Showing papers by "Sasithon Pukrittayakamee published in 1996"
TL;DR: The results suggest that the heart is remarkably resilient even in the face of heavy parasite sequestration and other vital organ dysfunction, and that deaths from cardiac arrhythmias in severe malaria are rare.
Abstract: Electrocardiographic monitoring over 24 h was performed with 53 patients with severe Plasmodium falciparum malaria (11 adults and 42 children) to assess the frequency of unrecognized cardiac arrhythmias. Nine patients (17%) died, 5 during the monitoring period and 4 afterwards. Pauses lasting 2-3 s were observed in 3 children, a single couplet in one, and a further child experienced frequent supraventricular ectopic beats which had not been detected clinically. In none of the patients who died could death be attributed to cardiac arrhythmia. Furthermore, no abnormality was detected which could have resulted from the often large doses of quinine, chloroquine or the artemisinin derivatives used for treatment. These results suggest that the heart is remarkably resilient even in the face of heavy parasite sequestration and other vital organ dysfunction, and that deaths from cardiac arrhythmias in severe malaria are rare. The need for routine cardiac monitoring of patients with severe and complicated P. falciparum malaria is questionable.
63 citations
TL;DR: It is suggested that a single intravenous infusion of DCA rapidly reduces hyperlactataemia in patients severely ill with malaria, and that DCA should be evaluated further as an adjunct to conventional antimalarial and supportive measures for such patients with lactic acidosis.
Abstract: 1 Dichloroacetate (DCA) is a promising treatment for lactic acidosis complicating severe malaria. The pharmacokinetics, pharmacodynamics and toxicity of dichloroacetate were evaluated in 11 patients with severe malaria, and their lactate responses compared with nine control patients in an open–label prospective study.
2 Intravenous DCA (46 mg kg-1 infused in 30 min) or saline placebo was given on admission to the study, and 12 h later, as an adjunct to standard quinine treatment.
3 An open one-compartment model with the following parameters described the pharmacokinetics of DCA after one dose (mean [s.d.]): v = 0.44(0.2) 1 kg-1; CL = 0.13[0.027] 1 h-1 kg-1; Cmax = 106[28] mg l-1; t1/2, = 3.4(2.2)h. After two doses of DCA (n = 9) the pharmacokinetic parameters were similar to those after the first dose.
4 DCA decreased venous plasma lactate concentrations by 42% of baseline values 8 h after admission, normalized arterial pH from a mean(s.d.) of 7.367(0.063) to 7.39(0.1), and decreased the calculated base deficit from 9.2(7.3) mEq 1-1 to 6. 4(10.4) mEq 1-1. In control patients lactate concentrations fell by ˜14% of baseline concentrations (P <0.02 compared with DCA recipients). Venous lactate concentrations fell a further 16% from baseline values after the second dose of DCA but this change was not significantly different from controls. There was no electrocardiographic or other evidence of toxicity associated with DCA.
5 These data suggest that a single intravenous infusion of DCA rapidly reduces hyperlactataemia in patients severely ill with malaria, and that DCA should be evaluated further as an adjunct to conventional antimalarial and supportive measures for such patients with lactic acidosis.
24 citations
TL;DR: Chloroquine does not potentiate the clinical response to quinine against resistant strains of uncomplicated falciparum malaria, nor does it convey any useful antipyretic effect.
Abstract: The efficacy and toxicity of oral quinine combined with oral chloroquine were studied in 50 Thai men with uncomplicated falciparum malaria. All were treated for 7 days with quinine sulphate (10 mg salt/kg every 8 h). Twenty-five of the patients, selected at random, were also given oral tetracycline (4 mg/kg four times daily) over the same period and the remainder were given chloroquine (25 mg base/kg over the first 3 days). There were no serious adverse effects. Overall fever-clearance times (FCT) and parasite-clearance times (PCT) in the chloroquine and tetracycline groups were not significantly different, with mean (S.D.) values of 51 (33) and 41 (27) h for FCT and 80 (25) and 83 (21) h for PCT, respectively. Most of the patients (18 in each group) were followed for > or = 2 months. Recrudescence rates (R1) were significantly higher in the chloroquine group than in the tetracycline group (39% v. 6%; P = 0.02), all recrudescences occurring within 4 weeks (18-25 days) of starting treatment. Subsequent parasitaemia with Plasmodium vivax, however, occurred less frequently in the chloroquine group (11%) than in the tetracycline group (33%) (P = 0.11) and took longer to develop in the chloroquine group [51 or 59 days compared with a mean (S.D.) value of 29 (10) days in the tetracycline group; P = 0.01]. Within the chloroquine group, FCT and PCT were both shorter in those with cure than in those with R1 resistance, with mean (S.D.) values of 41 (25) and 70 (33) h for FCT (P = 0.09) and 72 (20) and 100 (18) h for PCT (P = 0.01), respectively. Chloroquine does not potentiate the clinical response to quinine against resistant strains of uncomplicated falciparum malaria, nor does it convey any useful antipyretic effect.
19 citations