Cross-sectional interactions by malaria status were investigated between plasma alpha-tocopherol, retinol, and several carotenoids (lutein, beta-cryptoxanthin, lycopene, and alpha- and beta-carotene) and indicators of disease severity (blood parasite count, hemoglobin concentration), acute-phase response (plasma albumin and ceruloplasmin concentrations), hepatic involvement (plasma alanine aminotransferase), oxidant status and antioxidant status (plasma thiobarbituric acid-reactive material and ascorbate), nutritional (weight-for-age) and carrier protein [retinol binding protein (RBP)] status, and cholesterol concentration (as a proxy for lipoprotein) in 100 consecutively admitted children with malaria. There were 50 children with severe and 50 with mild malaria and 50 age- and sex-matched control subjects. alpha-Tocopherol, retinol, and all the carotenoid concentrations were lower in the patients than in the control subjects (P < 0.001). The differences were greater in severe than in mild malaria, except for lutein. In severe malaria only, both retinol and alpha-tocopherol correlated with albumin, ceruloplasmin, and RBP concentrations whereas in all three groups retinol correlated with RBP and alpha-tocopherol correlated with cholesterol (all P < 0.01)). Using multivariate analysis on data from all patients combined, cholesterol was the most significant factor explaining the variance in alpha-tocopherol (29%) whereas RBP was responsible for 95% of the variance in retinol. Plasma cholesterol and RBP values in turn (in the absence of alpha-tocopherol and retinol, respectively) were influenced primarily by acute-phase markers (mainly albumin and ceruloplasmin). Alanine aminotransferase (r = -0.17) and thiobarbituric acid-reactive material (r = -0.17) also showed a small contribution to the variance of RBP but 60-70% remained unexplained. In conclusion, low plasma lipid-soluble micronutrient concentrations in malaria are strongly influenced by the reductions in their carrier molecules, which, in turn, are low as a consequence of the acute-phase response.
To investigate Fe nutritional indices in malaria infection in children, haematology (blood haemoglobin, plasma ferritin, transferrin, Fe, and transferrin saturation), acute phase markers (albumin and caeruloplasmin) and liver function tests were studied in fifty consecutive cases of severe and mild falciparum malaria, fifty matched controls and twenty-three cases of asymptomatic malaria. Blood haemoglobin and transferrin were lower, while ferritin and transferrin saturation were higher, in groups with symptomatic malaria in comparison with the control group. The differences were greatest with the severest form of the disease. There were no differences between any of the groups in plasma Fe. Plasma transferrin correlated directly with albumin in asymptomatic, mild and severe malaria groups (r 0.48, 0.65 and 0.83; P < 0.05, P (0.01 and P < 0,001 respectively), and inversely with caeruloplasmin (r -0.65, -0.34 and -0.43; P < 0.01, P < 0.05 and P < 0.01 respectively). For ferritin, the correlation was inverse with albumin (r -0.65, -0.57 and -0.64; P < 0.01, P < 0.001 and P < 0.001 respectively and direct with caeruloplasmin (r 0.83, 0.21 and 0.49, P < 0.001, NS and P < 0401 respectively). Multiple regression analysis on data from all patients combined indicated that albumin, and to a lesser extent alanine aminotransferase (EC 2.6.1.2) activity, explained 62 % of the variance in transferrin. Caeruloplasmin, parasite count and albumin explained 59 % of the variance in ferritin, and transferrin and unconjugated bilirubin explained 62 % of the variance in Fe values. In conclusion, these data suggest that low transferrin and high ferritin values are primarily due to the acute phase response.
Plasma lipid peroxides were measured as malonyldialdehyde (MDA) by the thiobarbituric acid (TBA) method in 75 children suffering from Plasmodium falciparum malaria. Their riboflavin status was assessed by measuring erythrocyte glutathione reductase activation coefficients (EGRACs), and values greater than 1.40 were regarded as indicating biochemical deficiency. Plasma MDA was higher (p less than 0.001) in patients than in control subjects; the concentrations were 3.65 +/- 0.70 and 1.77 +/- 0.45 mumol/L (means +/- SD), respectively. The riboflavin-deficient group had higher plasma MDA values (3.98 +/- 0.70 mumol/L) than did the nondeficient group (3.30 +/- 0.68 mumol/L, p less than 0.001). Plasma MDA concentrations correlated with EGRACs (r = 0.46, p less than 0.01) in the patients. It is proposed that riboflavin deficiency restricts regeneration of reduced glutathione making the parasitized erythrocytes more vulnerable to destructive lipid peroxidation and increasing plasma lipid hydroperoxides.
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