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

Four of 21 patients with cerebral malaria developed hypoglycaemia, defined as plasma glucose concentration below 40 mg/dl (2.2 mmol/l). Two patients had spontaneous hypoglycaemia at admission and the other two developed it subsequent to quinine therapy. All recovered with continuous intravenous glucose infusion. Spontaneous hypoglycaemia in malaria has not earlier been reported from India.
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PMID:Spontaneous and quinine induced hypoglycaemia in severe falciparum malaria. 266 91

One hundred and ten patients with severe falciparum malaria have been admitted between 1985 and 1987. All had received quinine to the same protocol: 8.3 mg base/kg infused intravenously over 3 hours every eight hours. A systematic glycaemic supervision by capillary glycaemia every eight hours has been employed. Hypoglycaemia occurred in 17 patients (15.5%). Despite an early injection of glucose, recurrent hypoglycaemia was almost constant (16 over 17). The mortality of the group with hypoglycaemia is significantly higher (41% to 25%; 00.5 less than p less than 0.1). We have not found any connection between the risk of hypoglycaemia and elements of gravity of the access. If the part of the patient (age, pregnancy), high parasitemia and impaired hepatic gluconeogenesis have been finding, our results suggest than quinine-induced insulin secretion is the principal mechanism of this hypoglycaemia. Its high incidence and its severity impose preventive measures.
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PMID:[Severe hypoglycemia during a pernicious attack of Plasmodium falciparum malaria treated with quinine (study of 110 cases)]. 268 Jan 32

Cerebrospinal-fluid (CSF) lactate concentrations were elevated in all but 1 of 45 patients with cerebral malaria. They were significantly higher in patients who died (9.0 +/- 5.3 mmol/l, mean +/- SD) than in survivors (3.4 +/- 1.1 mmol/l, p = 0.0002) and had returned to normal values in each of 9 patients studied after recovery of consciousness. There was a significant negative correlation between CSF lactate and CSF glucose. All 11 patients with CSF lactate concentrations above 6 mmol/l died. CSF lactate is thus an important prognostic indicator in cerebral malaria and these findings suggest that hypoxia contributes to the pathogenesis of this disorder.
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PMID:Pathophysiological and prognostic significance of cerebrospinal-fluid lactate in cerebral malaria. 285 65

Hypoglycaemia, defined as a plasma glucose concentration below 2.2 mmol/l, developed in 15 of 47 prospectively studied Gambian children with severe chloroquine-sensitive falciparum malaria. 5 of these hypoglycaemic children died compared with 1 in the normoglycaemic group (p = 0.02). In contrast to previous observations in quinine-treated adults, in whom hypoglycaemia was associated with hyperinsulinaemia, plasma concentrations of insulin were appropriately low and plasma ketones were high. Raised plasma concentrations of lactate and alanine suggested impairment of hepatic gluconeogenesis. In African children, hypoglycaemia is an important and treatable manifestation of severe malaria and is unrelated to antimalarial treatment.
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PMID:Hypoglycaemia in African children with severe malaria. 288 30

1028 (99%) of the 1038 inhabitants of the West African village of Agbave and a random sample of 353 (12.4%) of the population of 2850 in Kati, another West African village, were screened for diabetes. Also recorded were their anthropometric data, dietary habits, possession of antibodies to malaria, and serum IgG concentrations. About 85% of the study population consumed cassava root at least once a day. The mean (SD) capillary random blood glucose concentration was 5.1 (1.1) mmol/l in men and 5.1 (0.6) in women. The mean (SD) body mass index was 20.2 (1.8) in men and 20.7 (2.3) in women. The mean blood glucose was similar whether cassava was consumed once daily, more than once daily, or less than once daily. None of the 1381 subjects examined had diabetes. This finding suggests that a high carbohydrate/cassava intake (84% of a mean daily supply of 1916 calories) combined with a low protein consumption (8% of caloric supply) does not cause diabetes. This does not support the World Health Organisation hypothesis that malnutrition-related diabetes exists, at least not in this West African rural population.
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PMID:Absence of diabetes in a rural West African population with a high carbohydrate/cassava diet. 288 81

