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Query: UMLS:C0024530 (malaria)
 44,886 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Untreated malaria for more than 4 days in eleven patients decreased significantly prealbumin, transferrin levels and increased SGOT activity when compared with a control group and a group of 10 malaria patients who were admitted to the hospital at an earlier stage of the infection. Total protein was significantly lower in the group of patients admitted after five to ten days to hospital compared with the control group. In all malaria patients independent of the duration of the acute infection the 1st post albumin peak in polyacrylamide gel electrophoresis (consisting mainly of Gc-globulin, alpha-1-antichymotrypsin and alpha-1 B-glycoprotein) and creatinine were found to be significantly higher compared with the control group.
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PMID:Alterations of human serum proteins and other biochemical parameters after five to ten days of untreated acute falciparum malaria. 33 73

To study the role of the erythrocyte membrane in the process of chloroquine accumulation, surface polypeptides were digested with a nonspecific protease from Streptomyces griseus. This treatment activated a saturable process of chloroquine accumulation with an affinity and a specificity similar to those of mouse erythrocytes infected with Plasmodium berghei CS (chloroquine susceptible). Studies of competitive inhibitors of chloroquine accumulation yielded the following approximate values for K(i): amodiaquine, 2 x 10(-7) M; quinacrine, 5 x 10(-7) M; quinine, 2 x 10(-6) M; and mefloquine, 2 x 10(-5) M. Lack of a substrate requirement distinguished this process from the one used by P. berghei and permitted the protease to be used in studies of infected erythrocytes. Protease treatment of erythrocytes infected with P. berghei CR (chloroquine resistant) produced a dramatic transformation. Instead of describing a sigmoid curve, the process of chloroquine accumulation became saturable and substrate dependent, with a K(diss) of approximately 10(-8) M; i.e., protease-treated erythrocytes infected with P. berghei CR now behaved similarly to those infected with P. berghei CS. Coating the erythrocyte surface with albumin completely inhibited the protease-activated process of chloroquine accumulation. These findings are presented as evidence that erythrocyte surface components determine the affinity with which chloroquine is accumulated and thereby determine whether or not the malaria parasite will be susceptible to the drug.
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PMID:Erythrocyte surface: novel determinant of drug susceptibility in rodent malaria. 35 16

A global review of the porblem of malaria accidentally transmitted by blood transfusion is reported in France during these ten last years. Biological and epidemiological studies of malariae are recorded. Among the factors involved in the transmission of malariae by blood transfuction, the persistence of the parasites in the donors is very important. It is often longer than usual in the subjects who have lived in endemic malarious areas for many years or are always travelling in these countries, because they are partly protected by their acquired immunity and may be carriers of asymptomatic infection. The viability of parasites in stored blood, red cells and preparations with platelets, leucocytes or plasma containing a few red cells with parasites is discussed. The prevention depended on the elimination of any blood donor who has ever had malaria appears to be the simplest method but it is also the most failible. The screening of donors by direct microscopy is obviously impracticable because of low density and often submicroscopic level of their parasitoemia. Screening donors by IFA test is the best method. If IFA test is negative four months after coming back from endemic areas and two months after ending suppressive therapeutic, whole blood, red cells, leucocytes, platelets and fresh plasma can be used on condition that the stay of donors in endemic areas had been not too long. If the stay in these countries was very long, blood will be only used for preparing lyophilized plasma, fibrinogen immunoglobulins or albumin.
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PMID:[Post-tranfusional malaria in France]. 98 71

