Displaying publications 61 - 80 of 275 in total

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  1. Mordi MN, Mansor SM, Navaratnam V, Wernsdorfer WH
    Br J Clin Pharmacol, 1997 Apr;43(4):363-5.
    PMID: 9146847
    AIMS: To determine the pharmacokinetics of artemether (ARM) and its principal active metabolite, dihydroartemisinin (DHA) in healthy volunteers.

    METHODS: Six healthy male Malaysian subjects were given a single oral dose of 200 mg artemether. Blood samples were collected to 72 h. Plasma concentrations of the two compounds were measured simultaneously by reversed-phase h.p.l.c. with electro-chemical detection in the reductive mode.

    RESULTS: Mean (+/- s.d.) maximum concentrations of ARM, 310 +/- 153 micrograms l-1, were reached 1.88 +/- 0.21 h after drug intake. The mean elimination half-life was 2.00 +/- 0.59 h, and the mean AUC 671 +/- 271 micrograms l-1 h. The mean Cmax of DHA, 273 +/- 64 micrograms l-1 was observed at 1.92 +/- 0.13 h. The mean AUC of DHA was 753 +/- 233 micrograms h l-1'. ARM and DHA were stable at < or = -20 degrees C for at least 4 months in plasma samples.

    CONCLUSIONS: The relatively short half-life of ARM may be one of the factors responsible for the poor radical cure rate of falciparum malaria with regimens employing daily dosing. In view of the rapid loss of DHA in plasma samples held at room temperature (26 degrees C) it is recommended to store them at a temperature of < or = -20 degrees C as early as possible after sample collection.

