Search

PURPOSE: The purpose of this study was to determine the effect of dapsone on platelet count in patients with human immunodeficiency virus (HIV)-related autoimmune thrombocytopeniag. PATIENTS AND METHODS: Eleven patients with HIV-related thrombocytopenia received dapsone (50 to 125 mg/day) for 2 to 43 months. Patients with the acquired immunodericiency syndrome were not enrolled. RESULTS: Of the 11 patients, six developed platelet counts above 50 X 10.sup.9/L and did not require any other specific therapy. No significant side effects were observed. CONCLUSION: We conclude that dapsone may be effective in some patients with HIV-related thrombocytopenia., Autoimmune thrombocytopenic purpura (AITP) is a systemic illness in which the platelet (cells which help preserve clotting mechanism in blood) count decreases and easy bruising of the skin occurs, along with a tendency to bleed. It is often seen in patients infected with the human immunodeficiency virus (HIV). A suitable treatment for this problem has not yet been found. This study examined the effectiveness of the drug dapsone to treat AITP in HIV-infected patients. The idea behind such therapy is that dapsone might be able to inhibit the destruction of platelets by macrophages, cells of the immune system that engulf cells and other matter identified as 'foreign'. Eleven HIV-infected patients with AITP were treated with 50 to 125 mg dapsone/day for between 2 and 43 months. The patients did not yet have AIDS and had not received antiviral therapy. Platelet counts were measured before, during, and after drug therapy. Results showed that platelet counts rose after therapy in 9 of the 11 patients, with counts rising above 50 billion per liter of blood - significantly better than the counts of 27 billion/L before therapy. Increases were persistent in eight of the nine patients that responded. There were no significant side effects of the drug therapy beyond some mild hemolysis (red cell destruction). The results indicate dapsone may be useful for treating some HIV-related cases of AITP. The mechanism by which it works is not clear. (Consumer Summary produced by Reliance Medical Information, Inc.)

ABSTRACTThe distribution and range of 50% inhibitory concentrations (IC50s) of doxycycline were determined for 747 isolates obtained between 1997 and 2006 from patients living in Senegal, Republic of the Congo, and Gabon and patients hospitalized in France for imported malaria. The statistical analysis was designed to answer the specific question of whether Plasmodium falciparumhas different phenotypes of susceptibility to doxycycline. A triple normal distribution was fitted to the data using a Bayesian mixture modeling approach. The IC50geometric mean ranged from 6.2 μM to 11.1 μM according to the geographical origin, with a mean of 9.3 μM for all 747 parasites. The values for all 747 isolates were classified into three components: component A, with an IC50mean of 4.9 μM (±2.1 μM [standard deviation]); component B, with an IC50mean of 7.7 μM (±1.2 μM); and component C, with an IC50mean of 17.9 μM (±1.4 μM). According to the origin of the P. falciparumisolates, the triple normal distribution was found in each subgroup. However, the proportion of isolates predicted to belong to component B was most important in isolates from Gabon and Congo and in isolates imported from Africa (from 46 to 56%). In Senegal, 55% of the P. falciparumisolates were predicted to be classified as component C. The cutoff of reduced susceptibility to doxycycline in vitro was estimated to be 35 μM.

ABSTRACTWe determined the level of in vitro resistance of Plasmodium falciparumparasites to standard antimalarial drugs, such as chloroquine, quinine, amodiaquine, halofantrine, mefloquine, cycloguanil, and pyrimethamine, and to new compounds, such as dihydroartemisinin, doxycycline, atovaquone, and lumefantrine. The in vitro resistance to chloroquine reached 75.5%. Twenty-eight percent of the isolates were intermediate or had reduced susceptibility to quinine. Seventy-six percent and 96% of the tested isolates showed in vitro resistance or intermediate susceptibilities to cycloguanil and pyrimethamine, respectively. Only 2% of the parasites demonstrated in vitro resistance to monodesethylamodiaquine. No resistance was shown with halofantrine, lumefantrine, dihydroartemisinin, or atovaquone. Halofantrine, mefloquine, and lumefantrine demonstrated high correlation. No cross-resistance was identified between responses to monodesethyl-amodiaquine, dihydroartemisinin, atovaquone, and cycloguanil. Since the level of chloroquine resistance in vitro exceed an unacceptable upper limit, high rates of in vitro resistance to pyrimethamine and cycloguanil and diminution of the susceptibility to quinine, antimalarial drugs used in combination, such as amodiaquine, artemisinin derivatives, mefloquine, lumefantrine, or atovaquone, seem to be appropriate alternatives for the first line of treatment of acute, uncomplicated P. falciparummalaria.