Study of urinary waste of chickens with acute Plasmodium gallinaceum malaria indicated that serum proteins of the globulin and albumin classes were passed. Protein extravasation did not begin until globulin-associated serum antigen and its antibody were detected in the blood. Both serum antigen and antibody were found in the wastes for as long as the antigen was present in the blood. Extracts of kidney tissues contained serum proteins that were not present in extracts from normal kidneys, and serum antigen and its antibody were both present. Frozen kidney sections reacted strongly with fluorescein-conjugated antibody to serum antigen, showing diffuse granular immunofluorescence characteristic of immune complex nephritis. Sections from chickens with nephritis induced by injections of malarious plasma also showed deposits of extravasated antigen. The experiments suggested that complexes of serum antigen and antibody served as a permeability factor, or activated other permeability factors and may have caused the glomerulonephritis associated with acute avian malaria. The passing of serum proteins in the urinary wastes after chickens had recovered from acute malaria suggested that persisting damage may have resulted.
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PMID:Pathogenesis of acute avian malaria. IV. Immunologic factors in nephritis of acute Plasmodium gallinaceum infections of chickens. 109 93

Liver function tests were performed in 165 hospitalized patients suffering from P. falciparum malaria with complications. Serum bilirubin was found increased in 33 patients, and 22 of them had unconjugated hyperbilirubinaemia. Serum alanine aminotransferase was increased in 5 patients, but only to mild to moderate levels. Serum alkaline phosphatase was increased in 11 patients, gamma-glutamyl transpeptidase in 3 patients. Serum total protein and albumin were significantly decreased but these were considered more as indicator of acute phase response. Liver cell necrosis was observed in one patient, and oedema and mononuclear cell infiltration in two patients. Though hepatomegaly and mild elevation of enzymes can be observed in a significant proportion of patients, involvement of liver leading to acute hepatitis or liver cell necrosis is a relatively uncommon complication in P. falciparum malaria.
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PMID:Hepatic changes in P. falciparum malaria. 128 32

Plasma levels of HDL, LDL, total cholesterol and triglycerides were measured in 60 patients with falciparum malaria (37 severe cases and 23 mild) and in 83 healthy individuals, to study malaria-induced changes in plasma lipids. Triglyceride levels were lower in the patients than in the controls but the difference was significant only for those with severe malaria (P < 0.001). In contrast, the levels of all the other plasma lipids were significantly higher (P < 0.001) in those with severe malaria than in those with mild malaria, and in the mild malaria cases compared with the controls. Initially LDL cholesterol was estimated by the Friedwald formula, but this gave negative values in a few cases of severe malaria. Plasma lipoproteins were therefore also measured by nephelometry; the estimated levels of S particles, corresponding to LDL, were then found to be lower in all malaria cases than in the controls (P < 0.001) but never negative. Interestingly, levels of L particles in the patients with severe malaria were significantly elevated compared with the other patients and controls (P < 0.001), indicating impaired metabolism of chylomicrons. Plasma albumin, considered a negative acute phase protein (i.e. its level decreases as a consequence of the acute phase response), was reduced significantly and was directly correlated to HDL cholesterol levels (r = 0.715 and r = 0.895, respectively) in both mild and severe malaria. Follow-up of 22 of the severe malaria cases three weeks after treatment indicated that, while triglycerides had returned to similar levels to those in the controls, total cholesterol levels were still elevated and could give misleading results if lipid profiles were used, immediately after malaria infection, to assess an individual's risk of developing atherosclerosis.
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PMID:Altered plasma lipid pattern in falciparum malaria. 130 1

The binding of quinine to human serum albumin (HSA), alpha 1-acid glycoprotein (AAG) and plasma obtained from healthy subjects (10 caucasians and 15 Thais) and from Thai patients with falciparum malaria (n = 20) has been investigated. In healthy volunteers, plasma protein binding expressed as the percentage of unbound quinine was 7.9-31.0% (69-92.1% bound). The mean percentage of unbound quinine found with essentially fatty acid-free HSA (40 g L-1) was 65.4 +/- 1.5% (mean +/- s.d.) and was comparable with the value (66.3 +/- 3.8%, mean +/- s.d.) for Fraction V HSA (40 g L-1). This suggests that fatty acids do not influence the plasma protein binding of quinine. Binding of quinine to 0.7 g L-1 AAG was high (mean unbound 61.0 +/- 5.0%), indicating that quinine is bound primarily to AAG and albumin, although other plasma proteins such as lipoproteins may be involved. The mean percentage of unbound quinine was slightly less in caucasians (14.8 +/- 6.7% unbound), compared with healthy Thai subjects (17.0 +/- 6.7% unbound). The higher binding of quinine in caucasian subjects was associated with a higher plasma AAG concentration observed in caucasians. Mean percentage of unbound quinine was significantly lower in Thai patients with malaria (10.9 +/- 4.0%) than in the healthy Thai subjects. The increase in the extent of quinine binding corresponded with the increase in the acute-phase reactant protein, AAG in the patients with malaria. Overall, when the data were combined there was a significant correlation (r = 0.846, P < 0.005) between the binding ratio (bound/unbound) of quinine and the plasma AAG concentration.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Plasma protein binding of quinine: binding to human serum albumin, alpha 1-acid glycoprotein and plasma from patients with malaria. 136 May 5

