Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0024530 (malaria)
 44,886 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 65-year-old woman was rehospitalized for increasing mental confusion 16 days after open heart surgery for mitral stenosis. A diagnosis of transfusion-acquired falciparum malaria was made from a routine peripheral blood smear 24 hours after admission. Because progressive encephalopathy developed while she was receiving antimalarial drugs, a therapeutic exchange transfusion was performed. Clinical improvement occurred promptly during the exchange, and the patient went on to complete recovery from her malaria. The putative blood donor involved met the currently accepted standards for blood donors.
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PMID:Transfusion malaria: treatment with exchange transfusion after delayed diagnosis. 703 44

Six cases of severe jaundice and encephalopathy due to falciparum hepatitis initially diagnosed as fulminant hepatic failure are reported. This rare presentation of falciparum malaria should be suspected in patients with persistent fever, jaundice, encephalopathy and hepatomegaly. The diagnosis should be further suspected when the liver function tests show a predominantly conjugated hyperbilirubinemia with only modest elevation of liver enzymes and alkaline phosphatase. Liver biopsy is valuable in establishing the diagnosis at all stages of the disease.
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PMID:Falciparum malaria or fulminant hepatic failure? 811 50

Malaria, the most important of all tropical diseases, causes approximately one million deaths per year. In Plasmodium falciparum malaria, the organs most affected are the brain, kidneys, lungs, and liver. Cerebral involvement is the most important lethal complication with a mortality rate of up to 50%. We report a patient with malignant, tertian falciparum malaria with an initial parasitemia rate of 60% and severe cerebral, hepatorenal, and pulmonary involvement. In addition to the severe diffuse encephalopathy, an initial neurologic examination showed signs of a pontine lesion that was confirmed by cerebral magnetic resonance imaging. We therefore conclude that cerebral malaria may be responsible for focal neurologic lesions that can be demonstrated by this procedure.
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PMID:Isolated pontine lesion in algid cerebral malaria: clinical features, management, and magnetic resonance imaging findings. 833 75

Epidemic emergencies have shown increasing trend in India and most parts of the country appear to be vulnerable to these emergencies. In this paper we present a profile of epidemic emergencies attended by the National Institute of Communicable Diseases in the last five years, to delineate aspects that will promote better preparedness and management. Water borne and water related disease epidemics constituted more than 70% of the epidemic emergencies in India. Non 01 cholera epidemics constituted one fourth of total cholera epidemics during 1991-95. Most of the hepatitis outbreaks were attributed to Non A Non B. The source of infection in majority of the cholera and jaundice epidemics was contaminated water. Dengue and resistant typhoid fever were among other emergencies reported during last five years. Some of these epidemic were reported to local health authorities as mysterious diseases due to lack of public health laboratory facilities. Encephalitis and encephalitis like epidemics in the form of Liquor poisoning and chronic Heat syndrome encephalopathy were also observed. The re-emerging disease epidemics like plague in Beed, Pneumonic plague in Surat and malaria in Rajasthan were also investigated during 1994. These observations indicate the weakness in the epidemiological and laboratory surveillance besides inadequacy in water management practices and other socio environmental reasons.
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PMID:Profile of epidemic emergencies in India during 1991-95. 881 Jan 49

Data were prospectively collected on 306 Kenyan children, including blood gases in 258 (75%). Severe malaria caused a predominantly high-anion-gap metabolic acidosis in at least 43% of children. Children with coma and respiratory distress (CM + RD) had greater evidence of renal dysfunction, lower mean pH and higher mean plasma osmolality than those with respiratory distress (RD) or coma (CM) as isolated findings (mean urea 10.7 vs. 6.0 vs. 4.3 mmol/l; mean creatinine 97 vs. 74 vs. 58 mumol/l; mean osmolality 301 vs. 288 vs. 283 mosmol/l; and mean pH 7.16 vs. 7.29 vs. 7.39, respectively, p < 0.001 for each comparison of CM + RD vs. RD or CM). In addition, children with CM + RD had a higher mean blood lactate (6.7 vs. 3.3 mmol/l, p < 0.001), a lower mean haemoglobin (5.5 vs. 7.0 g/dl, p = 0.002) and a lower mean age (26.4 vs. 41.9 months, p < 0.001) than children with CM and accounted for 15/24 (63%) of all deaths. These and previous data implicate hypovolaemia and renal impairment in the pathogenesis of metabolic acidosis in severe childhood malaria. In children who are acidotic, anaemia is strongly associated with lactic acidaemia and may therefore contribute to its pathogenesis. These data also imply that coma in acidotic children (CM + RD) and those with an isolated encephalopathy (CM) may result from quite different pathophysiological mechanisms.
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PMID:Acidosis in severe childhood malaria. 934 54

