Primaquine for preventing relapse in people with<i>Plasmodium vivax</i>malaria treated with chloroquine

Galappaththy, Gawrie N. L.; Tharyan, Prathap; Kirubakaran, Richard

doi:10.1002/14651858.cd004389.pub3

Cited by 59 publications

(65 citation statements)

References 139 publications

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“…91,96 Administration of primaquine therapy for less than 14 days is associated with higher relapse rates than 14 day regimens. 97 We therefore recommend that in vivax malaria, primaquine should be given at a dose of 30 mg daily for 14 days to prevent relapse along with treatment with chloroquine. (Grade 1C).…”

Section: Prevention Of Relapse In Ovale or Vivax Malariamentioning

confidence: 99%

UK malaria treatment guidelines 2016

Lalloo

Shingadia

Bell

et al. 2016

Journal of Infection

164

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1.Malaria is the tropical disease most commonly imported into the UK, with 1300-1800 cases reported each year, and 2-11 deaths. 2. Approximately three quarters of reported malaria cases in the UK are caused by Plasmodium falciparum, which is capable of invading a high proportion of red blood cells and rapidly leading to severe or life-threatening multi-organ disease. 3. Most non-falciparum malaria cases are caused by Plasmodium vivax; a few cases are caused by the other species of plasmodium: Plasmodium ovale, Plasmodium malariae or Plasmodium knowlesi. 4. Mixed infections with more than one species of parasite can occur; they commonly involve P. falciparum with the attendant risks of severe malaria. 5. There are no typical clinical features of malaria; even fever is not invariably present. Malaria in children (and sometimes in adults) may present with misleading symptoms such as gastrointestinal features, sore throat or lower respiratory complaints. 6. A diagnosis of malaria must always be sought in a feverish or sick child or adult who has visited malaria-endemic areas. Specific country information on malaria can be found at http://travelhealthpro.org.uk/. P. falciparum infection rarely presents more than six months after exposure but presentation of other species can occur more than a year after exposure. 7. Management of malaria depends on awareness of the diagnosis and on performing the correct diagnostic tests: the diagnosis cannot be excluded until more than one blood specimen has been examined. Other travel related infections, especially viral haemorrhagic fevers, should also be considered. 8. The optimum diagnostic procedure is examination of thick and thin blood films by an expert to detect and speciate the malarial parasites. P. falciparum and P. vivax (depending upon the product) malaria can be diagnosed almost as accurately using rapid diagnostic tests (RDTs) which detect plasmodial antigens. RDTs for other Plasmodium species are not as reliable. 9. Most patients treated for P. falciparum malaria should be admitted to hospital for at least 24 h as patients can deteriorate suddenly, especially early in the course of treatment. In specialised units seeing large numbers of patients, outpatient treatment may be considered if specific protocols for patient selection and follow up are in place. 10. Uncomplicated P. falciparum malaria should be treated with an artemisinin combination therapy (Grade 1A). Artemether-lumefantrine (Riamet(®)) is the drug of choice (Grade 2C) and dihydroartemisinin-piperaquine (Eurartesim(®)) is an alternative. Quinine or atovaquone-proguanil (Malarone(®)) can be used if an ACT is not available. Quinine is highly effective but poorly-tolerated in prolonged treatment and should be used in combination with an additional drug, usually oral doxycycline. 11. Severe falciparum malaria, or infections complicated by a relatively high parasite count (more than 2% of red blood cells parasitized) should be treated with intravenous therapy until the patient is well enough to continue with o...

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Section: Prevention Of Relapse In Ovale or Vivax Malariamentioning

confidence: 99%

UK malaria treatment guidelines 2016

Lalloo

Shingadia

Bell

et al. 2016

Journal of Infection

164

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“…2 Currently, a 14-day course of primaquine is the only treatment able to eradicate P. vivax liver hypnozoites and one of few drugs with gametocidal activity against P. falciparum. 3 However, primaquine therapy is contraindicated in patients with glucose-6-phosphate dehydrogenase (G6PD) deficiency, which is common in malaria-endemic regions. 4 G6PD deficiency is an X-linked disorder with multiple clinical phenotypes resulting from loss-of-function mutations in the G6PD gene (band Xq28).…”

Section: Introductionmentioning

confidence: 99%

Field Trial of the CareStart Biosensor Analyzer for the Determination of Glucose-6-Phosphate Dehydrogenase Activity in Haiti