The binding of the novel antimalarial drug, arteether, to human plasma, pure albumin and alpha 1-acid glycoprotein has been investigated by ultrafiltration, using [14C]arteether. The protein binding in plasma obtained from 11 healthy male subjects ranged from 73.4 to 81.8% bound, with a mean of 78.7 +/- 2.1%. The binding of drug in plasma was mainly accounted for by binding to albumin and alpha 1-acid glycoprotein. Scatchard analysis of the binding data revealed that the binding affinity of arteether to alpha 1-acid glycoprotein is much greater (20-fold) than that to albumin. This suggests that alpha 1-acid glycoprotein is the more important binding protein in plasma. This may have clinical importance due to alterations in plasma protein binding in patients with malaria, as the concentration of alpha 1-acid glycoprotein is markedly increased during malarial infection.
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PMID:The binding of the antimalarial arteether to human plasma proteins in-vitro. 136 44

Aflatoxin-albumin adduct levels were measured in serum samples obtained from a group of Gambian children. The relationships between exposure to aflatoxin and the prevalence of malaria, between exposure and humoral and cellular responses in vitro to defined malaria antigens and, amongst children with evidence of exposure to hepatitis B infection, between aflatoxin and carriage of the hepatitis B surface antigen (HBsAg), were assessed. Aflatoxin-albumin adduct was found in nearly all serum samples collected during a survey performed at the end of the dry season and levels of adduct were generally high (up to 720 pg aflatoxin-lysine equivalent/mg albumin). Higher levels of aflatoxin-albumin adduct were detected in Wollof children than in children of other ethnic groups and marked variation in mean adduct levels between villages was observed. Aflatoxin-albumin adduct levels were higher in children who were HbsAg positive and in children with Plasmodium falciparum parasitaemia than in controls. However, levels of adduct had no consistent effect on either malaria-specific antibody responses, lymphoproliferative responses in vitro, or morbidity from malaria during the subsequent rainy season. Much lower levels of aflatoxin-albumin adduct were detected in repeat samples obtained at the end of the rainy season. There was poor correlation between dry and rainy season levels of adduct in individual children. We have shown that Gambian children are exposed to high levels of aflatoxin. The seasonal variation of aflatoxin-albumin adduct and marked fluctuation of adduct with time in individual children need to be considered in the future planning of epidemiological studies using this marker of exposure.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Aflatoxin exposure, malaria and hepatitis B infection in rural Gambian children. 144 Aug 26

Biochemical alterations in 152 malaria patients infected with Plasmodium vivax were studied and the effect of parasitaemia on these changes was assessed. The degree of parasitaemia correlated positively with plasma uric acid, total and unconjugated bilirubin. A decrease in the levels of serum total protein, albumin, serum total, free and ester cholesterol was observed in vivax malaria. A follow-up study done on a section of the above patients after administration of chloroquine and primaquine for radical treatment of malaria showed the most of the alterations observed were bought back to normal. However, blood haemoglobin level was not restored to normal even after ten days of commencement of treatment.
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PMID:Biochemical alterations in Plasmodium vivax-infected malarial patients before and after radical treatment. 145 3


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