par Fondu, Pierre 
;Mozes, Nava;Neve, Pierre ;Sohet‐Robazza, Lucienne;Mandelbaum, Israel
Référence British journal of haematology, 44, 4, page (605-618)
Publication Publié, 1980
;Mozes, Nava;Neve, Pierre ;Sohet‐Robazza, Lucienne;Mandelbaum, Israel Référence British journal of haematology, 44, 4, page (605-618)
Publication Publié, 1980
Article révisé par les pairs
| Résumé : | Summary. In protein‐energy malnutrition (PEM), as observed in Kivu, the RBC have an increased ratio of surface area to volume which is demonstrated by the presence of target cells on light microscopy and cup cells with scanning electron microscopy. The osmotic fragility is decreased. These abnormalities can be attributed to the accumulation of cholesterol and phosphatidylcholine (PC) in the RBC membrane. The molar ratio of cholesterol to phospholipids is moderately increased. Several findings suggest that the cholesterol and PC build‐up results from disturbed exchanges in these lipids between the RBC and the plasma lipoproteins. Firstly, the osmotic fragility of a patient's RBC gradually becomes normal when the cells are transfused into a healthy recipient. Secondly, the cholesterol flux between the RBC and the plasma LDL seems to be low. Thirdly, the increase in RBC PC cannot be explained by a diminished fatty acids transport between the deep RBC PC pool and the RBC phosphatidylethanolamine (PE) pool. Finally complex disturbances of the plasma lipoproteins are obvious. It is improbable that the cholesterol and PC build‐up accounts for the premature RBC destruction which has been described in Kivu PEM. However, the observation of an increased fatty acid turnover in RBC PC and PE, as well as other data previously obtained in Kivu PEM, lead to the conclusion that membrane peroxidation may be a major cause of the shortened erythrocyte life‐span in this syndrome. Copyright © 1980, Wiley Blackwell. All rights reserved |
