RV, a 62 year old caucasian male was admitted to LH from the ER for prolonged epistaxis. Ten months prior to admission he had appeared at the ER with the same complaint. At that time the patient’s Hb, Hmct, MCH and MCHC were 12.3 g/dL, 29.2 percent, 35.8 pg and 42 percent respectively. All hematological and chemical assays used instrumentation from Beckman-Coulter Inc.( Brea, CA). The patient’s epistaxis was attributed to anti-platelet therapy with aspirin and clopidogrel for coronary artery disease and he was subsequently lost to follow-up. At his most recent ER appearance his Hb, Hmct, MCH and MCHC were 11.8 g/dL, 22.9 percent, 42.5 pg and 51.6 percent respectively. The patient was admitted to allow evaluation by ENT because of difficulty controlling his epistaxis. Shortly after admission, a CBC revealed nearly identical hematological parameters to those seen in the ER and the pathologist was telephoned. Attempts at warming the patient’s specimen and even acquiring another specimen brought to the lab in a water bath resulted in only trivial changes in the patient’s CBC. If however, patient plasma was replaced by an equal volume of isotonic diluent supplied by the manufacturer, the Hb, Hmct, MCH and MCHC dropped to 6.5 g/dL, 19.4 percent, 23.1 pg and 33.5 percent respectively. Examination of a smear revealed numerous rouleaux. Serum protein and albumin assays revealed concentrations of 9.7 and 2.7 g/dL respectively suggesting an increase in the globulin fraction. Subsequent SPE, IFE and quantitative nephelometry assays performed at our reference lab (ARUP; Salt Lake City, UT) indicated the presence of an IgM-kappa monoclonal protein [6.99 g/dL]. A presumptive diagnosis of Waldenstrom’s macroglobulinemia was confirmed by bone marow biopsy. It has long been known that an MCHC greater than 36 percent should prompt a careful investigation of the data [

Am J Clin Pathlol.
]. In this case the elevated concentration of IgM resulted in increased turbidity and a spuriously elevated Hb [
Arch Pathol Lab Med.
]. Yet the clue went unrecoginized by laboratory personnel as well as ordering physicians leading to a probable delay of nearly one year in the diagnosis of the patient’s underlying hematologiclal disorder.

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