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

Changes in plasma glucose and insulin concentrations were monitored over 24 hours in 28 African patients receiving quinine intravenously in an average dose of 8.5 mg base/kg over one hour eight hourly for severe malaria. The patients (nine children and 19 adults) were moderately undernourished; none was pregnant or had renal insufficiency. Plasma insulin concentrations rose during the infusion and then declined. Plasma glucose concentrations were decreased at two, three, and four hours after the start of the infusion. Insulin: glucose ratios were raised between half an hour and two hours after the start of the infusion. The three infusions of quinine increased plasma insulin concentrations in a similar way. In nine patients, including four children, plasma glucose concentrations fell below 2.8 mmol/l on one or two occasions. At the time of the hypoglycaemia plasma insulin concentrations were inappropriately high as shown by a consistent and often considerable increase in the insulin:glucose ratio. Hypoglycaemia that may pass unnoticed in comatose patients is thus a common complication of treating severe malaria with quinine, in particular in children. Its high incidence calls for attentive monitoring and preventive measures.
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PMID:High incidence of hypoglycaemia in African patients treated with intravenous quinine for severe malaria. 311 15

Severe falciparum malaria complicated by acute renal failure resulted in very high mortality. Ten patients with acute renal failure from falciparum malaria (infected rbc up to 80%) were continuously dialysed using Tenckhoff peritoneal catheter. Five were oliguric and BUN was maintained between 60 to 80 mg/dl (21.4 to 28.6 mmol/l) by hourly 1 to 1.5 liter dialysate exchange during the acute phase. The peritoneal urea clearance (mean +/- SD) was 12.1 +/- 1.2 ml/min with urea nitrogen removal of 13.4 +/- 2.3 g/day. In nonoliguric cases dialysis was also needed for additional removal of waste products since the remaining renal function could not cope with the hypercatabolic state. Peritoneal glucose absorption (135 to 565 g/day) gave considerable caloric supply without volume load and also contributed to the prevention of hypoglycemia. Varying degree of acute respiratory failure developed in all patients with 5 cases (2 oliguric and 3 nonoliguric) progressing to pulmonary edema. Swan-Ganz catheterization and hemodynamic study suggested the role of increased capillary permeability and volume overload from endogenous water formation in the development of pulmonary complication. Continuous removal of fluid and waste products minimized these problems and may prevent the progression of respiratory failure. One patient died of severe sepsis and the other nine survived. This study showed the beneficial contribution of continuous peritoneal dialysis in the management of acute renal failure from severe falciparum malaria.
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PMID:Continuous peritoneal dialysis in acute renal failure from severe falciparum malaria. 312 24

We reviewed the charts of 24 patients with malaria seen at the Queens Hospital Center, Jamaica, NY, over the past five years. Twenty-three patients were foreign citizens. Eighteen patients were infected with Plasmodium vivax and six with Plasmodium falciparum. Malaria was suspected on admission in 19 of the 23 hospitalized patients. Five patients were admitted with unrelated diagnoses, and four of these experienced diagnostic delay. All diagnoses were confirmed with thin blood smears. Twenty-one patients were febrile, and 18 patients had prominent gastrointestinal tract symptoms. Serum glucose level was increased in nine patients, and hypoglycemia occurred in one. Four patients also had intestinal parasites. Malaria should be suspected in travelers with gastrointestinal tract symptoms, and patients with malaria may have other parasitic infections. Most patients with P vivax infections can be treated as outpatients, since the course is usually uncomplicated.
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PMID:Malaria. A city hospital experience. 328 21

A patient with severe hypoglycaemia complicating cerebral malaria is reported. No other recognized cause of hypoglycaemia was detected during life or at autopsy. This case adds to the existing evidence that, through several possible mechanisms, cerebral malaria can give rise to life-threatening hypoglycaemia.
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PMID:Hypoglycaemia and cerebral malaria. 353 85

The authors have earlier proposed that tumor necrosis factor (TNF) might contribute to the pathology of malaria. Here they report the outcome of injecting recombinant human TNF/cachectin into normal mice and others with low parasitemias (6-35%) of Plasmodium vinckei. The object was to see how precisely the pathologic features of the terminal stages of this infection could be produced, when parasitemias are 70-80%. Hypoglycemia, mid-zonal liver damage, and pulmonary accumulation of neutrophils in the pulmonary vasculature, all of which are seen in severe P vinckei infection, occurred within 4-12 hours after the mildly infected mice received TNF/cachectin. Uninfected mice were much less susceptible. TNF/cachectin also increases plasma lactate, a change seen in both the human and rodent diseases. From these findings and the recent literature on TNF/cachectin, including its detection in serum from malarial patients, it seems likely that excessive release of this monokine could account for certain of the unexplained pathologic features of human malaria.
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PMID:Possible roles of tumor necrosis factor in the pathology of malaria. 366 78

