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Letters to the Editor |
Laboratory Medicine, Immunology, University Hospitals Leuven, Katholieke Universiteit Leuven, Leuven, Belgium
aAddress correspondence to this author at: Herestraat 49, 3000 Leuven, Belgium. Fax 32-16-34-70-42; e-mail xavier.bossuyt{at}uz.kuleuven.be.
To the Editor:
Capillary zone electrophoresis (CZE) of serum proteins is a well-accepted method used in clinical chemistry laboratories to separate serum proteins and detect monoclonal (M) proteins. The detection is based on ultraviolet absorbance measurements at 200 nm (Capillarys, Sebia) or at 214 nm (Paragon 2000, Beckman Coulter), which correspond to the absorption of peptide bonds in proteins. Compared with gel electrophoresis, CZE offers the advantage that all proteins are quantified. Most interferences on CZE are caused by exogenous nonprotein substances that also absorb at 200/214 nm, such as radioopaque agents and antibiotics (1). Gelatin-based plasma expanders have also been reported to cause interference. Gay-Bellile and Gijbels reported an increase in the ß/
-region on CZE in samples from patients who had received infusions with 500 mL Gelofusine(2)(3). This interference, however, could not be mistaken for a M-peak.
A 75-year-old woman admitted to the emergency room with symptoms of cardiogenic shock, liver failure, and renal failure was transferred to the coronary care unit. Approximately 24 h later, a serum sample was sent to the laboratory for serum protein electrophoresis. CZE with Capillarys showed an increase in the ß/-region with a suspected M-peak (Fig. 1A
). To further evaluate the unusual morphology on the CZE result, we performed CZE and immunofixation on a plasma sample obtained just before the patient’s transfer to the coronary care unit (Fig. 1B
). This sample showed hypoproteinemia (40 g/L) with hypoalbuminemia (18 g/L, 45%) and hypogammaglobulinemia (2 g/L, 6.5%) but no clear M-peak, except for a faint IgG-
band (Fig. 1B
inset). When we compared results from both time points, we observed a 17% decrease in total hemoglobin (from 900 to 750 g/L blood) and a 27% decrease in serum albumin protein (18 to 13 g/L serum), suggesting an increase in extracellular blood volume of 
40%. We contacted the cardiologists and learned that, because of an acute deterioration, the patient had received 2000–2500 mL Geloplasma (modified gelatin, 30 g/L; Fresenius Kabi) in the 24 h before the sample was taken for CZE. She died 4 h later.
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To confirm our observations, we used a hypoalbuminemic serum sample (35g/L, 47%) that also showed discrete hypogammaglobulinemia (8 g/L, 10%), which we diluted to a total protein content of 40 g/L (Fig. 1C
). After mixing the diluted sample with an equal volume of Geloplasma, we observed a similar increase in the ß/-region and a suspected M-peak (Fig. 1D
).
We report for the first time a pseudoparaproteinemia caused by the administration of Geloplasma. Previously, Gay-Bellile et al. (2) observed a polyclonal-like increase in the ß/-region on CZE in patients treated with Gelofusine. This interference, however, was much less pronounced than what we have observed. In healthy volunteers, approximately half of the Geloplasma is excreted in the urine after 6 h. The interference in the case we report was therefore most likely caused by the administration of large amounts of Geloplasma in combination with renal failure (urea 125 mg/dL; creatinine 211.3 µmol/L), hypoproteinemia, hypoalbuminemia, and hypogammaglobulinemia.
In conclusion, the administration of large amounts of Geloplasma can cause important CZE interference in the ß/-region, which can be confused with an M-protein in patient samples.
References
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