Vitamin E deficiency: A previously unrecognized cause of hemolytic anemia in the premature infant

1967 ◽  
Vol 70 (2) ◽  
pp. 211-220 ◽  
Author(s):  
Frank A. Oski ◽  
Lewis A. Barness
1974 ◽  
Vol 27 (10) ◽  
pp. 1158-1173 ◽  
Author(s):  
Lois Johnson ◽  
David Schaffer ◽  
Thomas R. Boggs

1994 ◽  
Vol 33 (1) ◽  
pp. 2-7 ◽  
Author(s):  
Benjamin S. Wilfond ◽  
Philip M. Farrell ◽  
Anita Laxova ◽  
Elaine Mischler

1968 ◽  
Vol 21 (1) ◽  
pp. 45-50 ◽  
Author(s):  
FRANK A. OSKI ◽  
LEWIS A. BARNESS

PEDIATRICS ◽  
1977 ◽  
Vol 59 (6) ◽  
pp. 995-997
Author(s):  
Steven J. Gross ◽  
Stephen A. Landaw ◽  
Frank A. Oski

A study was designed to determine if the presence of vitamin E deficiency during the first week of life played a contributory role in the shortened red cell life span observed in the premature infant. Carboxyhemoglobin values were used as an index of hemolysis. Ten infants received vitamin E administered intramuscularly in a total dose of 125 mg/kg during days 3 to 7 of life; ten infants served as controls. The mean percent carboxyhemoglobin level fell significantly from day 3 to day 8 in the treated group (1.08% to 0.78%) whereas the mean value remained unchanged at 0.96% in the control group. The administration of vitamin E appears to reduce but not eliminate the accelerated red cell destruction that characterizes the preterm infant.


Blood ◽  
1968 ◽  
Vol 32 (4) ◽  
pp. 549-568 ◽  
Author(s):  
HARRY S. JACOB ◽  
SAMUEL E. LUX

Abstract To understand more clearly the hemolytic anemia associated with administration of certain oxidant drugs, the mechanism by which H2O2 causes hemolysis in rat red cells, deficient in vitamin E was investigated. It was demonstrated that the locus of attack by H2O2 was the red cell membrane, in which one phospholipid, i.e., phosphatidyl ethanolamine, was specifically destroyed prior to the onset of hemolysis. No perturbation of intracellular components or metabolism was noted during peroxidative hemolysis. E-deficient red cells incorporated 14C-labelled fatty acids into this phosphatide at nearly twice the rate that in E-supplemented cells, reflecting the continual tendency of phosphatidyl ethanolamine to be destroyed. Young red cells were especially active in this regard and concomitantly were less vulnerable to damage by H2O2 both in vitro and when circulating in rats exposed to hyperbaric oxygenation. If, however, replacement of fatty acids in phosphatidyl ethanolamine was prevented by inhibition of metabolism or if fatty acids were enzymatically removed by a phospholipase-A, H2O2 hemolysis was potentiated. Hemolysis was also associated with, and potentiated by, loss of membrane sulfhydryl activity. It is suggested that hemolytic anemia may occur in patients with vitamin E deficiency (i.e., with steatorrhea) if oxidant drugs capable of generating H2O2 and oxidizing membrane thiols are administered. Two such cases are under investigation.


1974 ◽  
Vol 27 (10) ◽  
pp. 1158-1173 ◽  
Author(s):  
Lois Johnson ◽  
David Schaffer ◽  
Thomas R. Boggs

2017 ◽  
Vol 35 (03) ◽  
pp. 305-310 ◽  
Author(s):  
Emily Hatfield ◽  
Karen Garlitz ◽  
Philip Westgate ◽  
Henrietta Bada ◽  
Enrique Gomez-Pomar

Objective Vitamin E deficiency in premature infants has been associated with hemolytic anemia. Its incidence decreased after the supplementation of preterm formulas and parenteral nutrition with vitamin E. Despite this, some infants still develop hemolytic anemia and receive vitamin E. Study Design Retrospective analysis of 70 infants admitted to a level IV intensive care unit and who developed hemolytic anemia and were treated with vitamin E. Infants were classified into two groups based on whether or not they responded to vitamin E therapy. Statistical methods included the use of descriptive statistics and marginal logistic regression models. Results Low hematocrit and reticulocytosis before vitamin E administration were associated with adequate response to treatment. Thrombocytosis, iron treatment (duration and dose), gestational age, birth weight, and type of feedings were not. Infants who received a short duration of parenteral nutrition and were on oxygen responded to vitamin E therapy. Infants with a hematocrit ≤ 26% and reticulocyte of 36.1% were more likely to respond to vitamin E. Conclusion Although formulas and parenteral nutrition are supplemented with vitamin E; some preterm infants may still develop hemolytic anemia. Those with anemia, reticulocytosis, and oxygen requirement may benefit from additional vitamin E.


Circulation ◽  
1996 ◽  
Vol 94 (1) ◽  
pp. 14-18 ◽  
Author(s):  
Kunihisa Miwa ◽  
Yuko Miyagi ◽  
Akihiko Igawa ◽  
Keiko Nakagawa ◽  
Hiroshi Inoue

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