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Biomedical subjects

G Charmot

Publications and source records attributed to G Charmot.

At least 19 recordsLinked to original sources
PubMed1998

[Human transmission and plasmodium resistance].

There is no longer malaria transmission in Europe and North America, while the transmission decreases in sub-tropical areas and increases in tropical countries. Most of malarias are now due to Plasmodium falciparum and happen in Africa. In the regions where the transmission is high, malaria is stable, baby mortality is high, and protective immunity is achieved in early childhood. Falciparum resistant malaria originates from mutations on drug target decreasing affinity to antifols, or mutations preventing accumulation of chloroquine in parasitized red blood cells. Resistance is a rapid event following large use of antifols, even associated, while falciparum chloroquine resistance is now widespread. Resistance to quinine, mefloquine and halofantrine is still at low levels out of Thailand, as their use remains through medical hands. Non resistance was observed yet with artemisinin derivatives.

Africa↗
PubMed1997

[Reserve treatment for malaria: pros and cons].

Any discussion of stand-by treatment will raise several questions: to whom should it be prescribed? which drugs are advised for stand-by treatment, according to the expected sensitivity of the parasites, the chemoprophylaxis and the possible side effects of the drugs chosen? what information should be given to a potential user? under what circumstances should stand-by treatment be used? how can the use of stand-by treatment and its efficacy be evaluated? are there any data for the stand-by treatment in literature? what are the pros and cons for the use of stand-by treatment? what is the place for stand-by treatment in today's array of antimalarial treatment? All of these questions were discussed at a round table stating that while stand-by treatment is an important element in malarial prevention for travellers, it must not become synonymous with self-treatment. An initial prescription of stand-by treatment is essential with the physician informing the user of the conditions for its use and its risks. The use of stand-by treatment does not exempt the traveller from rigourously carrying out the extensive recommended preventive measures. If, in spite of these precautions, a traveller does come down with a presumed malarial fever, the use of stand-by treatment should not prevent him from consulting a physician. A physician is in the best position to indicate an available stand-by treatment which should be considered as a back-up treatment. Self-treatment should only be considered as a last resort given its limitations. In all cases, it is indispensable to consult a physician.

Acute Disease↗
PubMed1996

[Effects of chloroquine on the replication of a murine retrovirus].

The wide use of chloroquine (Cq) for prophylaxis and chemotherapy of malaria in Africa, and the increased spread of AIDS in areas of this continent where malaria is endemic, raised the question of a possible interaction between chloroquine intake and HIV infection. Indeed, hydroxychloroquine and chloroquine itself have been shown to inhibit HIV-1 replication in vitro, hydroxychloroquine being proposed as a potential useful adjunctive therapy in the treatment of HIV-1 infection. On the other hand, chloroquine has been reported to enhance the replication of Semliki forest and encephalomyocarditis viruses in a mouse model. In an attempt to elucidate Cq effect on retroviral replication, we have studied the effect of various concentrations of chloroquine in vitro (0.1 nmol/l to 25 mumol/l) on Friend retrovirus (FV)-infected fibroblasts of mice and in vivo (2 to 30 mg/kg) on FV-infected mice. No reduction in the number of virus foci was found in chloroquine-treated fibroblasts cultures. In chloroquine treated-infected mice, no differences were observed in the spleen weights, except an increase at 10 mg/kg. A decrease in splenocyte virus titer was only observed at 10 and 30 mg/kg. No differences in the median survival time was observed up to 30 mg/kg. The authors concluded that chloroquine seemed to have variable effects on viral replication in vivo depending on the dosage, but has no influence on the course of FV-induced disease.

Animals↗
PubMed1993

[Treatment of bilharziasis].

Specific treatment of bilharziosis is obviously simplified by praziquantel which, unfortunately, is not easily available in endemic areas. Nevertheless, the major problem is an early treatment before the occurrence of severe sequellae. Mass chemoprophylaxis remains needed and, if possible, with praziquantel. For economic purposes, we have often to use either oxamniquine or niridazole-metrifonate combination.

Humans↗
PubMed1992

[Contribution of molecular genetics to the understanding of chemoresistance of Plasmodium falciparum].

Resistance to pyrimethamine and proguanil is due to a single point mutation in the gene that codes for dihydrofolate reductase. A single mutation gives rise to resistance to only one of the drugs. Resistance to both drugs results from several mutations. Chloroquine resistance phenotype is due to a rapid efflux of the drug from the parasite's digestive vacuole. This efflux is associated with a transmembrane permeability glycoprotein, or P-gp, which is similar to the protein implicated in the multidrug resistant phenotype of some cancer cells. However, one or several other poorly understood major gene(s) may be involved. Drugs which can inhibit the supposed affinity of P-gp for chloroquine are under study.

ATP Binding Cassette Transporter, Subfamily B, Mem↗
PubMed1991

[Hemolytic anemia associated with minor salmonellosis in an HIV positive, G6PD deficient Congolese woman].

Haemolytic anaemia in G6PD-deficient patients with thyphoid fever is well known, but there is only one case-report associated with non-typhic salmonella fever. We report here a case observed in a black african young woman whose HIV infection has been discovered on this occasion. Because of the high prevalence of HIV infection, salmonellosis and G6PD deficiency in sub-saharian Africa, an increasing number of such haemolytic anaemias should be expected in this geographic area.

Adult↗
PubMed1990

[HIV infection and malaria].

In sub-Saharian Africa, most HIV seropositive subjects carry either haematozoa (especially children) or antimalarial antibodies. Despite a transient decrease in cell-mediated immunity during malarial paroxysms, Plasmodium falciparum malaria does not seem to influence the course of the HIV infection. Paroxysms may be slightly more frequent or slightly more severe in HIV seropositive subjects, but they raise no diagnostic or therapeutic problem. Some cases of HIV contamination have been attributed to the blood transfusions required by malaria-induced anaemia. Prophylactic measures include early chemotherapy of malaria and detection of dangerous blood donors, if necessary by quick tests. Modern HIV tests avoid most of the false-positive reactions sometimes observed during malaria.

Africa, Northern↗