    Matched MeSH terms: Antimalarials/administration & dosage; Antimalarials/blood; Antimalarials/pharmacokinetics*
  2. Navaratnam V, Mordi MN, Mansor SM
    J Chromatogr B Biomed Sci Appl, 1997 Apr 25;692(1):157-62.
    PMID: 9187395
    A selective reproducible high-performance liquid chromatographic assay for the simultaneous quantitative determination of the antimalarial compound artesunic acid (ARS), dihydroartemisinin (DQHS) and artemisinin (QHS), as internal standard, is described. After extraction from plasma, ARS and DQHS were analysed using an Econosil C8 column and a mobile phase of acetonitrile-0.05 M acetic acid (42:58, v/v) adjusted to pH 5.0 and electrochemical detection in the reductive mode. The mean recovery of ARS and DQHS over a concentration range of 50-200 ng/ml was 75.5% and 93.5%, respectively. The within-day coefficients of variation were 4.2-7.4% for ARS and 2.6-4.9% for DQHS. The day-to-day coefficients of variation were 1.6-9.6% and 0.5-8.3%, respectively. The minimum detectable concentration for ARS and DQHS in plasma was 4.0 ng/ml for both compounds. The method was found to be suitable for use in clinical pharmacological studies.
    Matched MeSH terms: Antimalarials/blood*; Antimalarials/pharmacokinetics
  3. Cox-Singh J, Zakaria R, Abdullah MS, Rahman HA, Nagappan S, Singh B
    Am J Trop Med Hyg, 2001 6 27;64(1-2):28-31.
    PMID: 11425158
    Dihydropteroate synthase (dhps) and dihydrofolate reductase (dhfr) alleles were typed in 67 Malaysian Plasmodium falciparum isolates. The isolates were collected from two geographically distinct locations: 51 from Sabah, Malaysian Borneo, where sulfadoxine/pyrimethamine (SDX/PYR) is used to treat uncomplicated malaria and 16 from Peninsular Malaysia where in vivo resistance to SDX/PYR has been reported. A total of seven dhps alleles were identified with no significant difference in allele frequency between the 2 populations. Two of the dhps alleles described here have not been previously reported. Four dhfr alleles were detected in 67 P. falciparum isolates. Eighty-seven percent of the isolates from the Peninsula, where clinical SDX/PYR failure has been reported, had dhfr alleles with triple point mutations while all of the isolates from Sabah had dhfr alleles with 2 or less point mutations. The difference in dhfr allele frequency between the two populations was highly significant. There was no correlation between in vitro PYR response and accumulation of dhfr point mutations.
    Matched MeSH terms: Antimalarials/therapeutic use
  4. Lyn PC, Fernandez E
    Med J Aust, 1987 Mar 16;146(6):335-6.
    PMID: 2950306
    Matched MeSH terms: Antimalarials/adverse effects*
  5. William T, Menon J, Rajahram G, Chan L, Ma G, Donaldson S, et al.
    Emerg Infect Dis, 2011 Jul;17(7):1248-55.
    PMID: 21762579 DOI: 10.3201/eid1707.101017
    The simian parasite Plasmodium knowlesi causes severe human malaria; the optimal treatment remains unknown. We describe the clinical features, disease spectrum, and response to antimalarial chemotherapy, including artemether-lumefantrine and artesunate, in patients with P. knowlesi malaria diagnosed by PCR during December 2007-November 2009 at a tertiary care hospital in Sabah, Malaysia. Fifty-six patients had PCR-confirmed P. knowlesi monoinfection and clinical records available for review. Twenty-two (39%) had severe malaria; of these, 6 (27%) died. Thirteen (59%) had respiratory distress; 12 (55%), acute renal failure; and 12, shock. None experienced coma. Patients with uncomplicated disease received chloroquine, quinine, or artemether-lumefantrine, and those with severe disease received intravenous quinine or artesunate. Parasite clearance times were 1-2 days shorter with either artemether-lumefantrine or artesunate treatment. P. knowlesi is a major cause of severe and fatal malaria in Sabah. Artemisinin derivatives rapidly clear parasitemia and are efficacious in treating uncomplicated and severe knowlesi malaria.