BAEPs and SEPs were studied in 25 patients of enteric encephalopathy in acute phase and the results were compared with 25 healthy control persons. In the study the important observations of BAEPs were delayed peak latency of wave III, wave V and delayed ILP I-V, and of SEPs was prolonged peak latency of N20. The electrophysiological evidence suggests metabolic cause for the coma and the SEP changes were similar to those observed in cerebral malaria reported earlier in this laboratory.
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PMID:Brainstem auditory evoked potentials (BAEPs) and somatosensory evoked potentials (SEPs) in enteric encephalopathy (EE). 940 31

Patients infected with the malaria parasite Plasmodium falciparum may develop a diffuse reversible encephalopathy, termed cerebral malaria. It is unclear how the intraerythrocytic parasite, which sequesters in the cerebral microvasculature but does not enter the brain parenchyma, induces this neurological syndrome. Adhesion of parasitized red blood cells in the brain microvasculature is mediated by specific receptors on the host endothelium, including intercellular adhesion molecule (ICAM)-1, CD36 and CD31. Leucocyte binding to cerebral endothelial cells in culture induces intracellular signalling via ICAM-1. The hypothesis that parasitized red blood cells binding to receptors on cerebral endothelial cells causes changes in the integrity of the blood-brain barrier was tested. Immunohistochemistry was used to examine the blood-brain barrier in human cerebral malaria, with antibodies to macrophage and endothelial activation markers, intercellular junction proteins, and plasma proteins. The distribution of the cell junction proteins occludin, vinculin and ZO-1 were altered in cerebral malaria cases compared to controls. While fibrinogen was the only plasma protein detected in the perivascular space, there was widespread perivascular macrophage activation, suggesting that these cells had been exposed to plasma proteins. It was concluded that functional changes to the blood-brain barrier occur in cerebral malaria, possibly as a result of the binding of parasitized red blood cells to cerebral endothelial cells. These changes require further examination in vitro.
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PMID:Evidence of blood-brain barrier dysfunction in human cerebral malaria. 1047 50

Although cerebral malaria is the most common acute encephalopathy arising in children in Africa little is known of its effect upon the longer-term cognitive development of survivors. In Kenya, we compared the performance of 87 survivors of severe malaria with impaired consciousness to matched community controls on a wide range of tasks, not less than 42 months post illness episode. The presence of cognitive impairment was then related to both the pattern of symptoms at the time of the acute illness and the presence of gross neurological impairment on discharge. Significant group differences were found in areas of cognitive functioning suggestive of widespread impairment in the development of the ability to initiate, plan and carry out tasks (the executive functions). On tasks of more discrete cognitive skills (information processing) there were no significant group differences, although impaired performance was found more frequently in the severe malaria group. The odds ratio associated with the development of cognitive impairment following severe malaria with impaired consciousness was found to be 4.48 (95% CI 1.22, 16.47). A combination of 4 signs (coma, hypoglycaemia, seizures, and absence of hyperpyrexia) proved to have greater accuracy than the presence of gross neurological sequelae in predicting cognitive impairment (95% vs 93% specificity, 67% vs 58% sensitivity).
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PMID:Cognitive sequelae of severe malaria with impaired consciousness. 1069 14

Cerebral malaria is one of the commonest causes of an acute neurological syndrome in malaria-endemic areas. However, there are few detailed reports of findings on clinical neurological examination of the condition. The neurological features of cerebral malaria in 103 children aged 5 years or less were studied in Ibadan, Nigeria, an area of high malaria transmission. The correlation of these features with prognosis was also studied. Convulsions occurred in 87% of subjects and were in most cases of a generalized tonic-clinic nature. Abnormalities of posture were observed in 41%, abnormal tone in 70% and abnormal deep tendon reflexes in 74%. Absent corneal reflexes were found in about 14%. The time interval between the last seizure episode and presentation in hospital, abnormal posture (decerebrate or decorticate), absence of corneal reflex and depth and duration of coma were indicators of poor prognosis. In this study, cerebral malaria presented with non-specific features of diffuse, symmetrical, upper motor neurone dysfunction, and some specific neurological features were associated with poor prognosis. It is important that cerebral malaria be considered in any child with features of acute encephalopathy in a malaria-endemic area. Careful clinical examination of such children is essential as neurological features of the condition may provide a clue to prognosis.
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PMID:Neurological features of cerebral malaria in Nigerian children. 1071 24

Cerebral malaria may be the most common non-traumatic encephalopathy in the world. The pathogenesis is heterogeneous and the neurological complications are often part of a multisystem dysfunction. The clinical presentation and pathophysiology differs between adults and children. Recent studies have elucidated the molecular mechanisms of pathogenesis and raised possible interventions. Antimalarial drugs, however, remain the only intervention that unequivocally affects outcome, although increasing resistance to the established antimalarial drugs is of grave concern. Artemisinin derivatives have made an impact on treatment, but other drugs may be required. With appropriate antimalarial drugs, the prognosis of cerebral malaria often depends on the management of other complications-for example, renal failure and acidosis. Neurological sequelae are increasingly recognised, but further research on the pathogenesis of coma and neurological damage is required to develop other ancillary treatments.
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PMID:Cerebral malaria. 1099 May


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