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)

We report on a serious case of malaria due to Plasmodium falciparum. Although the 46-year-old Swiss female had strictly followed the recommended prophylaxis with proguanil and chloroquine she was infected during a stay in Namibia which had lasted several month. The patient had poor prognostic signs such as encephalopathy (cerebral malaria), a parasitemia of 34% but only moderate renal impairment. Instead of the classical treatment with quinine, the patient was treated with a constant infusion of quinidine over 3 days which was combined with an exchange transfusion of approximately 2 liters on the first day of treatment. All clinical signs of the infection improved within less than 2 days as did the parasitemia. The patient was discharged after a hospital stay of 11 days. Quinidine as opposed to quinine may be more readily available, less toxic and more efficacious. Treatment with quinidine must carefully be monitored. Exchange blood transfusions may be an important additional therapeutic modality in severe plasmodium falciparum malaria.
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PMID:[Continuous quinidine infusion and blood exchange transfusion in severe tropical malaria: a case report]. 192 63

The in vitro response of P. falciparum to amodiaquine, quinine and quinidine was assessed in Tanga region where chloroquine resistance is established, to determine baseline susceptibility levels which could guide health care deliverers on the suitability of these drugs for the treatment of falciparum malaria in the areas studied. Amodiaquine resistance was observed in all of the three areas. 16.7%, 24.0% and 14.7% of successful in vitro tests showed resistance to amodiaquine in Korogwe, Muheza and Tanga respectively. The in vitro response to quinine and quinidine showed that P. falciparum strains in the three areas are very sensitive to the two drugs. Only 1.9%, 4.5% and 1.4% of successful quinine tests showed resitance in Korogwe, Muheza and Tanga respectively. Quinidine showed activity which is twice higher than that of quinine and only 1 isolate in Tanga showed resistance response to quinidine.
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PMID:The in vitro response of Plasmodium falciparum to amodiaquine, quinine and quinidine in Tanga region, Tanzania. 220 87

Over the last decade, chloroquine-resistant falciparum malaria has spread to other areas from its original foci in Southeast Asia and South America. Additionally, new knowledge about the life-cycle of the malaria parasite, and about the pharmacokinetic properties of antimalarial drugs, has emerged. It is appropriate to reassess our approach to prevention and management of malaria with these factors in mind. Antimalarial drugs can be classified in two ways: biologically as tissue schizontocides, hypnozoitocides, blood schizontocides, gametocytocides or sporontocides; or by a mixed chemical/biological classification as 8-aminoquinolines, antimetabolites and (again) blood schizontocides. Chloroquine resistance in P. falciparum can now be found in most areas where malaria occurs. Malarial strains moderately resistant to the chloroquine group of drugs (chloroquine and mepacrine) are generally susceptible to the aryl amino alcohols such as quinine. Indeed, quinine is the most widely used drug for treating malaria due to chloroquine-resistant strains, followed by a 7-day course of tetracycline where some resistance to quinine is also found. Alternatively, the course of quinine may be followed by sulfadoxine/pyrimethamine or the newer quinoline derivative, mefloquine. Quinidine has also shown activity against quinine-resistant strains. Prophylaxis of chloroquine-resistant strains is best undertaken with daily proguanil (chloroguanide), and weekly chloroquine. In severe malaria, including cerebral malaria, an intravenous loading dose of quinine should be considered, and plasma concentration monitoring may be advisable to assist with dosage adjustment. In patients with severe renal insufficiency, there is evidence that the elimination of chloroquine is prolonged, and dosage adjustments may be necessary. Other recent findings on the pharmacodynamic properties, mechanisms of action and toxicity of antimalarial drugs are also discussed.
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PMID:Antimalarial drugs. An update. 354 65

Quinidine has proved more effective than quinine against chloroquine-resistant Plasmodium falciparum both in vitro and in patients with uncomplicated disease. To examine the effectiveness and pharmacokinetics of quinidine for this use, we treated 14 patients who had severe falciparum malaria with intravenous quinidine gluconate; a loading dose of 15 mg of the base per kilogram of body weight was followed by 7.5 mg per kilogram every eight hours. Two of the five patients with cerebral malaria died, but parasitemia was eliminated in the 12 survivors. Two patients had recurrent parasitemia on Days 25 and 28. Times required for parasite clearance and elimination of fever (49.4 +/- 17.8 and 69.5 +/- 18.7 hours, respectively) were comparable to those in earlier studies with a loading dose of quinine. Quinidine appears to have a larger volume of distribution than quinine. The elimination half-life was 12.8 hours, the volume of distribution was 1.68 liters per kilogram, total clearance was 1.75 ml per kilogram per minute, and urinary clearance was 0.62 ml per kilogram per minute. Electrocardiographic changes were common but there were no dysrhythmias. In two patients, blood pressure fell during the initial infusion of quinidine. Quinidine gluconate is more widely available than quinine in many countries, and our findings show that it is effective in severe falciparum malaria.
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PMID:Intravenous quinidine for the treatment of severe falciparum malaria. Clinical and pharmacokinetic studies. 388 62

Fourteen patients with falciparum malaria were successfully treated with oral quinidine. Twelve of these patients were followed for 35 days without recrudescence. In six patients the infection had already recrudesced after antimalarial treatment, which in two cases had included a full course of quinine. Quinidine caused no cardiotoxicity, although the electrocardiogram QTc interval was prolonged by more than 25% in four patients. In-vitro cultures from nine of these patients and a further seven patients with falciparum malaria showed that the minimum inhibitory concentration was consistently lower for quinidine than for quinine. Quinidine is an effective antimalarial drug for Plasmodium falciparum infections and may be more potent than quinine.
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PMID:Quinidine in falciparum malaria. 611 23

The blood schizontocidal activity of the four main Cinchona alkaloids against Plasmodium falciparum was compared in 46 fresh parasite isolates, using an in-vitro test measuring the drug-specific inhibition of schizont maturation. The studies were conducted in June-August 2001 at Mae Sot, northwestern Thailand, an area where quinine alone is no longer able to eliminate infections with P. falciparum. Quinidine showed the highest blood schizontocidal activity, followed by cinchonine, cinchonidine and finally quinine, which was identified as the least active compound. The isolates showed marked heterogeneity in their response to the Cinchona alkaloids. There was also high correlation of activity among all four alkaloids. The mean EC50 values for quinine, quinidine, cinchonine and cinchonidine were 144 nM, 80 nM, 104 nM and 225 nM, respectively, and the EC99 values 8040 nM, 861 nM, 1176 nM and 6531 nM. The EC99 values for quinine and cinchonidine are beyond the therapeutic concentration range and those for quinidine within it. For cinchonine, values are likely to be within this range, but toxicological and pharmacokinetic studies on this compound are required for clarifying its potential future role in the treatment of falciparum malaria.
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PMID:In-vitro response of Plasmodium falciparum to the main alkaloids of Cinchona in northwestern Thailand. 1550 79