    Matched MeSH terms: Antimalarials/administration & dosage*; Antimalarials/therapeutic use
  6. Azidah AK, Mohd Faizal MA, Lili HY, Zeehaida M
    Trop Biomed, 2014 Mar;31(1):31-5.
    PMID: 24862042 MyJurnal
    Plasmodium knowlesi has been recently identified as the "fifth human malaria species" following the discovery in Malaysian Borneo of a large focus of this simian malaria parasite in humans. Even though it shares microscopic similarities with Plasmodium malariae, it may cause severe illness with risk of fatality. We describe a case of P. knowlesi infection causing multi-organ failure in a patient who was successfully managed due to early recognition of the infection. Clinicians in this region should be more aware of the infection as it is not as rare as previously thought. This case write up highlight the case of severe malaria infection which presented with multi organ involvement which is caused by P. knowlesi.
    Matched MeSH terms: Antimalarials/administration & dosage*
  7. Chan KL, Choo CY, Abdullah NR
    Planta Med, 2005 Oct;71(10):967-9.
    PMID: 16254833 DOI: 10.1055/s-2005-864188
    Among the quassinoids isolated from Eurycoma longifolia Jack, eurycomanone was identified as the most potent and toxic inhibitor of the chloroquine-resistant Gombak A isolate of Plasmodium falciparum. Several diacylated derivatives of eurycomanone, 1,15-di-O-isovaleryleurycomanone, 1,15-di-O-(3,3-dimethylacryloyl)- eurycomanone and 1,15-di-O-benzoyleurycomanone were synthesized by direct acylation with the respective acid chlorides. The monoacylated 15-O-isovaleryleurycomanone was synthesized by selective protection of the other hydroxy groups of eurycomanone with trimethylsilyl trifluoromethanesulphonate to enable the exclusive acylation of its C-15 hydroxy group. This was followed by the removal of the protecting groups with citric acid. The diacylated eurycomanones exhibited lower antiplasmodial activity against the Gombak A isolates and lower toxicity in the brine shrimp assay when compared to eurycomanone. In contrast, the monoacylated derivative displayed comparable antiplasmodial potency to eurycomanone, but its toxicity was reduced. Thus, preliminary studies of the synthesized acylated eurycomanones have shown that acylation only at the C-15 hydroxy group may be worthy of further antimalarial investigation.
    Matched MeSH terms: Antimalarials/administration & dosage; Antimalarials/chemical synthesis; Antimalarials/pharmacology*; Antimalarials/therapeutic use
  8. Nurhidanatasha Abu Bakar, Zainal Abidin Abu Hasan, Nurul Izza Nordin, Bohari Mohamad Yamin
    Sains Malaysiana, 2007;36:39-44.
    Ferrocene plays an important role in chemistry and industry. The structure and bonding discovered in ferrocene has led to new developments in organometallic chemistry, and the discovery of entirely new organometallic compounds. The high stability of this compound is also related to its interesting electrochemical properties that makes it effective electrochemical, reduction and combustion catalysts. Nevertheless, ferrocenyl derivatives are also capable of enhancing the activity of certain biological compounds. Indeed, recently ferrocene and its derivatives have been incorporated into antimalarial agents. Therefore, the evaluation of the possible toxic effects of ferrocene derivative called ferrocenium tetrachloroantimonate (C10H10FeSbCl4 or FC) on acute and subchronic toxicity tests using different dose concentrations according to the body weight for different time interval was carried out