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

One hundred and ninety-two male malaria patients admitted to two different hospitals within 1 year, were studied. There were 74 malaria cases with glucose-6-phosphate dehydrogenase (G-6-PD) deficiency and 118 G-6-PD normal malaria cases, randomly selected as a control group. History of dark urine, and the presence of jaundice, haematocrit, total bilirubin and parasite count on day of admission were not significantly different comparing both groups. The number of observed complications did not differ either. Distinctions were detected in abnormal symptoms and in some laboratory parameters in patients with Plasmodium falciparum infection. G-6-PD deficient patients had significantly less gastrointestinal disturbances (P = 0.006), higher serum glutamic oxalacetic transaminase (P = 0.009) and significantly lower blood urea nitrogen (P = 0.007) when compared with the control group. These findings indicate that G-6-PD deficiency when the variants are aggregated, in male adult patients has no significant influence on the clinical presentation of malaria.
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PMID:Glucose-6-phosphate dehydrogenase deficiency in Thailand: the influence on the clinical presentation of malaria in male adult patients. 329 88

31 pairs of patients with complicated falciparum malaria (with anaemia, jaundice, raised blood urea, hyperpyrexia or more than 2% of erythrocytes parasitized) were treated with artemether or quinine. All patients in the artemether group survived but 2 of those treated with quinine died. Fever clearance time and parasite clearance time of patients treated with artemether were significantly shorter than in the quinine-treated group. One patient who failed to respond to quinine within 72 h was saved with artemether. Follow-up of the patients showed that 9 of 23 (39.1%) recrudesced on day 28 in the artemether group. In the quinine group the recrudescence rate was 9% (2 of 22). Hence artemether may be considered as one of the drugs of choice for severely ill patients; it may even be better than quinine.
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PMID:A controlled clinical trial of artemether (qinghaosu derivative) versus quinine in complicated and severe falciparum malaria. 332 42

The prevalence and pathogenesis of renal involvement was investigated in 74 patients with malarial infections. A rise in proteinuria of 150 to 5,000 mg per day was seen in 12 out of 27 patients with Plasmodium falciparum infections. SDS-polyacrylamide gel electrophoresis revealed either an increase in albumin and high molecular weight proteins alone or an increase in low and high molecular weight proteins. Serum creatinine and urea were increased in 5 patients. In P. vivax infections, 8 out of 46 patients developed a proteinuria level of up to 462 mg per day. Low and, to a lesser degree, high molecular weight proteins were increased. In one patient with quartan malaria infection, proteinuria rose as far as 432 mg per day. There was a correlation between the appearance of proteinuria and fever; however, there was no correlation between the amount of proteinuria and the height of fever. It is therefore unlikely that a rise in temperature is the only cause of proteinuria in malarial infections. The electrophoretic analyses of proteinuria indicate that in malarial infections, glomerular as well as tubular lesions may cause reversible proteinuria.
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PMID:Origin of proteinuria in human malaria. 389 Jan 20

A study of 125 children aged 0-6 months who were seen at Kenyatta National Hospital for acute diarrhea was conducted between 1982-1983 to determine the benefits of oral rehydration therapy (ORT) in treatment of diarrheal illness. At admission, specimens of stool, blood and urine were collected and examine for bacterial, parasitic, and viral agents (including malaria), serum electrolytes, urea, white cell counts and hematocrit. Children were started on oral rehydration solution (ORS) unless severly dehydrated, in which case intravenous therapy was initiated. 84% of the children were successfully treated with ORS alone regardless of etiological agent found; 15% required IV therapy initially, then were placed on ORS. Average hospital stay was 56.2 hours. Cost of treatment by ORT is less than 20% the cost of IV therapy. When investigators surveyed other health institutions, they found that ORT was used alone in less than 10% of all children seen with diarrhea. A side benefit of ORT is the utilization of mothers in preparation and administration of solution, reducing the demand on hospital staff. Since 20% of all pediatric admissions at Kenyatta are due to acute diarrheal disease, use of ORT would reduce costs tremendously. Initiation of ORT at home may prevent development of dehydration altogether.
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PMID:Management of acute childhood diarrhoea with oral rehydration therapy at Kenyatta National Hospital, Nairobi, Kenya. 400 16

Of 140 patients with malignant tertian malaria seen during 1956 to 1967 10 died. Death was caused by cerebral malaria in all cases. Since 1968 more intensified treatment has resulted in the complete recovery of three patients and the partial recovery of one, all of whom had been in a cerebral malaria coma for various periods of time before admission and in whom a fatal outcome was expected. In these cases a polypragmatic therapeutic approach using intravenous low molecular weight dextran, besides the usual quinine and fluids, corticosteroids, heparin and urea, separately or combined, was adopted.
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PMID:New concepts in treatment of malignant tertian malaria with cerebral involvement. 555 Dec 49

