Suwaporn AnantrakulsilYaowapa ManeeratPolrat WilairatanaSrivicha KrudsoodChaiyong ArunsuriyasakVichai AtichartakarnRatchanok KumsiriKovit PattanapanyasatSornchai LooareesuwanRatchanee UdomsangpetchNational Institutes of Health, BethesdaMahidol UniversityInstitute of PathologyFaculty of Medicine, Ramathibodi Hospital, Mahidol UniversityRangsit UniversityFaculty of Medicine, Siriraj Hospital, Mahidol University2018-06-212018-06-212005-05-01Southeast Asian Journal of Tropical Medicine and Public Health. Vol.36, No.3 (2005), 543-551012515622-s2.0-24944509624https://repository.li.mahidol.ac.th/handle/20.500.14594/17001The mechanism of anemia in severe falciparum malaria is still not completely understood. The purpose of this study was to determine whether apoptosis in the erythroid lineage causes anemia in falciparum malaria. Bone marrow aspirated from 8 severe falciparum malaria patients, 3 normal volunteers and 5 retrospective normal bone marrow smears were investigated. By light microscopic study, 5 of 8 hyperparasitemic patients had hypocellular bone marrows and erythroid hypoplasia, whereas the other 3 patients had normal cellularity. The mean myeloid:erythroid ratio of these 5 patients was significantly (p ≤ 0.05) higher than normal. Apoptosis of bone marrow nucleated cells (BMNC) could be determined from the exposure of phosphatidylserine (PS) on the cell membrane but not DNA fragmentation (180-250 bp) or ultrastructural morphology. The percentages of apoptotic BMNC and apoptotic erythroid cells in bone marrow from each patient and controls varied from low to high, and were not associated with parasitemia. This study suggests that destruction of erythroid lineage, particularly through apoptosis regulation, cannot solely account for anemia in falciparum malaria.Mahidol UniversityMedicineArticleSCOPUS