in an in vivo model. Results showed that FC was acutely toxic with the LD50 value of 194.70 mg/kg body weight (BW) with signs of toxicity associated with respiratory depression. In the 28-day acute toxicity test, the dose of 100 mg/kg BW resulted in 60 % mortality with signs of gross toxicity, adverse pharmacological effects or abnormal behaviors during the 28 days observation. While in the 90-day subchronic toxicity test at the lower dose of 10 mg/kg BW, however, showed no significant differences (p>0.05) in the mortality rates, and showed no sign of toxicity. These results indicated that FC had different toxicity levels, and mice appeared to tolerate well at the lower dose of 10 mg/kg BW.
    Matched MeSH terms: Antimalarials
  9. Min TH, Khairul MF, Low JH, Che Nasriyyah CH, A'shikin AN, Norazmi MN, et al.
    Exp Parasitol, 2007 Apr;115(4):387-92.
    PMID: 17118354
    Chloroquine (CQ) and mefloquine (MQ) are no longer potent antimalarial drugs due to the emergence of resistant Plasmodium falciparum. Combination therapy has become the standard for many regimes in overcoming drug resistance. Roxithromycin (ROM), a known p-glycoprotein inhibitor, is reported to have antimalarial activity and it is hoped it will potentiate the effects of both CQ/MQ and reverse CQ/MQ-resistance. We assayed the effects of CQ and MQ individually and in combination with ROM on synchronized P. falciparum (Dd2 strain) cultures. The IC(50) values of CQ and MQ were 60.0+/-5.0 and 16.0+/-3.0 ng/ml; these were decreased substantially when combined with ROM. Isobolograms indicate that CQ-ROM combinations were relatively more synergistic (mean FICI 0.70) than MQ-ROM (mean FICI 0.85) with their synergistic effect at par with CQ-verapamil (VRP) (mean FICI 0.64) and MQ-VRP (mean FICI 0.60) combinations. We conclude that ROM potentiates the CQ/MQ response on multidrug-resistant P. falciparum.
    Matched MeSH terms: Antimalarials/pharmacology*
  10. Hou LJ, Raju SS, Abdulah MS, Nor NM, Ravichandran M
    Jpn J Infect Dis, 2004 Oct;57(5):198-202.
    PMID: 15507775
    Chloroquine (CQ)-resistant Plasmodium falciparum appears to decrease CQ accumulation in its food vacuole by enhancing its efflux via an active membrane pump, which has been reported to be a P-glycoprotein-like transporter. Rifampicin (RIF) is a P-glycoprotein inhibitor and also has some antimalarial activity. It is hoped that a combination of choloroquine-rifampicin (CQ + RIF) would be advantageous in the treatment of CQ-resistant malaria. Swiss albino mice were inoculated with CQ-resistant P. berghei intraperitoneally, and studied for the effect of CQ versus the combination of CQ + RIF at various doses on the clearance of parasitemia, the survival of the mice, and the recrudescence of malaria. Paradoxically, RIF decreased the survival rate and rate of clearance of parasitemia and increased the rate of recrudescence significantly when combined with various doses of CQ. Our results indicated that RIF worsened the course of the disease, and we concluded that RIF should not be combined with CQ in the treatment of malaria.
    Matched MeSH terms: Antimalarials/administration & dosage*
  11. Habas K, Nganwuchu C, Shahzad F, Gopalan R, Haque M, Rahman S, et al.
    Expert Rev Anti Infect Ther, 2020 12;18(12):1201-1211.
    PMID: 32749914 DOI: 10.1080/14787210.2020.1797487
    INTRODUCTION: Coronavirus disease 2019 (COVID-19) was first detected in China in December, 2019, and declared as a pandemic by the World Health Organization (WHO) on March 11, 2020. The current management of COVID-19 is based generally on supportive therapy and treatment to prevent respiratory failure. The effective option of antiviral therapy and vaccination are currently under evaluation and development.

