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Iron replacement is often indicated for treatment of iron deficiency This may improve the anemia but may also cause a transient increase in hemolysis For unclear reasons, prednisone is effective in decreasing hemolysis, and some patients can be managed effectively with alternateday steroids In severe cases and cases of transformation to myelodysplasia, allogeneic bone marrow transplantation has been used to treat the disorder The anti-complement C5 antibody eculizumab has been shown to be effective in reducing hemolysis and transfusion requirements
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Brodsky RA New insights into paroxysmal nocturnal hemoglobinuria Hematology Am Soc Hematol Educ Program 2006: 24 8 [PMID: 17124035] Hillmen P et al Effect of eculizumab on hemolysis and transfusion requirements in patients with paroxysmal nocturnal hemoglobinuria N Engl J Med 2004 Feb 5;350(6):552 9 [PMID: 14762182]
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Clinical Findings
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G6PD deficiency is an X-linked recessive disorder affecting 10 15% of American black males Female carriers are rarely affected only when an unusually high percentage of cells producing the normal enzyme is inactivated
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A Symptoms and Signs
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Patients are usually healthy, without chronic hemolytic anemia or splenomegaly Hemolysis occurs as a result of oxidative stress on the red blood cells, generated either by infection or exposure to certain drugs Common drugs initiating hemolysis include dapsone, primaquine, quinidine, quinine, sulfonamides, and nitrofurantoin Even with continuous use of the offending drug, the hemolytic episode is self-limited because older red blood cells (with low enzyme activity) are removed and replaced with a
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population of young red blood cells with adequate functional levels of G6PD Severe G6PD deficiency (as in Mediterranean variants) may produce a chronic hemolytic anemia
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B Laboratory Findings
Between hemolytic episodes, the blood is normal During episodes of hemolysis, there is reticulocytosis and increased serum indirect bilirubin The red blood cell smear is not diagnostic but may reveal a small number of bite cells cells that appear to have had a bite taken out of their periphery This indicates pitting of hemoglobin aggregates by the spleen Heinz bodies may be demonstrated by staining a peripheral blood smear with cresyl violet; they are not visible on the usual Wright-Giemsa stained blood smear Specific enzyme assays for G6PD may reveal a low level but may be misleading if they are performed shortly after a hemolytic episode when the enzyme-deficient cohort of cells has been removed In these cases, the enzyme assays should be repeated weeks after hemolysis has resolved In severe cases of G6PD deficiency, enzyme levels are always low
polymer formation, and its presence markedly retards sickling Other factors that increase sickling are those that lead to formation of deoxyhemoglobin S, eg, acidosis and hypoxemia, either systemic or locally in tissues Prenatal diagnosis is now available for couples at risk of producing a child with sickle cell anemia DNA from fetal cells can be directly examined, and the presence of the sickle cell mutation can be accurately and definitively diagnosed Genetic counseling should be made available to such couples
Clinical Findings
A Symptoms and Signs
The hemoglobin S gene is carried in 8% of American blacks, and one birth out of 400 in American blacks will produce a child with sickle cell anemia The disorder has its onset during the first year of life, when hemoglobin F levels fall as a signal is sent to switch from production of -globin to -globin Chronic hemolytic anemia produces jaundice, pigment (calcium bilirubinate) gallstones, splenomegaly, and poorly healing ulcers over the lower tibia The chronic anemia may become life-threatening when severe anemia is produced by hemolytic or aplastic crises The latter occur when the ability of the bone marrow to compensate is reduced by viral or other infection or by folate deficiency Hemolytic crises may be related to splenic sequestration of sickled cells (primarily in childhood, before the spleen has been infarcted as a result of repeated sickling) or with coexistent disorders such as G6PD deficiency Acute painful episodes due to acute vaso-occlusion may occur spontaneously or be provoked by infection, dehydration, or hypoxia Clusters of sickled red cells occlude the microvasculature of the organs involved These episodes last hours to days and produce acute pain and lowgrade fever Common sites of acute painful episodes include the bones (especially the back and long bones) and the chest Acute vaso-occlusion may also cause strokes due to sinus thrombosis and priapism Vaso-occlusive episodes are not associated with increased hemolysis Repeated episodes of vascular occlusion affect a large number of organs, especially the heart, lungs, and liver Ischemic necrosis of bone occurs, rendering the bone susceptible to osteomyelitis due to staphylococci or (less commonly) salmonellae Infarction of the papillae of the renal medulla causes renal tubular concentrating defects and gross hematuria, more often encountered in sickle cell trait than in sickle cell anemia Retinopathy similar to that noted in diabetes is often present and may lead to blindness Pulmonary hypertension may develop and is associated with a poor prognosis These patients are prone to delayed puberty An increased incidence of infection is related to hyposplenism as well as to defects in the alternative pathway of complement On examination, patients are often chronically ill and jaundiced There is hepatomegaly, but the spleen is not palpable in adult life The heart is enlarged, with a hyperdynamic precordium and systolic murmurs Nonhealing ulcers of the lower leg and retinopathy may be present
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