American Journal of Hematology 33:282-283 (1990)

Letter to the Editor: MCHC in lntravascular Hemolysis Anemias have been classified by the size and hemoglobin content or red cells. Of the red cell indices, the mean corpuscular volume (MCV) has proven to be the most useful in the classification of anemia. The mean corpuscular hemoglobin concentration (MCHC) generally parallels the MCV, being reduced in iron deficiency anemia and thalassemia, and is reported to be elevated only in spherocytic anemias and certain hemoglobinopathies [2,6]. Elevations in the MCHC to greater than 50.0 g/dl were reported in two patients with acute intravascular hemolysis due to clostridial septicemia. This increase was likely spurious due to the presence of extracellular hemoglobin. Experimental data and other cases of hemolytic anemia support this hypothesis. Case 1: A 72-year-old male was admitted with fever and abdominal pain. The hemoglobin (HGB) was 15.3 gidl, red blood cell count (RBC) 4.96 X 10l2/L, hematocrit (HCT) 46.1%, MCV 93 fl, mean corpuscular hemoglobin (MCH) 30.8 pg, MCHC 33.2 g/dl, white cell count (WBC) 6.1 X 109/L, and platelet count (Plt) 139 X 109/L. Over the next few hours he began to bleed around the intravenous catheters, and the urine became dark. Repeat HGB was 7.8 g/dl, RBC 1.95 x 10l2/L, HCT 14.0%, MCV 71 fl, MCH 39.9 pg, MCHC 56.1 g/dl, WBC 15.6 X 109/L, Plt 48 X 109/L, prothrombin time (PT) 30.2 sec, and partial thromboplastin time (PTT) 63 sec. Blood cultures grew Clostridium perfringens. He became hypotensive and died. At autopsy, an acute clostridial hepatic abscess was detected. Case 2: A 76-year-old male was admitted with fever and abdominal pain. The HGB was 11.6 g/dl, RBC 2.9 X lO'*/L, HCT 23.0%, MCV 80 fl, MCH 40 pg, MCHC 50.1 g/dl, WBC 26.6 X 109/L, and Plt 37 x 109/L. He died with a cardiac arrest. At autopsy, acute cholecystitis and a clostridial hepatic abscess were identified. Blood cultures grew Clostridium perlfringens.

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These cases illustrate that the MCHC may be elevated in acute intravascular hemolysis. As automatic blood cell analyzers calculate the MCHC by dividing the HGB by the product of the MCV and RBC (HGB/[MCVX RBC]), free plasma hemoglobin would be predicted to elevate the MCHC. In vitro Coulter counter analysis of whole blood which was mixed with varying proportions of hemolyzed blood supports this hypothesis (Fig. 1). Calculation of red cell indices in other cases of acute intravascular hemolysis demonstrate that this finding is not limited to clostridial sepsis. Infection with Leptospira, Toxoplasma, and Plasmodium caused the MCHC to rise [4,5,8] as did autoimmune intravascular hemolysis [3]. An increased MCHC is not, however, found in all cases of intravascular hemolysis. In one report of microangiopathic hemolytic anemia, only two of 25 cases had an elevated MCHC [l]. One of seven cases of pyruvate kinase deficiency was associated with an elevated MCHC [7]. Before the use of blood cell analyzers, hematocrits were performed manually and direct observation of the plasma could detect hemolysis. Now blood counts may be made without an opportunity to note the color of plasma. In some cases, the elevated MCHC may be the first clue to the presence of hemolysis and may prompt consideration of the diagnosis of acute intravascular hemolysis. Sandra Buys

Division of Hematology and Oncology Catherine Craven

Division of Anatomic Pathology University of Utah Medical Center Salt Lake City, Utah 84132

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Letter to the Editor

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Fig. 1. In vitro lysis of red cells causes an elevation in the MCH and MCHC. Blood from a healthy volunteer was anticoagulated with ethylenediaminetetraacetic acid (EDTA) and sonicated (Heat Systems Ultrasonic) until the microhematocrit was less than 0.01. Sonicated blood was mixed with unsonicated blood at concentrations from 10 to 90%.

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Samples of the blood mixtures, sonicated blood, and normal blood were analyzed on a Coulter S-plus V. The hemoglobin concentration and MCV were unchanged. The RBC and HCT fell; the MCH and MCHC rose. The hatched bar indicates the normal range of the MCHC. Lysis of 10% of the RBC caused the MCHC to become abnormal.

REFERENCES 1. Brain MC, Dacie JV, Hourihane DOB: Microangiopathic haemolytic anemia: The possible role of vascular lesions in the pathogenesis. Br J Haematol 8:358-374, 1962. 2. Charache S , Conley CL, Waugh DF, Ugorets RJ, Spurrell RJ: Pathogenesis of hemolytic anemia in homozygous C disease. J Clin Invest 46: 1795-181 I , 1967. 3. Crowley LV, Bouroncle BA: Studies on the specificity of autoantibodies in acquired hemolytic anemia. Blood 11:700-707, 1956. 4. Kalderon AE, Kikkawa Y, Bernstein J: Chronic toxoplasmosis associ-

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ated with severe hemolytic anemia, Arch Intern Med 114:95-102, 1964. Ridgon RH: A consideration of the mechanism of death in acute Plasmodium falciparum infection. Am J Hyg 36269-275, 1942. Schilling RF: Hereditary spherocytosis: A study of splenectomized persons. Semin Hemdtol 13:169-176, 1976. Tanaka KK, Valentine WN, Miwa S: Pyruvate kinase deficiency: A hereditary nonspherocytic hemolytic anemia. Blood 19:267-295, 1962. Trowbridge A, Green JB, Bonnett JD, Shohet SB, Ponnappa BD, McCombs WB: Hemolytic anemia associated with Leptospirosis. Am J Clin Pathol 76493-498, 1981.

MCHC in intravascular hemolysis.

American Journal of Hematology 33:282-283 (1990) Letter to the Editor: MCHC in lntravascular Hemolysis Anemias have been classified by the size and h...
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