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)

This study was done in the Paediatric in-patient department of Chittagong Medical College Hospital (CMCH), Chittagong, Bangladesh to identify and quantify the prognostic factors associated with increased mortality in severe malaria (SM) cases. All the patients with parasitologically confirmed clinical syndromes of SM, admitted between June 1997 and May 1998, were included. A total of 53 consecutive cases were studied. Cerebral malaria (CM) was the commonest type of SM, observed in 36(68%) cases, second commonest type was severe anaemia 13(25%). More than one type of severe manifestations were present in 23(44%) cases. Overall case fatality rate (CFR) was 17% and it was 30% among those who had multi-organ manifestations. Important poor prognostic clinical variables were Blantrye coma score (BCS) score of 0 and 1 on day 1 (OR = 7.78) and day 2(OR = 40.0), multi-organ manifestations (OR = 6.8) and in-hospital complications (OR = 5.18). Important poor prognostic laboratory variables were day 2 parasite count > 50,000/cmm (OR = 5.5), blood glucose < 2.2 mmol/l (OR = 21.5) and raised CSF protein > 50 mg/dl (OR = 7.0). It can be concluded that certain clinical variables e.g. low BCS on day 1 & 2, multi-organ manifestations, in-hospital complications; and laboratory variables e.g. high parasite count, low blood glucose level, raised CSF protein levels are associated with increased mortality rate in SM cases.
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PMID:Prognostic factors relating to outcome of severe malaria among children in Bangladesh. 1169 95

Hypoglycaemia is an important complication in severe malaria, ascribed to an inhibition of gluconeogenesis. However, the only data available suggested that in severe malaria, total glucose production is increased. We measured glucose production and gluconeogenesis after an overnight fast in all seven patients with cerebral malaria (CM) consecutively admitted to Bao Loc General hospital over a 2-year period, and in six healthy sex- and age-matched controls. Glucose production was measured by infusion of [6,6-(2)H(2)]glucose and the contribution of gluconeogenesis by oral ingestion of (2)H(2)O. Compared to controls, plasma glucose concentration was 42% higher in CM patients (p=0.004), and glucose production was doubled (p=0.003). Gluconeogenesis contributed 100% of the total glucose in CM patients but only 58% in controls (p=0.003). The plasma concentrations of the substrates for gluconeogenesis and the glucoregulatory hormones were not different between patients and controls, except for an increase in lactate and cortisol in the patients. Cerebral malaria is associated with increases rather than decreases in plasma glucose, glucose production and gluconeogenesis, and there is no contribution of glycogenolysis to glucose production. Factors other than malaria per se are involved in the pathogenesis of hypoglycaemia associated with CM.
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PMID:Glucose production and gluconeogenesis in adults with cerebral malaria. 1174 92

Cerebral malaria is a life threatening sequel of Plasmodium falciparum infection and contributes significantly to malaria mortality, especially among children. Accumulation of macrophages and proliferation of microglial cells play key roles in cerebral malaria and are thought to contribute to the pathophysiological alterations observed in these patients, which include enhanced adherence of infected erythrocytes to the cerebral vasculature by expression and secretion of proinflammatory molecules, disruption of the blood-brain barrier, recruitment of other inflammatory cells to the lesion site. In this review, recent advances in the understanding of the involvement of macrophages/microglial cells in the development of cerebral malaria are summarized.
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PMID:Macrophages/microglial cells in patients with cerebral malaria. 1210 Oct 73

Cerebral malaria remains a major cause of childhood morbidity. Quinine is the drug of choice for which resistance is now emerging. A total of 77 children admitted to Khartoum Children Emergency Hospital who conform to WHO criteria of cerebral malaria were randomly allocated to receive either artemether (1.6 mg/kg body wt., repeated after 12 hrs and then daily for four days) or quinine (10 mg/kg body wt in 10 ml/kg body wt of 5% dextrose in 0.9% saline intravenously. Repeated every 8 hrs and changed to oral administration when the child was able to drink to finish seven days). Response to therapy was evaluated using fever clearance time (FCT), time of regaining consciousness (TRC) and parasite clearance time (PCT). The FCT (mean+SD), TRC and PCT for the artemether-treated group were 32 (+13) hrs, 21 (+11) hrs and 36 (+18) hrs, respectively, while for the quinine-treated group the respective figures were 36 (+18), 26 (+15) hrs and 41 (+12) hrs. The response to artemether was slightly better than that of quinine, but the differences between the two groups were not statistically significant. The outcome in terms of cure rate, neurological sequalae and case fatality was also comparable.
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PMID:The efficacy of artemether versus quinine in the treatment of cerebral malaria. 1221 38

Cerebral malaria is the main cause of death in severe Plasmodium falciparum infection and is one of the most important medical emergencies. No conclusive theory exists on the pathogenesis of cerebral malaria, although it has been shown that the level of tumor necrosis factor correlates well with the severity of symptoms. Involvement of the intracerebral capillaries by the malaria parasites interferes with microcirculation in the brain, leading to cerebral anoxia, oedema, and cell death. Cerebral oedema is not, however, consistently found in all cases. The condition is more commonly seen in nonimmune people, children below five years old, and in pregnancy. Nonetheless, any degree of impairment of cerebral functions given infection with P. falciparum warrants clinical consideration of cerebral malaria unless proved otherwise. Basic principles of management should include maintenance of patent airways, care of bowel, bladder, skin; regular blood sugar estimation; intravenous or oral Quinine 10 mg per body weight every eight hours for 5-10 days; intravenous glucose; daily parasite count; exchange transfusion and hemodialysis when indicated. Steroids should never be used.
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PMID:Cerebral malaria -- its management. 1228 4