The incidence of hypoglycaemia and the role of quinine in its causation was assessed in 46 patients with severe Plasmodium falciparum malaria. Plasma glucose and immunoreactive insulin were estimated before, during and after quinine therapy. In 5 patients the plasma glucose was in the hypoglycaemic range, the lowest value being 0.67 mmol/litre (12 mg/dl) in a pregnant patient. Most of the remaining patients showed a significant fall in plasma glucose (P less than 0.05), but not to the hypoglycaemic range, and an increase in plasma insulin after quinine (P less than 0.01). A good correlation was found between these changes (r = 0.79, P less than 0.01). Patients with severe P. falciparum malaria, particularly those on quinine therapy, should be watched carefully for developing hypoglycaemia.
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PMID:Hypoglycaemia in severe falciparum malaria. 305 51

Life threatening hypoglycaemia has been closely associated with the use of quinine, but the effect of quinidine and the synthetic antimalarials on the homoeostasis of glucose has not been investigated. In volunteers given a fixed dose of 500 mg base and patients with malaria given a quinidine loading dose (15 mg base/kg) mean (SEM) plasma insulin concentrations rose from 6.1 (1.5) mU/l to 10.9 (4.4) mU/l (p less than 0.02) and 10.4 (2.0) mU/l to 18.5 (5.3) mU/l (p less than 0.04), respectively. Plasma glucose concentrations fell from 4.5 (1.1) mmol/l (81 (20) mg/100 ml) to 4.0 (0.3) mmol/l (72 (5) mg/100 ml) in volunteers (p less than 0.04) and from 5.7 (1.3) mmol/l (102 (23) mg/100 ml) to 4.8 (1.6) mmol/l (86 (29) mg/100 ml) in patients (p less than 0.05). One of two patients with cerebral malaria and acute renal failure became profoundly hypoglycaemic (plasma glucose concentration 1.4 mmol/l (25 mg/100 ml), plasma insulin concentration 3.1 mU/l). Hypoglycaemia may occur in any severely ill fasting patient given parenteral quinidine. The other antimalarials tested, chloroquine, amodiaquine, mefloquine, and halofantrine, did not stimulate the release of insulin, an important advantage that should be taken into account when treatment is chosen for Plasmodium falciparum malaria.
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PMID:Hypoglycaemia and antimalarial drugs: quinidine and release of insulin. 308 30

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

BCNU [1,3-bis(2-chloroethyl)-1-nitrosourea] and its less toxic derivative HeCNU [1-(2-chloroethyl)-3-(2-hydroxyethyl)-1-nitrosourea] are clinically-used antitumour drugs. In erythrocytes BCNU is a highly specific inhibitor of the enzyme glutathione reductase [H. Frischer and T. Ahmad, J. Lab. clin. Med. 89, 1080 (1977)]. When treating erythrocytes in vitro, 50% enzyme inhibition was obtained with 1 microM BCNU or 3 microM HeCNU within 2 hr. The two drugs were used for preparing red cell populations with various levels of glutathione reductase activity; complete inhibition (greater than or equal to 98%) was only achieved when the medium contained glucose as a source of reducing equivalents. The erythrocytes were then tested in drug-free media as host cells for the malaria parasite Plasmodium falciparum. In the range of 0-300 mU/ml cells, there was a correlation between glutathione reductase activity and parasite growth; erythrocytes with an activity of less than 20 mU/ml did not serve as host cells for P. falciparum at all although these erythrocytes were viable. When the culture medium was supplemented with 20 mM glutathione (GSH), parasite growth was normal irrespective of the glutathione reductase level in the erythrocytes. This is consistent with the finding that poisoning glutathione reductase led to a 10-fold decrease of the cytosolic GSH level. Our results corroborate the concept that intraerythrocytic inhibition of glutathione reductase mimicks the biochemistry of drug-sensitive glucose-6-phosphate dehydrogenase deficiency (favism), an inherited condition which confers protection from malaria.
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PMID:Glutathione reductase-deficient erythrocytes as host cells of malarial parasites. 327 13


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