Are MpI glycosylation defects in polycythemia vera secondary to artifactual hypoglycemia?
In their report on altered processing of the thrombopoietin receptor (Mpl) in patients with polycythemia vera, Moliterno and Spivak1 (Oct 15 issue) show that Mpl glycosylation is associated with disease progression. The authors demonstrate that the nonglycosylated Mpl isoform has reduced expression and is impaired in its ability to transit to the cell membrane, thus rendering the cells resistant to thrombopoietin.1,2 While the authors suggest that these findings indicate that Mpl glycosylation defects may serve as a marker for disease progression, an alternate hypothesis should be entertained. Artifactual hypoglycemia has been reported to occur in polycythemia vera and is caused by in vitro autoglycolysis due to an exaggerated consumption of glucose by blood cells.3 In polycythemia vera, this phenomenon can occur even with only modest leukocytosis and may be due to both red and white cell-induced enhanced glycolysis.4,5 Serum glucose concentrations can drop significantly within 2 hours
