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Iron deficiency decreases hemolysis in sickle cell anemia / Anemia ferropriva diminui hemólise em anemia falciforme
Castro, Oswaldo; Medina, Adriana; Gaskin, Peter; Kato, Gregory J; Gordeuk, Victor R.
  • Castro, Oswaldo; Howard University Center for Sickle Cell Disease. Washington. US
  • Medina, Adriana; Howard University College of Medicine. Department of Medicine. Washington. US
  • Gaskin, Peter; Howard University College of Medicine. Department of Pediatrics. Washington. US
  • Kato, Gregory J; Institute National Institutes of Health. Bethesda. US
  • Gordeuk, Victor R; University College of Medicine. Center for Sickle Cell Disease Howard. Washington. US
Rev. bras. hematol. hemoter ; 31(1): 51-53, jan.-fev. 2009. graf, tab
Article in English | LILACS | ID: lil-511179
ABSTRACT
A woman with homozygous sickle cell disease developed severe iron deficiency due to long-standing uterine bleeding. At this point, the serum lactic dehydrogenase level was normal and the reticulocyte count was only minimally elevated. This suggested that the low red cell hemoglobin concentration that resulted from iron deficiency also decreased Hb S polymerization and lowered the hemolytic rate. Iron replacement led first to a substantially improved hemoglobin concentration with only a minimal increase in the hemolytic rate and secondarily to a modest further improvement in the hemoglobin concentration and a marked increase in the hemolytic rate. The hematologic changes observed in this patient, and those in other iron deficient sickle cell patients reported in the literature, suggest that it may be appropriate to consider the induction of an intermediate iron deficient stage as experimental treatment in adult sickle cell patients.
RESUMO
Uma mulher com anemia falciforme homozigose para a Hb S evoluiu com anemia ferropriva grave devido a sangramento uterino prolongado. A dosagem de dehidrogenase lática era normal e a contagem de reticulócitos estava levemente aumentada. Isto sugere que concentrações baixas de hemoglobina, que resulta de anemia ferropriva, também diminuem a polimeração de Hb S e reduz a taxa de hemólise. O complemento de ferro levou, primeiramente, a uma concentração substancialmente maior de hemoglobina com apenas um aumento mínimo na taxa hemolítica e subsequentemente a um aumento leve adicional na concentração da hemoglobina e um aumento notável na taxa hemolítica. As mudanças hematológicas observadas nesta paciente e aquelas em outras pacientes com anemia falciforme e também deficientes de ferro relatadas na literatura sugerem que pode ser interessante considerar a indução de deficiência de ferro como tratamento experimental em pacientes adultos com anemia falciforme.

Full text: Available Index: LILACS (Americas) Language: English Journal: Rev. bras. hematol. hemoter Journal subject: Hematology Year: 2009 Type: Article Affiliation country: United States Institution/Affiliation country: Howard University Center for Sickle Cell Disease/US / Howard University College of Medicine/US / Institute National Institutes of Health/US

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Full text: Available Index: LILACS (Americas) Language: English Journal: Rev. bras. hematol. hemoter Journal subject: Hematology Year: 2009 Type: Article Affiliation country: United States Institution/Affiliation country: Howard University Center for Sickle Cell Disease/US / Howard University College of Medicine/US / Institute National Institutes of Health/US