We studied the occurrence, clinical manifestations, and mechanism of hypoglycemia in patients with falciparum malaria in eastern Thailand. Hypoglycemia, which was often severe and recurrent, occurred in 17 patients, including 12 in a series of 151 patients with cerebral malaria. Thirty episodes were investigated. Plasma concentrations of insulin and C peptide were inappropriately high, and lactate and alanine concentrations were significantly higher than in patients with falciparum malaria who were normoglycemic (P less than 0.05). Sixteen patients had received quinine; plasma quinine and insulin concentrations were correlated at the time of hypoglycemia (P = 0.007). In seven healthy fasting volunteers intravenous quinine increased the mean plasma insulin concentration (+/- S.D.) from 8.9 +/- 3.1 to 17.1 +/- 8.4 mU per liter (P = 0.02) and reduced the mean plasma glucose concentration from 88 +/- 20 to 68 +/- 23 mg per deciliter (P = 0.002). Our observations indicate that in falciparum malaria quinine-induced insulin secretion may precipitate hypoglycemia, but other factors, including the large glucose requirements of the malaria parasites may also contribute. This important complication, associated with pregnancy and severe disease, must be excluded in all patients with falciparum malaria who have impaired or deteriorating consciousness.
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PMID:Severe hypoglycemia and hyperinsulinemia in falciparum malaria. 634 77

Measures of malaria control have proved inadequate in many parts of the tropics. The recent rise in the incidence of malaria has been associated with the spread of drug-resistant strains of Plasmodium falciparum. Chloroquine therapy is now ineffective in many parts of Asia and South America, and resistance to this drug is emerging in Africa. There are few alternative drugs available. Quinine remains effective against P. falciparum in Southeast Asia. Reappraisal of quinine therapy has led to important modifications in dosage recommendations and recognition of a major complication of severe malaria associated with its use--hypoglycaemia. Severe malaria has been neglected as a subject for clinical investigation, and there is little information available on which to base rational treatment. Most of the drugs used in addition to antimalarial agents for cerebral malaria have not been critically tested, except dexamethasone which has been shown to be harmful. Simple, but difficult to organize, intensive nursing of patients with cerebral malaria will improve the prognosis. However, even in the best hands, the mortality rate never falls below 20%.
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PMID:Management of Plasmodium falciparum malaria. 648 99

A total of 1783 patients were admitted in Govt. Medical College Hospital, Jabalpur with fever in 1993. Out of these 152 (8.5%) patients had cerebral malaria, of which 39 (25.6%) patients died. Age and sex-wise break-up indicated that males suffered more (p < 0.01) from malaria and majority of patients belonged to 16-40 yrs age-group. Mortality was significantly higher in patients with hyperparasitaemia, hypoglycaemia and delayed diagnosis and treatment. Comatose condition was the main determinant of death.
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PMID:Cerebral malaria in Jabalpur, India. 758 31

The presenting features of 195 children with cerebral malaria were analysed to determine which correlated with severity of coma and anaemia. The children, who came from a single community in southern Zambia, were enrolled in an ongoing blinded drug trial in 1992 and 1993. Children with deep coma (scoring 0-2) had significantly longer duration of coma before presentation (P = 0.019) and were more likely to have been treated with chloroquine (P = 0.022) than children with light coma (scoring 3 or 4 on the Blantyre coma scale). Children with severe anaemia (haematocrit < 18%) were younger (P = 0.005), had been febrile longer (P = 0.005), had splenomegaly (P < 0.005) and hypoglycaemia (P < 0.008) more often and were more likely to have been treated with chloroquine (P < 0.005) than those without severe anaemia. The counts of asexual parasites in the peripheral blood were not significantly correlated with depth of coma or severity of anaemia. The observed widespread and uncontrolled use of chloroquine has probably led to the development of resistant malaria and of many severe complications despite early consultation. While early treatment of febrile illnesses in young children and immediate medical attention for altered consciousness must be emphasized in the community approach to severe malaria, our data indicate that effective public health measures will be difficult to develop in the face of a high prevalence of chloroquine resistance.
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PMID:Predictors of severity of illness on presentation in children with cerebral malaria. 766 13

In this review the old concept of severe malaria as a toxic disease is re-examined in the light of recent discoveries in the field of cytokines. Animal studies suggest that the induction of TNF by parasite-derived molecules may be partly responsible for cerebral malaria and anemia, while hypoglycaemia may be due to direct effects of similar molecules on glucose metabolism. These molecules appear to be phospholipids and we suggest that when fully characterized they might form the basis of antitoxic therapy for malaria.
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PMID:Malaria: toxins, cytokines and disease. 767 8


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