Weppelmann

Fricken

Wilfong

et al. 2017

The American Journal of Tropical Medicine and Hygiene

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Throughout many developing and tropical countries around the world, malaria remains a significant threat to human health. One barrier to malaria elimination is the ability to safely administer primaquine chemotherapy for the radical cure of malaria infections in populations with a high prevalence of glucose-6-phosphate dehydrogenase (G6PD) deficiency. In the current study, a field trial of the world's first quantitative, point-of-care assay for measuring G6PD activity was conducted in Haiti. The performance of the CareStart Biosensor Analyzer was compared with the gold standard spectrophotometric assay and genotyping of the allele in schoolchildren ( = 343) from the Ouest Department of Haiti. In this population, 19.5% of participants (67/343) had some form of G6PD deficiency (< 60% residual activity) and 9.9% (34/343) had moderate-to-severe G6PD deficiency (< 30% residual activity). Overall, 18.95% of participants had the presence of the A-allele (65/343) with 7.87% (27/343) considered at high risk for drug-induced hemolysis (hemizygous males and homozygous females). Compared with the spectrophotometric assay, the sensitivity and specificity to determine participants with < 60% residual activity were 53.7% and 94.6%, respectively; for participants with 30% residual activity, the sensitivity and specificity were 5.9% and 99.7%, respectively. The biosensor overestimated the activity in deficient individuals and underestimated it in participants with normal G6PD activity, indicating the potential for a systematic measurement error. Thus, we suggest that the current version of the biosensor lacks adequate sensitivity and should be improved prior to its use as a point-of-care diagnostic for G6PD deficiency.

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“…It is also used as a prophylactic drug against all major forms of human malaria and in combination with clindamycin for the treatment as well as prophylaxis of Pneumocystis pneumonia in human immunodeficiency virus/acquired immunodeficiency syndrome (HIV/AIDS) patients (Tekwani and Walker, 2006;Kim et al, 2009). The utility of PQ has also been shown in the prevention and blocking of transmission of Plasmodium falciparum malaria (Hill et al, 2006;White et al, 2012), and recently its use has been proposed as a key strategy in malaria control and elimination efforts (White, 2008;Fernando et al, 2011;John et al, 2012;Galappaththy et al, 2013). However, the therapeutic utility of PQ is limited because of its due to severe hemolytic toxicity in individuals with glucose 6-phosphate dehydrogenase deficiency (Youngster et al, 2010;Baird, 2012;Ganesan et al, 2012;Howes et al, 2013) Synthesis and testing of many different 8-AQs in the 1940s led to the discovery of PQ, with its 4-amino-1-methylbutyl side chain ( Fig.…”

Section: Introductionmentioning

confidence: 99%

Enantioselective Pharmacokinetics of Primaquine in Healthy Human Volunteers

et al. 2015

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Primaquine (PQ), a racemic drug, is the only treatment available for radical cure of relapsing Plasmodium vivax malaria and blocking transmission of P. falciparum malaria. Recent studies have shown differential pharmacologic and toxicologic profiles of individual PQ enantiomers in rodent, dog, and primate animal models. This study was conducted in six healthy adult human volunteers to determine the plasma pharmacokinetic profile of enantiomers of PQ and carboxyprimaquine (cPQ), the major plasma metabolite. The individuals were orally administered PQ diphosphate, equivalent to 45-mg base, 30 minutes after a normal breakfast. Blood samples were collected at different time intervals, and plasma samples were analyzed for enantiomers of PQ and cPQ. Plasma PQ concentrations were low and variable for both parent enantiomers and peaked around 2-4 hours. Peak (2)-(R)-PQ concentrations ranged from 121 ng/ml to 221 ng/ml, and peak (+)-(S)-PQ concentrations ranged from 168 ng/ml to 299 ng/ml. The cPQ concentrations were much higher and were surprisingly consistent from subject to subject. Essentially all the cPQ detected in plasma was (2)-cPQ. The peak concentrations of (2)-cPQ were observed at 8 hours (range: 1104-1756 ng/ml); however, very high concentrations were sustained through 24 hours. (+)-cPQ was two orders of magnitude lower than (2)-cPQ, and in a few subjects it was detected but only under the limit of quantification. In vitro studies with primary human hepatocytes also suggested more rapid metabolism of (2)-PQ compared with (+)-PQ. The results suggest more rapid metabolism of (2)-PQ to (2) cPQ compared with (+)-PQ. Alternatively, (+)-PQ or (+)-cPQ could be rapidly converted to another metabolite(s) or distributed to tissues. This is the first clinical report on enantioselective pharmacokinetic profiles of PQ and cPQ and supports further clinical evaluation of individual PQ enantiomers.

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Primaquine for preventing relapse in people withPlasmodium vivaxmalaria treated with chloroquine

Cited by 59 publications

References 139 publications

UK malaria treatment guidelines 2016

UK malaria treatment guidelines 2016

Field Trial of the CareStart Biosensor Analyzer for the Determination of Glucose-6-Phosphate Dehydrogenase Activity in Haiti

Enantioselective Pharmacokinetics of Primaquine in Healthy Human Volunteers

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