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)

The mutant genotype at codon 76 of the pfcrt gene (T76) has been proposed as a molecular marker for surveillance of chloroquine (CQ)-resistant Plasmodium falciparum malaria but this proposal has not been validated by population-based surveys. In 1998-99, in 6 Ugandan sentinel sites, the prevalence of P. falciparum infections with the T76 genotype and the level of CQ use were measured by community surveys, and CQ resistance was determined by in-vivo tests on 6-59-month-old children with clinical malaria. The prevalence of T76 was not related to the overall clinical (early and late treatment failure: ETF + LTF; r = 0.14, P = 0.78) or parasitological (RI + RII + RIII; r = 0.17, P = 0.73) CQ resistance. However, the percentage of individuals carrying only infections with the T76 genotype (T76 alone) increased with increasing ETF (r = 0.76, P = 0.07) and type RIII parasitological failure (r = 0.69, P = 0.12). Similarly, the ratio between T76 and K76 (the wild type) prevalences (T76/K76) was strongly and positively correlated with ETF (r = 0.85, P = 0.03) and RIII (r = 0.82, P = 0.04). Moreover, T76 alone (r = 0.90, P = 0.01) as well as T76/K76 (r = 0.90, P = 0.01) significantly increased with increasing community CQ use. T76 alone and T76/K76 can be useful markers to estimate the ETF and RIII prevalence as well as the amount of CQ use in the community.
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PMID:Role of the pfcrt codon 76 mutation as a molecular marker for population-based surveillance of chloroquine (CQ)-resistant Plasmodium falciparum malaria in Ugandan sentinel sites with high CQ resistance. 1247 88

Following the high rate of chloroquine-resistant Plasmodium falciparum, Ethiopia changed the national drug policy in 1999 from chloroquine to sulfadoxine/pyrimethamine (SP) as first line. However, the useful therapeutic lifespan of SP may be limited by the rapid emergence of resistance. We conducted a study between October and November 2001 to examine the current extent of SP resistance to P. falciparum in Amhara Region, Northern Ethiopia. A total of 93 patients with uncomplicated P. faliciparum malaria were studied from Habru (n=50) and Weizazirt (n=43) localities. Drug resistance was evaluated using the 14-day WHO in vivo test protocol. Parasitological resistance to SP was found to be 32.0% (16/50) and 4.7% (2/43) in Harbu and Weizazirt localities, respectively. The corresponding clinical failure rates were 20.0% (10/50) and 4.7% (2/43). Of the parasitological failure at Harbu, 9 patients were classified as RI, 6 as RII and one as RIII type response. Among the clinical failures, 7 were LTF while the remaining 3 were ETF. Nevertheless, there was hardly any patient with RII/RIII or ETF response, and only two patients each with RI and LTF response were seen from Weizazirt locality. Therefore, the study underscores the presence of varying level of SP resistance to P. falicparum in the areas studied. Whereas SP remains quite effective in the treatment of uncomplicated P. falciparum in Weizazirt locality, the observed high rate of resistance from Harbu is alarming and an area of concern.
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PMID:Development of resistance by Plasmodium falciparum to sulfadoxine/pyrimethamine in Amhara Region, Northwestern Ethiopia. 1637 May 50