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Pages 276-295

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From page 276...
... Thus in sickle cell anemia the hematocrit is almost invariably less than thirty per cent; in the genetic variants of sicklemia the degree of anemia is less often severe, and individuals with sickle trait do not ordinarily have anemia. Anemia might occur in individuals with sickle trait, however, if chronic oxygen deprivation results in sufficient reduction of the oxygen tension of the blood.
From page 277...
... The cause for transient marrow aplasia is not clearly understood and aplastic crises occur in disorders other than sicklemia. The following case is illustrative of the clinical course of sickle cell anemia with an aplastic crisis.
From page 278...
... 2. Aplastic crisis in sickle cell anemia.
From page 279...
... Infarction of the spleen in individuals with genetic variants of sickle cell anemia, such as sickle-hemoglobin C disease or sickle-thalassemia, has occurred at lower altitudes than in individuals with sickle trait. Only gross infarction has been recognized in patients with sicklemia who were in airplane flight,3 ~ but few instances of gross splenic infarction with pain, fever, and shock have been observed in any form of sicklemia when not airborne.
From page 281...
... Renal hemorrhage, which is most often unilateral and frequently massive, is encountered in patients with sickle cell Preemie, the genetic variants of sickle cell disease, and in sickle cell trait. Most of the reported cases have been in sickle trait.
From page 282...
... C.: Sickle cell anemia, a molecular disease, Science 110: 543, 1949.
From page 283...
... P reaction B - Abnormalities of red cell morphology C- Fetal hemoglobin factor Etc.
From page 284...
... 'B' may be assigned to the defect resulting in morphologic alterations such as anisocytosis, poikilocytosis, ovalocytosis, and target cells, and 'C' to the role played by Hb F Other letters might be assigned to stippling, stromal defects, and so forth, although all or most of these may be involved in a single genetic aberration.
From page 285...
... Thus, sickling in combination with thalassemia suggests thalassemia-lIb S disease. Greatly increased numbers of target cells in an otherwise uncomplicated case of thalassemia may point to a combination with fIb C
From page 286...
... Its most striking feature outside of the genetic and hemoglobin abnormalities is the presence of up to 60-80 per cent target cells and the consequent shift in the osmotic fragility curve to the right. Thalassemia-Hb E disease has been recognized with increasing frequency in Thailand, Burma, and Indonesia and except in a few minor respects, mimics Cooley's anemia.
From page 287...
... Hemoglobin C trait. The combination of hemoglobin C and normal adult hemoglobin in asymptomatic individuals was first detected in family studies;7 however, large scale surveys for abnormal hemoglobins revealed hemoglobin C trait in 2 to 3 per cent of American Negroes.
From page 288...
... Studies of eight offspring of sickle cell and normal individuals revealed only hemoglobin C trait or sickle cell trait in the offspring (figs. 1 and 2~; it seems probable that genes responsible for sickle cell hemoglobin and hemoglobin C are allelic or are closely linked.~3 FIGS.
From page 289...
... and 3) large renumbers of target cells in the stained smears.
From page 290...
... . Erythrocyte survival times of 40 to 60 days, with one-half survival times of 13 to 24 days were observed.S' 15, i7, 2~, 9~, 94 The data are consistent with the assumption that the shortened survival time is related to an intracorpuscular defect.
From page 291...
... Nucleated erythrocytes have been found in many of the peripheral blood smears. The most impressive finding on blood smear was the increased number of target cells, frequently with erythrocyte "folding" (fig.
From page 292...
... Splenomegaly and target cells are more constant findings than is anemia. Only one patient has developed evidence of "hypersplenism"; patients with anemia and thrombocytopenia returned to normal following splenectomy.
From page 293...
... While most of the reported patients have had some increment of normal adult hemoglobin in addition to hemoglobins C' and A, the amount of hemoglobin A nary be so small tot accurate determination is difficult. Consequently, a study of the hemoglobin of other members of the family is a more reliable way of establishing the diagnosis of hemoglobin C-thalassemia than analysis of the hemoglobin of the affected individual alone.
From page 294...
... W., and Peel, J V.: A new inherited abnormality of hemoglobin and its interaction with sickle cell hemoglobin, Blood 6: 1240, 1951.
From page 295...
... M.: Observations on the inheritance of sickle cell hemoglobin and hemoglobin C, i.


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