    AREAS COVERED: A literature search was performed using PubMed between December 1, 2019-June 23, 2020. This review highlights the current state of knowledge on the viral replication and pathogenicity, diagnostic and therapeutic strategies, and management of COVID-19. This review will be of interest to scientists and clinicians and make a significant contribution toward development of vaccines and targeted therapies to contain the pandemic.

    EXPERT OPINION: The exit strategy for a path back to normal life is required, which should involve a multi-prong effort toward development of new treatment and a successful vaccine to protect public health worldwide and prevent future COVID-19 outbreaks. Therefore, the bench to bedside translational research as well as reverse translational works focusing bedside to bench is very important and would provide the foundation for the development of targeted drugs and vaccines for COVID-19 infections.

    Matched MeSH terms: Antimalarials/therapeutic use
  12. Krishna S, Augustin Y, Wang J, Xu C, Staines HM, Platteeuw H, et al.
    Trends Parasitol, 2021 01;37(1):8-11.
    PMID: 33153922 DOI: 10.1016/j.pt.2020.10.003
    Artemisinin-based combination therapies (ACTs) have demonstrated in vitro inhibition of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). Artemisinins have also shown anti-inflammatory effects, including inhibition of interleukin-6 (IL-6) that plays a key role in the development of severe coronavirus disease 2019 (COVID-19). There is now sufficient evidence for the effectiveness of ACTs, and in particular artesunate/pyronaridine, to support clinical studies for COVID-19 infections.
    Matched MeSH terms: Antimalarials/therapeutic use*
  13. Islahudin F, Ting KN, Pleass RJ, Avery SV
    Antimicrob Agents Chemother, 2013 Nov;57(11):5787.
    PMID: 24123347 DOI: 10.1128/AAC.01688-13
    Matched MeSH terms: Antimalarials/pharmacology*
  14. Cahyo Budiman, Carlmond Goh Kah Wun, Lee, Ping Chin, Rafida Razali, Thean, Chor Leow
    MyJurnal
    FK506-binding protein35 of Plasmodium knowlesi (Pk-FKBP35) is a member of peptidyl prolyl cis-trans isomerase (PPIase) and is considered as a promising avenue of antimalarial drug target development. This protein is organized into the N-terminal domain responsible for PPIase catalytic activity followed and the tetratricopeptide repeat domain for its dimerization. The protease-coupling and protease-free assays are known to be the common methods for investigating the catalytic properties of PPIase. Earlier, the protease-coupling assay was used to confirm the catalytic activity of Pk-FKBP35 in accelerating cis-trans isomerization of the peptide substrate. This report is aimed to re-assess the catalytic and substrate specificity of Pk-FKBP35 using an alternative method of a protease-free assay. The result indicated that while Pk-FKBP35 theoretically contained many possible cleavage sites of chymotrypsin, experimentally, the catalytic domain was relatively stable from chymotrypsin. Furthermore, under protease-free assay, Pk-FKBP35 also demonstrated remarkable PPIase catalytic activity with kcat/KM of 4.5 + 0.13 × 105 M−1 s−1, while the kcat/KM of active site mutant of D55A is 0.81 + 0.05 × 105 M−1 s−1. These values were considered comparable to kcat/KM obtained from the protease-coupling assay. Interestingly, the substrate specificities of Pk-FKBP35 obtained from both methods are also similar, with the preference of Pk-FKBP35 towards Xaa at P1 position was Leu>Phe>Lys>Trp>Val>Ile>His>Asp>Ala>Gln>Glu. Altogether, we proposed that protease-free and protease-coupling assays arereliable for Pk-FKBP35.
    Matched MeSH terms: Antimalarials
  15. Islahudin F, Pleass RJ, Avery SV, Ting KN
    J Antimicrob Chemother, 2012 Oct;67(10):2501-5.
    PMID: 22763566 DOI: 10.1093/jac/dks253
    OBJECTIVES: Recent work with the yeast model revealed that the antiprotozoal drug quinine competes with tryptophan for uptake via a common transport protein, causing cellular tryptophan starvation. In the present work, it was hypothesized that similar interactions may occur in malaria patients receiving quinine therapy.

