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Patients with homozygous sickle cell anemia and -thalassemia have a somewhat milder form of hemolysis because of a slower rate of sickling related to reduced MCHC within the red blood cell Patients who are double heterozygotes for sickle cell anemia and -thalassemia are clinically affected with sickle cell
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Table 13 9 Hemoglobin distribution in sickle cell syndromes
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Genotype AA AS SS S 0-thalassemia S +-thalassemia AS, -thalassemia Hb, hemoglobin Normal Sickle trait Sickle cell anemia Sickle -thalassemia Sickle -thalassemia Sickle trait Clinical Diagnosis Hb A 97 99% 60% 0 0 10 20% 70 75% 0 40% 86 98% 70 80% 60 75% 25 30% Hb S Hb A2 1 2% 1 2% 1 3% 3 5% 3 5% 1 2% Hb F < 1% < 1% 5 15% 10 20% 10 20% < 1%
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syndromes Sickle 0-thalassemia is clinically very similar to homozygous SS disease Vaso-occlusive crises may be somewhat less severe, and the spleen is usually not infarcted Hematologically, the MCV is usually low, in contrast to the normal MCV of sickle cell anemia Hemoglobin electrophoresis (Table 13 9) reveals no hemoglobin A but will show an increase in hemoglobin A2, which is not present in sickle cell anemia Sickle +-thalassemia is a milder disorder than homozygous SS disease, with fewer crises The spleen is usually palpable The hemolytic anemia is less severe, and the hematocrit is usually 30 38%, with reticulocytes of 5 10% Hemoglobin electrophoresis shows the presence of some hemoglobin A
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necessary Patients with chronic hemolytic anemia should receive folate supplementation and avoid known oxidative drugs In rare cases, splenectomy may be required
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Acquired anemia caused by IgG autoantibody Spherocytes and reticulocytosis on peripheral blood smear Positive Coombs test
HEMOGLOBIN C DISORDERS
Hemoglobin C is formed by a single amino acid substitution at the same site of substitution as in sickle hemoglobin but with lysine instead of valine substituted for glutamine at the 6 position Hemoglobin C is nonsickling but may participate in polymer formation in association with hemoglobin S Homozygous hemoglobin C disease produces a mild hemolytic anemia with splenomegaly, mild jaundice, and pigment (calcium bilirubinate) gallstones The peripheral blood smear shows generalized red cell targeting and occasional cells with rectangular crystals of hemoglobin C Persons heterozygous for hemoglobin C are clinically normal Patients with hemoglobin SC disease are double heterozygotes for S and C These patients, like those with sickle +-thalassemia, have a milder hemolytic anemia and milder clinical course than those with homozygous SS disease There are fewer vaso-occlusive events, and the spleen remains palpable in adult life However, persons with hemoglobin SC disease have more retinopathy and more ischemic necrosis of bone than those with SS disease The hematocrit is usually 30 38%, with 5 10% reticulocytes and few irreversibly sickled cells on the blood smear Target cells are more numerous than in SS disease Hemoglobin electrophoresis will show approximately 50% hemoglobin C, 50% hemoglobin S, and no increase in hemoglobin F levels
Nagel RL et al The paradox of hemoglobin SC disease Blood Rev 2003 Sep;17(3):167 78 [PMID: 12818227]
General Considerations
Autoimmune hemolytic anemia is an acquired disorder in which an IgG autoantibody is formed that binds to the red blood cell membrane The antibody is most commonly directed against a basic component of the Rh system present on most human red blood cells When IgG antibodies coat the red blood cell, the Fc portion of the antibody is recognized by macrophages present in the spleen and other portions of the reticuloendothelial system The interaction between splenic macrophage and the antibody-coated red blood cell results in removal of red blood cell membrane and the formation of a spherocyte because of the decrease in surface-to-volume ratio of the red blood cell These spherocytic cells have decreased deformability and become trapped in the red pulp of the spleen because of their inability to squeeze through the 2mcm fenestrations When large amounts of IgG are present on red blood cells, complement may be fixed Direct lysis of cells is rare, but the presence of C3b on the surface of red blood cells allows Kupffer cells in the liver to participate in the hemolytic process because of the presence of C3b receptors on Kupffer cells Approximately 50% of all cases of autoimmune hemolytic anemia are idiopathic The disorder may also be seen in association with systemic lupus erythematosus, chronic lymphocytic leukemia, or lymphomas It must be distinguished from drug-induced hemolytic anemia Penicillin (and other drugs) coats the red blood cell membrane, and the antibody is directed against the membrane drug complex The Coombs antiglobulin test forms the basis for diagnosis of these immune hemolytic disorders The Coombs reagent is a rabbit IgM antibody raised against human IgG or human complement The direct Coombs test is performed by mixing the patient s red blood cells with the Coombs reagent and looking for agglutination, which indicates the presence of antibody on the red blood cell surface The indirect Coombs test is performed by mixing the patient s serum with a panel of type O red blood cells After incubation of the test serum and panel red blood cells, the Coombs reagent is added Agglutination in this system indicates the presence of free antibody in the patient s serum
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