Severe Hemolytic Anemia Associated With Vitamin E Deficiency in Infants With Cystic Fibrosis

1994 ◽  
Vol 33 (1) ◽  
pp. 2-7 ◽  
Author(s):  
Benjamin S. Wilfond ◽  
Philip M. Farrell ◽  
Anita Laxova ◽  
Elaine Mischler
Keyword(s):  
Cystic Fibrosis ◽  
Vitamin E ◽  
Hemolytic Anemia ◽  
Vitamin E Deficiency

Application of a new test for vitamin E deficiency to cystic fibrosis

1987 ◽  
Vol 146 (5) ◽  
pp. 512-514 ◽  
Author(s):  
H. A. Cynamon ◽  
J. N. Isenberg
Keyword(s):  
Cystic Fibrosis ◽  
Vitamin E ◽  
Vitamin E Deficiency

Hemolytic Anemia in Vitamin E Deficiency

1968 ◽  
Vol 21 (1) ◽  
pp. 45-50 ◽  
Author(s):  
FRANK A. OSKI ◽  
LEWIS A. BARNESS
Keyword(s):  
Vitamin E ◽  
Hemolytic Anemia ◽  
Vitamin E Deficiency

AVITAMINOSIS E IN CYSTIC FIBROSIS OF THE PANCREAS

PEDIATRICS ◽  
1958 ◽  
Vol 22 (3) ◽  
pp. 494-506
Author(s):  
William A. Blanc ◽  
Joseph D. Reid ◽  
Dorothy H. Andersen
Keyword(s):  
Cystic Fibrosis ◽  
Smooth Muscle ◽  
Vitamin E ◽  
Gastrointestinal Tract ◽  
Striated Muscle ◽  
Vitamin E Deficiency ◽  
Severe Vitamin ◽  
Second Year ◽  
Avitaminosis E ◽  
Ceroid Pigment

Ceroid-pigment is present in the smooth muscle fibers of the gastrointestinal tract of patients with cystic fibrosis of the pancreas. It is first seen during the second year of life. It is found in all patients of 5 years of age and older, and the amount increases with age. It has not been found in other pediatric conditions with the exception of biliary atresia and cirrhosis of the liver. Extensive ceroid deposit probably represents an expression of prolonged and severe vitamin-E deficiency, related to protracted malabsorption of fat-soluble tocopherols. Alterations of striated muscle appear to be rare and minimal in cystic fibrosis of the pancreas.

scholarly journals Symptomatic vitamin E deficiency in cystic fibrosis.

1985 ◽  
Vol 60 (2) ◽  
pp. 162-164 ◽  
Author(s):  
A M Bye ◽  
D P Muller ◽  
J Wilson ◽  
V M Wright ◽  
M B Mearns
Keyword(s):  
Cystic Fibrosis ◽  
Vitamin E ◽  
Vitamin E Deficiency

Reversible tremor in an infant with vitamin E deficiency and cystic fibrosis

The Lancet ◽  
2021 ◽  
Vol 398 (10295) ◽  
pp. 156
Author(s):  
Tommaso Lo Barco ◽  
Anna Ludovica Ghobert ◽  
Francesca Lucca ◽  
Giulia Galati ◽  
Jacopo Proietti ◽  
...  
Keyword(s):  
Cystic Fibrosis ◽  
Vitamin E ◽  
Vitamin E Deficiency

Vitamin E Deficiency Neuropathy in Children with Fat Malabsorption Studies in Cystic Fibrosis and Chronic Cholestasis

1989 ◽  
Vol 570 (1 Vitamin E) ◽  
pp. 156-169 ◽  
Author(s):  
RONALD J. SOKOL ◽  
NANCY BUTLER-SIMON ◽  
JAMES E. HEUBI ◽  
SUSAN T. IANNACCONE ◽  
H. JUHLING McCLUNG ◽  
...  
Keyword(s):  
Cystic Fibrosis ◽  
Vitamin E ◽  
Vitamin E Deficiency ◽  
Chronic Cholestasis ◽  
Fat Malabsorption

scholarly journals Degradation of Membrane Phospholipids and Thiols in Peroxide Hemolysis: Studies in Vitamin E Deficiency

Blood ◽  
1968 ◽  
Vol 32 (4) ◽  
pp. 549-568 ◽  
Author(s):  
HARRY S. JACOB ◽  
SAMUEL E. LUX
Keyword(s):  
Fatty Acids ◽  
Vitamin E ◽  
Hemolytic Anemia ◽  
Phosphatidyl Ethanolamine ◽  
Red Cells ◽  
Membrane Phospholipids ◽  
Vitamin E Deficiency ◽  
Red Cell Membrane ◽  
Inhibition Of Metabolism

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.

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