry analyzers. Can you explain the mechanism/phenomenon?

A The diagnosis of acute pancreatitis is indicated by a predictable rise and fall in the levels of serum amylase and lipase in the setting of an appropriate clinical picture. Derangements in several other parameters, such as trypsinogen, as partate and alanine aminotransferase, hematocrit, and C-reactive protein, are also informative in terms of etiology and prognosis. (1) In addition, varying, but often significant, degrees of hemolysis are sometimes seen in these patients.

Massive hemolysis can cause acute pancreatitis. (2) Normally, free heme circulating in the plasma is bound and cleared by haptoglobin and other serum proteins. In cases of rapid, severe hemolysis, this protective mechanism can be overwhelmed, allowing free heme to directly activate neutrophils and to incite release of proinflammatory and leukocyte chemotactic cytokines. (2) How this leads to acute pancreatitis remains unclear, but a recent study implicated interaction of heme with an intercellular adhesion molecule (ICAM-1) and a leukocyte chemotactic cytokine (MCP-1). (3)

Somewhat more perplexing are cases where hemolysis is identified (sometimes quite incidentally) secondary to acute pancreatitis. This is most commonly seen in cases exhibiting significant pancreatic necrosis and hemorrhage. Goth, et al, argue that hemorrhage results from destruction of vascular structures by proteolytic and other enzymes released from dying pancreatic acinar cells. Why markers of hemolysis are subsequently present in the peripheral circulation is not known, but the authors, nonetheless, identified increased serum hemoglobin, hematin, lactate dehydrogenase and erythrocyte-derived catalase, and decreased haptoglobin in these patients.(4) Further research is necessary to fully understand these findings.

--Craig Midgen, MD

Department of Pathology

Oregon of Health and Science University

Portland, Oregon

References

(1.) McPherson RA, Pincus MR, eds. Henry's Clinical Diagnosis and Management by Laboratory Methods. 21st ed. Philadelphia, PA: Saunders Elsevier; 2007.

(2.) Saruc M, Yuceyar H, Turkel N, et al. An experimental model of hemolysis induced acute pancreatitis. Brazilian J Med Biol Res. 2003;36:879-886.

(3.) Saruc M, Yuceyar H, Turkel N, et al. The role of heme in hemolysis-induced acute pancreatitis. Med Sci Monit. 2007;13(3):BR67-72.

(4.) Goth L. Origin of serum catalase activity in acute pancreatitis. Clin Chim Acta. 1989; 186:39-44.

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Edited by Daniel M. Baer, MD

Daniel M. Baer, MD, is professor emeritus of laboratory medicine at Oregon Health and Science University in Portland, OR, and a member of MLO's editorial advisory board.
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Title Annotation:Answering your questions
Author:Midgen, Craig
Publication:Medical Laboratory Observer
Date:Aug 1, 2008
Words:487
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