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

Transcobalamin II (TCII) levels have been reported to be elevated in patients with many clinical conditions including proliferative reticuloendothelial system. As reactive macrophage hyperplasia frequently occurs in patients with malaria, the objective of the present study was to determine TCII in patients with Plasmodium falciparum with cerebral symptoms. The studies were performed on 14 cerebral malaria patients as well as 60 normal subjects. The mean values of serum vitamin B12 and TCII levels were significantly higher in the patient group and 6 and 7 patients had serum vitamin B12 and TCII levels higher than the normal values. There was direct relationship between serum TCII levels and BUN or creatinine levels. These findings indicated that raised serum TCII level occurred only in patients with renal insufficiency. A decreased glomerular fiLtration rate reduced the amount of vitamin B12 and TCII-B12 that filtered through the glomeruli resulting in the reduced proximal tubular cells uptake and its degradation of TCII. This reduced lysosomal enzyme activity, therefore, prolongs the intravascular TCII survival and increased secretion of TCII into the circulation. Therefore, serum TCII levels were elevated in these cerebral malaria patients.
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PMID:Abnormally elevated serum transcobalamin II levels in patients with cerebral malaria. 775 77

In a retrospective study we analyzed the clinical and blood chemical data of 12 patients with severe tropical malaria in the intensive care units of the University Hospital Zurich and the Stadtspital Triemli, Zurich, between 1991 and 1994. None of the 12 patients had been exposed to malaria before or had taken drugs for chemoprophylaxis. 7 patients survived, 5 died from complications of malaria. According to the criteria of severe tropical malaria defined by the WHO, the following pathological clinical and blood chemical parameters were noted on admission: cerebral coma (2/12); blood hemoglobin < 5 g/dl (0/12), < 8 g/dl (2/12); serum creatinine > 265 mumol/l (3/12); blood glucose < 2.2 mmol/l (0.12); circulatory collapse/shock (0/12); bleeding/signs of disseminated intravascular coagulation in laboratory tests (4/12); acidosis with pH < 7.25 (1/12). Further signs of severe tropical malaria were: hyperparasitemia > 5% (9/12); qualitative and quantitative disturbances of consciousness (6/12); thrombocytopenia < 30 x 10(9)/l (9/12); hyponatremia 125-135 mmol/l (9/12), < 125 mmol/l (2/12); rhabdomyolysis with creatine kinase > 1000 U/l (4/12). The basic treatment consisted of parenteral quinine hydrochloride in all patients; doxycycline was added in 8 cases, clindamycin in 3. Adjuvant therapy with desferrioxamin was given in 3 cases. 6 patients had exchange transfusions. Parasitemia cleared in all patients within 5 to 6 days. Later in the course, 5 patients developed acute respiratory distress syndrome, 6 required hemofiltration due to oliguria, and one became comatose.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Intensive care aspects in severe tropical malaria: clinical aspects, therapy and prognostic factors]. 777 Jul 59

The relation between the immune response and the clinical features of severe falciparum malaria was studied in Burundian adults with (n = 31) and without (n = 17) cerebral involvement. At the time of admission, mean values for age, temperature, and blood levels of hemoglobin, creatinine, bilirubin, and glucose were similar in the two groups. Plasma levels of tumor necrosis factor alpha, interferon gamma, interleukin 10 (IL-10), and soluble intercellular adhesion molecule 1 were similarly elevated in the two groups. Mean parasite counts and mean plasma levels of soluble E-selectin were higher in severe noncerebral malaria than in cerebral malaria and were correlated with each other. After adjustment for parasitemia, levels of soluble E-selectin remained higher in noncerebral malaria. All seven patients who died had cerebral disease. These patients had higher levels of creatinine, bilirubin, IL-10, and soluble E-selectin than did patients with nonfatal cerebral malaria. After adjustment for creatinine and bilirubin levels, IL-10 and soluble E-selectin concentrations were similar in fatal and nonfatal cases of cerebral infection. In these African adults, none of the immunologic variables investigated was specific to cerebral malaria or to a fatal outcome.
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PMID:Immunologic and biochemical alterations in severe falciparum malaria: relation to neurological symptoms and outcome. 781 67

