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Unmasking hidden risks: A case of primaquine-induced intravascular hemolysis in G-6-PD deficient malaria patient.

Travel Med Infect Dis

October 2024

Thai Travel Clinic, Hospital for Tropical Diseases, Faculty of Tropical Medicine, Mahidol University, Bangkok, 10400, Thailand; Department of Clinical Tropical Medicine, Faculty of Tropical Medicine, Mahidol University, Bangkok, 10400, Thailand. Electronic address:

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Article Synopsis
  • The study focuses on the effectiveness of 8-aminoquinolines (primaquine and tafenoquine) in curing Plasmodium vivax malaria by targeting hypnozoites, with a specific look at the role of methaemoglobin levels as a potential indicator for preventing malaria recurrence.
  • The researchers conducted a systematic review of clinical studies from 2000 to 2022 and examined data from 1,747 patients treated with primaquine to analyze the relationship between methaemoglobin concentration and the time to malaria recurrence.
  • Their findings suggest that higher methaemoglobin levels may correlate with a lower risk of P. vivax recurrence, indicating the potential use of methaemoglobin as
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Background: pneumonia (PJP) is an opportunistic infection caused by the yeast-like fungus . As recommended by some guidelines, the first-line treatment for this infection is trimethoprim-sulfamethoxazole (TMP-SMX), and the second-line treatment includes drugs such as dapsone, pentamidine, primaquine, Atovaquone, clindamycin, and caspofungin. Glucose-6-phosphate dehydrogenase (G6PD) deficiency is an X-linked gene disorder in which treatment with oxidizing drugs, such as sulfonamides, dapsone, primaquine, can directly destroy hemoglobin present in red blood cells (RBCs), thereby inducing methemoglobin and hemolysis.

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Primaquine-5,6-Orthoquinone Is Directly Hemolytic to Older G6PD Deficient RBCs in a Humanized Mouse Model.

J Pharmacol Exp Ther

September 2024

Department of Pathology, University of Virginia School of Medicine, Charlottesville, Virginia (K.H.D.-C., A.M.H., J.C.Z.); Carter Immunology Center, University of Virginia, Charlottesville, Virginia (K.H.D.-C., A.M.H., J.C.Z.); Department of Biochemistry and Molecular Genetics, University of Colorado Anschutz Medical Campus, Aurora, Colorado (J.A.R., T.N., F.I.C., A.I., A.D-A.); University of Maryland, School of Medicine, Center for Blood Oxygen Transport and Hemostasis, Department of Pediatrics, Baltimore, Maryland (D.R.L., P.W.B.); Center for Biomedical Engineering and Technology, and Department of Physiology, University of Maryland School of Medicine, Baltimore, Maryland (E.A.L., J.P.Y.K.); University of Maryland School of Medicine, Department of Pathology, Baltimore, Maryland (M.S.P., P.W.B.); National Center for Natural Products Research, School of Pharmacy, University of Mississippi, University, Mississippi (L.A.W.); and GlobaCure, Birmingham, Alabama (B.L.T.)

Article Synopsis
  • Primaquine and Tafenoquine are the only drugs that can cure malaria completely, but they pose risks for individuals with G6PD deficiency, potentially causing severe blood cell damage.
  • The study introduces a new mouse model replicating a specific human G6PD variant, allowing researchers to observe how a metabolite called 5,6-POQ affects red blood cells.
  • The research indicates that 5,6-POQ is not just a harmless byproduct of drug metabolism but actively contributes to the destruction of older red blood cells in G6PD-deficient individuals, challenging previous assumptions about its role.
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Primaquine-induced hemolysis in a Colombian patient with glucose-6-phosphate dehydrogenase deficiency.

Travel Med Infect Dis

September 2024

Facultad de Medicina, Universidad Militar Nueva Granada, Bogotá, D.C., Colombia; Servicio de Infectología, Hospital Militar Central, Bogotá, D.C., Colombia; Servicios y Asesorías en Infectología - SAI, Bogotá, D.C., Colombia. Electronic address:

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