Protein-energy malnutrition in Kivu is associated with a discrete normocytic, normochromic anemia. An attempt to define the physiopathology of this anemia disclosed the following results. As compared with local controls, both iron and total iron binding capacity were low, but with siderophilin saturation and sideroblast counts either normal or elevated; serum and erythrocyte folate was normal, plasma vitamin B12 was normal or elevated, and serum ascorbic acid was normal or elevated. The riboflavin nutritional status was normal. During refeeding, iron and riboflavin deficiencies became apparent. Characteristic findings on admission were the presence of giant erythroblasts and a diminished erythrocyte survival time implicated to an intracorpuscular hemolysis. Two results from the present study could contribute to explanation for the aforementioned abnormalities: low plasma vitamin E levels and, perhaps more importantly, low plasma selenium levels. In conclusion, the anemia of protein-energy malnutrition, as observed in Kivu, is a classifiable nonadaptive anemia that cannot be explained by isolated iron or vitamin deficiencies and whose physiopathology is distinct from that of the anemia of chronic disorders. It is suggested that a selenium deficiency may play an important role in the pathogenesis of this anemia.

Rats were either fed a 12 % fat diet for 3 weeks, or rendered obese by administration of a 40 % fat diet for 6 months. In both cases, the rate of insulin secretion evoked by glucose in incubated pieces of pancreatic tissue was lower than that observed in tissue from control animals fed diets containing only 3 to 4 % fat. This reduction in

SummaryThe in vitro incorporation and transport of plasma nonesterified fatty acids into phospholipids of red cell membranes have been studied in cystic fibrosis and healthy children.Red blood cells were labeled in vitro by an active "acyltransferase"-dependent incorporation of radioactively labeled nonesterified fatty acids. [3HI-Palmitic and ['4CI-linoleic acid, bound to albumin, have been studied simultaneously because it has been shown before that the concentration of palmitic acid increases and the concentration of linoleic acid decreases both in the plasma nonesterified fatty acid fraction and in the various phospholipids of the erythrocyte membranes of cystic fibrosis patients.The labeled cells were reincubated in autologous serum and the radioactivity present in the serum lipids and in the major phospholipid fractions of the erythrocyte membranes was measured.A general conclusion is that the in vitro turnover of labeled palmitic and linoleic acids in the phospholipids of the erythrocyte membranes is higher for cystic fibrosis patients than for healthy children. No difference is detectable between the in vitro behaviour of ['4CI-linoleic versus [3HI-palmitic acid in cystic fibrosis patients compared with healthy children.clusion of that study (8) is that the fatty acid composition of the plasma cholesterol esters of CF patients without pancreatic insufficiency is significantly different from the results obtained for agematched controls (8). Furthermore, it was found that the fatty acid patterns of the various phospholipid fractions of the RBC membranes are abnormal in CF patients with pancreatic insufficiency (24). A positive correlation was observed between the fatty acid changes of both plasma and RBC phospholipid fractions (Rogiers, V., unpublished data).One of the mechanisms, playing a major role in the continuous in vivo renewal of RBC lipids consists of the active incorporation of plasma NEFA's into the phospholipids of the RBC membrane (28, 29). Consequently it is possible that this process could be partly responsible for the abnormalities observed in the RBC membranes of CF patients. On the other hand, abnormal fatty acid patterns intrinsic to the C F membranes could support the hypothesis of a possible defect in fatty acid metabolism.In order to obtain more information concerning the active incorporation process of plasma NEFA's into the phospholipids of the RBC membranes of CF patients, a number of incorporation and reincubation experiments with labeled NEFA's have been carried out. RBCs of healthy and CF children were incubated with [14C1-linoleic and [3H1-palmitic acid bound to albumin. The labeled RBC'S were reincubated in their autologous serum.

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.

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