The association between Schistosoma mansoni infection and kidney lesions was investigated in school children selected from three primary schools in Machakos District, Kenya, namely Miu (n = 159), Kitengei (n = 160) and Misuuni (n = 99) schools. The children were examined parasitologically for S. mansoni infection, clinically for enlargement of the liver and spleen, and biochemically for proteinuria and serum and urine creatinine. High prevalences of S. mansoni infection, ranging from 84-96%, were seen in all the schools, but the geometric mean intensity of egg excretion varied, being relatively low in Misuuni (31 eggs/g), medium in Miu (182 eggs/g) and high in Kitengei (413 eggs/g). The prevalence of pathological proteinuria (> or = 200 mg/l) in the schools ranged from 10.1% in Miu to 28.8% in Kitengei. No difference in the levels of proteinuria was noted between age or sex groups. No association between intensity of infection and pathological proteinuria was observed in any of the schools, nor was any correlation between organomegaly and proteinuria observed. However, significant correlations between malaria and organomegaly (p < 0.001) and between malaria and proteinuria (p < 0.05) were observed when pooling data from all schools. These findings suggest that S. mansoni induced nephrotic syndromes are not common in children from this highly endemic area of Kenya.
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PMID:A survey of Schistosoma mansoni induced kidney disease in children in an endemic area of Machakos District, Kenya. 786 51

1. To assess the association between vitamin A, vitamin E and the clinical course of severe malaria, serial morning blood samples were taken from 24 Vietnamese patients, aged 18-62 years, receiving intensive treatment for complicated Plasmodium falciparum infections. A single fasting blood sample was also taken from 10 control subjects aged 22-45 years. Serum retinol, carotene and vitamin E concentrations were measured by h.p.l.c. 2. Admission serum retinol concentration was depressed relative to that of the control subjects (0.69 +/- 0.35 versus 1.86 +/- 0.41 mumol/l mean +/- SD, P < 0.001) and correlated inversely with indices of hepatic function, but positively with the simultaneous serum creatinine concentration (P < 0.05). During the first week of treatment, serum retinol concentration increased in parallel with improving liver function, whereas serum creatinine concentration remained elevated in the majority of patients. Serum alpha- and beta-carotene concentrations remained depressed throughout. 3. Serum vitamin E concentration, corrected for total serum cholesterol concentration in the form of a ratio, was also depressed at presentation (3.1 +/- 1.8 x 10(3) versus 4.2 +/- 0.8 x 10(3) in control subjects; P < 0.05), but tended to be higher than the control value at the time of discharge (0.1 > P > 0.05); there was a significant correlation between admission ratio and parasite clearance time (P = 0.04). 4. On the basis of this and previous studies, vitamin A replacement could be considered in selected severely ill patients without renal impairment. As found previously in animal models, depressed vitamin E levels may have a beneficial effect on the course of malarial infection.
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PMID:Serum vitamin A and E concentrations in acute falciparum malaria: modulators or markers of severity? 787 37

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

This article reports the findings of a study conducted to identify the relationship between HIV infection and cerebral malaria in Burundi. Study subjects were selected from hospital patients diagnosed with cerebral malaria. The Glasgow scale was used for unconscious patients as a measurement for admission into this study. Parasite density was determined with Giemsa-stained thick blood smears. HIV-1 testing was done by enzyme-linked immunosorbent assay (ELISA) techniques and positives were confirmed by Western blot. All patients received 10 mg of quinine per kg of body weight as an initial dose by intravenous infusion. This regimen was followed by a daily dose of 25 mg/kg body weight via intravenous infusion. If after 2 days the patient could take treatment orally, it was switched. This treatment regimen lasted 5-7 days total. Statistical analysis was performed using the Mann-Whitney U test, the Fisher exact test, and the Chi-square test. Of the 31 study patients, 22 were male and 9 were female. 7 (22.6%) died within the first 96 hours. The surviving 24 patients had a mean coma recovery time of 33.7 +or- 25.8 hours. No neurological damage was noted. The mean Glasgow score was 8.3 +or- 2.7 for the whole group of 31 patients. The mean malaria parasitemia was 11,920 (95% CI: 643-221,018) parasites/mcl of blood. Plasma levels of creatinine were higher in fatal cases than in patients who survived (307.2 +or- 261.8 mcmol/L vs. 135.1 +or- 55.3 mcmol/L). Of the 31 patients, 12 (38.7%) had antibodies to HIV-1. No relationship between positive HIV-1 and cerebral malaria was found, and no patient showed any clinical symptoms of acquired immunodeficiency syndrome.
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PMID:Prognostic indicators in adult cerebral malaria: a study in Burundi, an area of high prevalence of HIV infection. 802 53