This study sought to estimate the frequency of ocular complications in malaria and its prognostic value in Mali. A total of 140 children (aged 6 months to 9 years) with severe malaria (105 with cerebral malaria, 35 without neurological complications) were compared with 34 children with mild malaria and 82 children with nonmalarial fever. Ocular lesions were rare in the mild malaria group (5.8%). Retinal hemorrhages occurred in 11.8% of the children in the severe noncerebral malaria group. Cerebral malaria was associated with retinal hemorrhages (22.9%) and retinal edema (10.5%). No association was found between ocular signs such as retinal hemorrhages or retinal edema and mortality. Exudates, papilledema, and the presence of cottonwool spots were associated with an increased risk of death. Coma score and convulsions were significantly associated with death but not with ocular signs. The presence of retinal signs in a child in a malaria-endemic area may signal a case of severe malaria.
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PMID:Ocular lesions associated with malaria in children in Mali. 1236 65

Cerebral malaria is a major killer in the developing world, but we still know very little about the causes of this disease. How does Plasmodium falciparum cause such a devastating neurological disease while it is in the brain vasculature? Why do some patients die, whereas others survive? What processes contribute to disease in the brain, and can we reverse them? Here, the latest evidence from post-mortem, in vitro and animal studies is reviewed to highlight the role of blood-brain barrier breakdown in cerebral malaria. Blood-brain barrier integrity is disturbed during severe malaria, causing leakage of cerebral vessels. Understanding how this happens and how it contributes to the pathogenesis of coma may provide new opportunities for the treatment of cerebral malaria.
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PMID:Breaking down the blood-brain barrier: signaling a path to cerebral malaria? 1237 86

Cerebral malaria is one of the most common nontraumatic encephalopathies in the world. Children living in sub-Saharan Africa bear the brunt of the disease, but cerebral malaria is being seen increasingly in adults throughout the world, including outside malarious areas. There are differences in the clinical presentation and pathophysiology between African children and nonimmune adults from any region. Mortality is high (10-20%). Parenteral antimalarials are the only interventions that have been shown to affect outcome. The cinchona alkaloids (quinine and quinidine) are the mainstay of antimalarial treatment, but the artemisinin derivatives are increasingly being used. Aggressive treatment and prevention of convulsions may be important, particularly in children. Other ancillary treatments that can be used to augment standard antimalarial drugs, such as exchange blood transfusions, osmotic diuretics and pentoxifylline, may improve outcome but have not been subjected to rigorous clinical trials. There is little support for corticosteroids or deferoxamine (desferrioxamine) in cerebral malaria. Other adjuncts have not been adequately tested. Further research is required on drugs that interfere with the pathophysiological processes to prevent neurological complications and death.
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PMID:Cerebral malaria: optimising management. 1261 95

Cerebral malaria (CM), one of the most serious complications of Plasmodium falciparum infection, is characterized by the sequestration of infected erythrocytes (IEs) in cerebral microvascular beds. The precise mechanisms involved in the onset of neuropathology remain unknown, but parasite sequestration in the brain, metabolic disturbances, and host immune responses all play a role. Studies in a murine model of CM showed a potential role for host cells, especially platelets, in the pathogenesis of CM. Indeed, urokinase plasminogen activator receptor (uPAR; CD87) deficiency attenuates the severity of CM, most likely by its important role in platelet kinetics and trapping. These results led us to evaluate whether platelets have a role in the human disease. By immunostaining of brain samples from Malawian patients, we determined that the surface of platelet accumulation and the proportion of vessels filled with platelets were significantly higher in patients who died of CM than in those who died of other causes. We then investigated the role of platelets in IE cytoadhesion in vitro, using CD36-binding IE (IECD36) and CD36-deficient (CD36DEF) brain microvascular endothelial cells (ECs). Coincubation studies indicated that platelets can induce strong IECD36 binding to CD36DEF ECs and, conversely, can hide constitutively expressed falciparum receptors such as chondroitin sulfate A. Thus, platelets may provide an adhesion receptor to microvascular beds originally devoid of it. This novel mechanism of cytoadhesion may reorient the sequestration of different parasite phenotypes and play an important role in the pathogenesis of severe malaria.
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PMID:Pathophysiology of cerebral malaria: role of host cells in the modulation of cytoadhesion. 1279 44

Of 1857 Plasmodium falciparum malaria patients hospitalized from 1995 to 1998, 608 had severe malaria and 83 died. Acute renal failure, jaundice and respiratory distress were common in adults whereas children frequently had severe anaemia. Cerebral malaria occurred equally in adults and children but recovery from coma was quicker in children. Multiple complications caused high mortality in adults.
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PMID:Complications and mortality patterns due to Plasmodium falciparum malaria in hospitalized adults and children, Rourkela, Orissa, India. 1288 8


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