    PATIENTS AND METHODS: A direct observational study was conducted in which plasma levels of drug and amino acids (tryptophan, tyrosine and phenylalanine) were monitored during quinine treatment of malaria patients with Plasmodium falciparum infections.

    RESULTS: Consistent with competition for uptake from plasma into cells, plasma tryptophan and tyrosine levels increased ≥2-fold during quinine therapy. Plasma quinine levels in individual plasma samples were significantly and positively correlated with tryptophan and tyrosine in the same samples. Control studies indicated no effect on phenylalanine. Chloroquine treatment of Plasmodium vivax-infected patients did not affect plasma tryptophan or tyrosine. During quinine treatment, plasma tryptophan was significantly lower (and quinine significantly higher) in patients experiencing adverse drug reactions.

    CONCLUSIONS: Plasma quinine levels during therapy are related to patient tryptophan and tyrosine levels, and these interactions can determine patient responses to quinine. The study also highlights the potential for extrapolating insights directly from the yeast model to human malaria patients.

    Matched MeSH terms: Antimalarials/administration & dosage*; Antimalarials/pharmacology
  16. Hoon AH, Lam CK, Wah MJ
    Antimicrob Agents Chemother, 1995 Mar;39(3):626-8.
    PMID: 7793863
    Malaysian, TGR (Thailand), and Gambian (West African) Plasmodium falciparum isolates were cultured in vitro by the candle jar method and were characterized for their susceptibilities to present antimalarial drugs by the modified in vitro microtechnique. Results showed that 93 and 47% of the Malaysian isolates were resistant at 50% inhibitory concentrations of 0.1415 to 0.7737 and 0.1025 to 0.1975 microM, respectively, while the rest were susceptible to choloroquine and cycloguanil at 0.0376 and 0.0306 to 0.0954 microM, respectively. All isolates were susceptible to mefloquine, quinine, and pyrimethamine at 0.0026 to 0.0172, 0.0062 to 0.0854, and 0.0149 to 0.0663 microM, respectively. In contrast, the Gambian isolate was susceptible to multiple drugs at 0.0024 to 0.0282 microM; TGR was resistant to chloroquine at 0.8147 microM but was susceptible to mefloquine, quinine, cycloguanil, and pyrimethamine at 0.0024, 0.0096, 0.0143, and 0.0495 microM, respectively.
    Matched MeSH terms: Antimalarials/pharmacology*
  17. Thriemer K, Bobogare A, Ley B, Gudo CS, Alam MS, Anstey NM, et al.
    Malar J, 2018 Jun 20;17(1):241.
    PMID: 29925430 DOI: 10.1186/s12936-018-2380-8
    The goal to eliminate malaria from the Asia-Pacific by 2030 will require the safe and widespread delivery of effective radical cure of malaria. In October 2017, the Asia Pacific Malaria Elimination Network Vivax Working Group met to discuss the impediments to primaquine (PQ) radical cure, how these can be overcome and the methodological difficulties in assessing clinical effectiveness of radical cure. The salient discussions of this meeting which involved 110 representatives from 18 partner countries and 21 institutional partner organizations are reported. Context specific strategies to improve adherence are needed to increase understanding and awareness of PQ within affected communities; these must include education and health promotion programs. Lessons learned from other disease programs highlight that a package of approaches has the greatest potential to change patient and prescriber habits, however optimizing the components of this approach and quantifying their effectiveness is challenging. In a trial setting, the reactivity of participants results in patients altering their behaviour and creates inherent bias. Although bias can be reduced by integrating data collection into the routine health care and surveillance systems, this comes at a cost of decreasing the detection of clinical outcomes. Measuring adherence and the factors that relate to it, also requires an in-depth understanding of the context and the underlying sociocultural logic that supports it. Reaching the elimination goal will require innovative approaches to improve radical cure for vivax malaria, as well as the methods to evaluate its effectiveness.
    Matched MeSH terms: Antimalarials/therapeutic use*
  18. Barrett JP, Behrens RH
    J Travel Med, 1996 Mar 01;3(1):60-61.
    PMID: 9815425
    Chloroquine-resistant Plasmodium vivax was originally reported in Papua, New Guinea by Reickman in 1989.1 In the same year, in Colombia, South America, Arias and Corredor2 reported relapses of 11 patients suffering from vivax malaria, following a chloroquine-primaquine regimen. Garavelli and Corti3 suggested chloroquine-resistant Plasmodium vivax may be present in Brazil following these therapeutic relapses. Further therapeutic failures in returned travelers from South America were reported by Moore et al (1994).4 We report vivax malaria in a group of expeditioners visiting Guyana who, whereas compliant with antimalarial chemoprophylaxis, developed clinical malaria, adding evidence to the presence of chloroquine-resistant Plasmodium vivax in South America. Raleigh International is a youth development charity that undertakes environmental and community projects around the world. These are usually in remote locations. Nine expeditions in countries such as Chile, Belize, Zimbabwe, Uganda, and Malaysia are organized annually. A project manager and a medical officer are placed at each site, along with approximately 10 venturers (age 17-25.) Participants are of all nationalities, but, at present, they are predominantly British.
    Matched MeSH terms: Antimalarials
  19. Clyde DF, DuPont HL, Miller RM, McCarthy VC
    Trans R Soc Trop Med Hyg, 1970;64(6):834-8.
    PMID: 4924648
    Matched MeSH terms: Antimalarials/therapeutic use*
  20. Zaid OI, Abd Majid R, Sidek HM, Noor SM, Abd Rachman-Isnadi MF, Bello RO, et al.
    Trop Biomed, 2020 Mar 01;37(1):29-49.
    PMID: 33612716
    Treatment Failure with chloroquine is one of the challenges that faced the dedicated efforts to eradicate malaria This study aims at investigating the impact of treatment failure with chloroquine on the progression of the disease-induced histo-pathogenic and immunogenic outcomes. To achieve this, Rane's protocol with modifications was applied on a model of Plasmodium berghei ANKA infected ICR mice to determine the dose response curve of chloroquine and to screen the treatment impact on the disease progression. Chloroquine was given at 1, 5, 10, 15 and 20 mg/kg once the parasitemia reached to 20-30% (the experimental initiation point). During the subsequent days, the mice were monitored for changes in the clinical signs, hematology parameters and the progress of the parasitemia until the parasitemia reached to 60-70% (the experimental termination point) or up to 10 days after chloroquine administration in case of achieving a complete eradication of the parasite. At the end, the mice were exsanguinated and their blood and organs were collected for the biochemistry and the histology study. A complete eradication of the parasite was achieved at 20 mg/kg while recrudescence was observed at the lower doses. At 1 mg/kg, the parasite growth was comparable to that of the positive control. The histo-pathogenic and immunogenic changes were stronger in the groups that experienced recrudescence (at 5 and 10 mg/kg). All in all, the study highlights the possibility of having a worsened clinical condition when chloroquine is given at its sub-therapeutic doses during malaria treatment.
    Matched MeSH terms: Antimalarials/administration & dosage*; Antimalarials/therapeutic use
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