Fewer than 2% of hemolyzed blood samples are due to in vivo hemolysis (1). In this patient with a relatively mild episode of pancreatitis, multiple hemolyzed specimens raised concerns of in vivo hemolysis because of the concurrent findings of a haptoglobin concentration of 56 mg/dL, at the lower region of the reference interval, and a decrease in hemoglobin from 14.6 to 13.8 g/dL. From the clinician's perspective, the minor decrease in hemoglobin was more likely explained by the administration of intravenous hydration rather than hemolysis. Acute hemolytic anemia in pancreatitis is usually secondary to disseminated intravascular coagulation as a result of severe complications not evident in this patient.
Proving in vivo hemolysis in this situation is difficult. Increased lactic dehydrogenase activities can result from in vitro hemolysis. The reticulocyte count is often within reference intervals in acute hemolysis owing to a delay in marrow response. The presence of schistocytes or “shift” reticulocytes in a peripheral blood smear could have pointed to in vivo hemolysis. Serum haptoglobin, despite being an acute-phase reactant, remains the best test of in vivo hemolysis. Hemolyzing patients who have inflammation indicated by increased C-reactive protein concentrations will usually have low haptoglobin concentrations of <30 mg/dL (2) because the haptoglobin–hemoglobin complex is cleared from the circulation with a half-life of 10 to 30 min. Repeating the haptoglobin analysis 24 h later would have been helpful to evaluate whether the hemolyzed specimens were due to continuing intravascular hemolysis, because haptoglobin requires 5 days to regenerate. One might speculate that the circulation of pancreatic enzymes may have resulted in subclinical membrane abnormalities, making the red cells more susceptible to the common preanalytic causes of specimen hemolysis (1). A less likely cause was the local release of hemoglobin into the circulation by the damaging effect of the released enzymes on in situ hematomas, thereby mimicking intravascular hemolysis.
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Authors' Disclosures or Potential Conflicts of Interest: No authors declared any potential conflicts of interest.
- Received for publication March 18, 2011.
- Accepted for publication March 26, 2012.
- © 2012 The American Association for Clinical Chemistry