Overhydration can contribute to fatal complications of falciparum malaria, even though renal function may be normal. In this context, the role of inappropriate secretion of antidiuretic hormone (ADH) has been controversial. Therefore, we have analyzed ADH serum concentrations together with serum osmolality and sodium levels in serum and urine of 17 consecutively studied patients with severe falciparum malaria. Serum sodium levels were low in 13 of 17 patients upon admission and returned to normal levels during antiparasitic therapy. Urine sodium levels were low in seven of 13 patients before treatment and increased during therapy. Urine sodium concentrations were high, however, in the remaining six patients. Serum osmolality was lower in these six patients than in the other seven hyponatremic patients (P < 0.002). In relation to serum osmolality, ADH levels were inappropriately high in these six patients, which confirms the presence of inappropriate secretion of ADH. Serum creatinine levels were not higher in these six patients than in those without inappropriate secretion of ADH. Inappropriate secretion of ADH seemed to be a major cause of hyponatremia, since other factors that could lead to this condition were not found in these six patients. In conclusion, we have shown, that human falciparum malaria can be associated with inappropriate secretion of ADH.
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PMID:Inappropriate secretion of antidiuretic hormone and hyponatremia in severe falciparum malaria. 820 10

Serum transcobalamin II (TCII) levels were determined in 56 patients with P. falciparum malaria infection. They were divided into 3 groups: severe (malarial parasite > 5% or patients with cerebral malaria or renal insufficiency), moderate (1-5% infection without complications) and mild (1% infection). Elevated serum TCII values were found only in patients with severe malaria infection. These values correlated directly with parasitemia, blood urea nitrogen and creatinine, but were not correlated with alkaline phosphatase. As 17 patients with azotemia had elevated serum TCII levels while other 3 patients with normal BUN and creatinine concentrations had serum TCII levels within the normal limits. These findings indicated that malarial patients with renal insufficiency had increased serum TCII. A possible mechanism is the reduced TCII-B12 that filtered through the glomeruli due to the reduced renal blood flow with the decreased its uptake by proximal tubular cells resulting in the decreased degradation of TCII by the tubular lysosomal enzymes. Determination of serum TCII level may be used as an indicator of renal function in malarial patients with renal insufficiency.
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PMID:Serum transcobalamin II levels in patients with malaria infection. 852 19

A 44-year-old Spanish woman travelled in Kenya without doing correct malarial prophylaxis. Upon her return to Spain, she suffered from Plasmodium falciparum malaria. She was initially treated with chloroquine for three days, but her state worsened and she was admitted to our intensive care unit. On admission, parasitaemia was 22%. She had hyperpyrexia, obtundation, hypotension, tachycardia, tachypnoea, jaundice, digestive haemorrhage, petechiae in her soles, oliguria with elevation of serum uraemia and creatinine, anaemia, thrombocytopaenia, hypoproteinaemia, hyponatraemia, hypocalcaemia, metabolic acidosis and parameters of disseminated intravascular coagulation. She was given quinine, sulfadoxine-pyrimethamine and clindamycin. An exchange transfusion was performed, during which an acute pulmonary oedema appeared, initially with high pulmonary artery wedge pressure. She required mechanical ventilation for 16 days and haemodialysis for 11 days. She remained in coma and had seizures which required diazepam, phenitoin and thiopentone. She received a total amount of 22 units of packed erythrocytes, 55 of platelets and 15 of plasma. After the first week, she had nosocomial infection due to Escherichia coli, Staphylococcus and Pseudomonas aeruginosa and was treated with the corresponding antibiotics. She cured completely. This case report gives us the possibility of discussing on frequent problems in the prevention and treatment of malaria, and on the treatment of severe, life-threatening malaria in the setting of the intensive care unit.
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PMID:[Multiple organ failure in Plasmodium falciparum malaria]. 853 25


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