The disposal of immune complexes by the glomerulus and the participation of infiltrating monocytes were studied in acute malaria-associated glomerulonephritis. Young Sprague-Dawley rats were infected with Plasmodium berghei. Parasitemia reached a maximum after 8 to 12 days, ending by day 20. In all infected rats, renal immunofluorescence microscopy showed in all glomeruli granular deposition of rat IgG, IgM, and C3 in a mesangial distribution. The staining was strongest from days 8 to 12, then diminished and disappeared after day 32. By contrast, electron-dense deposits were rarely seen before day 16 when they became detectable in the mesangial matrix, particularly along the inner aspect of the glomerular basement membrane. They were most conspicuous on days 20 and 34 and disappeared by day 100. Few monocytes were detected in the glomeruli by electron microscopy and by histochemistry for nonspecific esterase. Highest counts of esterase-positive monocytes were found on day 10 (means 2.9 per glomerulus, range 0 to 5; normal control range 0 to 1). Total glomerular cell counts were transiently elevated on days 10 and 20. Renal functional damage of malarial rats was mild as reflected by a transient increase of urinary protein excretion, whereas serum urea values remained in the normal range. The results suggest that elimination of glomerular immune deposits in acute malarial glomerulonephritis of rats involves their gradual condensation and degradation in the mesangium which reduces detection by immunofluorescence while leading to formation of transient electron-dense deposits. In this model, the efficient disposal of glomerular immune deposits by the mesangium appears to minimize the infiltration of monocytes and to prevent aggravation of the glomerular injury.
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PMID:Mesangial disposal of glomerular immune deposits in acute malarial glomerulonephritis of rats. 703 93

We report two patients who had cerebral malaria, heavy parasitemia, hyperbilirubinemia, hypercatabolism with rapid rises of blood urea and serum creatinine and acute renal failure. There was no evidence of intravascular hemolysis. Renal biopsy was consistent with acute tubular necrosis. Both patients responded to treatment with intravenous quinine and dialysis.
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PMID:Acute renal failure in falciparum malaria. 767 79

Plasma from immune (residents of malaria infested areas) and non immune (European travellers) patients suffering from cerebral malaria, severe or mild, was analyzed for the presence of soluble tumor necrosis factor receptors. On admission of the subjects, sTNF-R55 and sTNF-R75 levels were significantly elevated in all groups and correlated with TNF-alpha. Except for sTNF-R55 whose levels were higher in severe than in mild malaria, no correlation was observed between soluble receptors and clinical status. Nevertheless, sTNF-R55 and sTNF-R75 were significantly more elevated in patients who died (10.7 +/- 2.3 ng/ml and 94.9 +/- 31 ng/ml, respectively) than in those surviving (5.5 +/- 0.4 ng/ml and 37.4 +/- 5.4 ng/ml respectively). A marked correlation was observed between soluble receptors levels and some biological markers of gravity like creatinine, urea, and bilirubin. In 13 non immune patients, circulating soluble receptors levels decreased significantly after 7 days when clinical and biological malaria features had disappeared, but TNFsR75 remained above normal levels. After a fortnight of treatment in 17 immune patients, sTNF-R55 and sTNF-R75 remained elevated. However, the ratios of TNF-alpha/s TNF-R55 and 75 were not higher in the cases of cerebral malaria or fatal outcome. Further studies are required to determine if elevated levels of sTNF-R55 and sTNF-R75 are beneficial, due to the inhibition of TNF-alpha or whether they are detrimental since they stabilize this deleterious cytokine.
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PMID:Plasma levels of TNF-alpha soluble receptors correlate with outcome in human falciparum malaria. 794 68

The study evaluated six Plasmodium falciparum antigen extracts to be used in the IgG and IgM enzyme-linked immunosorbent assays (ELISA), for malaria diagnosis and epidemiological studies. Results obtained with eighteen positive and nine negative control sera indicated that there were statistically significant differences among these antigen extracts (Multifactor ANOVA, p < 0.0001). Urea, sodium deoxycholate and Zwittergent antigen extracts performed better than did the three others, their features being very similar for the detection of IgG antibodies. Urea, alkaline and sodium deoxycholate antigen extracts proved to be better than the others for the detection of IgM antibodies. A straight line relationship was found between the optical densities (or their respective log10) and the log10 of antibody dilutions, with a very constant slope. Thus serum titers could be determined by direct titration and by two different equations, needing only one serum dilution. For IgM antibody detections, log10 expression gave results that better correlated with direct titration (95% Bonferroni). For IgG antibody detections, the titer differences were not significant. The reproducibility of antibody titers and antigen batches was also evaluated, giving satisfactory results.
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PMID:Malaria serology: performance of six Plasmodium falciparum antigen extracts and of three ways of determining serum titers in IgG and IgM-ELISA. 799 52

Intraerythrocytic malaria parasites degrade hemoglobin as a principal source of amino acids for parasite protein synthesis. We have previously identified a Plasmodium falciparum trophozoite cysteine proteinase as a putative hemoglobinase and shown that specific inhibitors of this proteinase block the hydrolysis of globin and the development of cultured parasites. We now show that the murine malaria parasite Plasmodium vinckei has an analogous cysteine proteinase with similar biochemical properties to the P. falciparum proteinase, including an acid pH optimum, a preference for the peptide proteolytic substrate benzyloxycarbonyl (Z)-Phe-Arg-7-amino-4-methylcoumarin, and nonomolar inhibition by seven peptide fluoromethyl ketone proteinase inhibitors. Thus, P. vinckei offers a model system for the in vivo testing of the antimalarial properties of cysteine proteinase inhibitors. One of the proteinase inhibitors studied, morpholine urea (Mu)-Phe-Homophenylalanine (HPhe)-CH2F strongly inhibited the P. vinckei cysteine proteinase in vitro and rapidly blocked parasite cysteine proteinase activity in vivo. When administered four times a day for 4 d to P. vinckei-infected mice, Mu-Phe-HPhe-CH2F elicited long-term cures in 80% of the treated animals. These results show that peptide proteinase inhibitors can be effective antimalarial compounds in vivo and suggest that the P. falciparum cysteine proteinase is a promising target for chemotherapy.
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PMID:Inhibition of a Plasmodium vinckei cysteine proteinase cures murine malaria. 845 35


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