scholarly journals Low plasma haptoglobin is a risk factor for life-threatening childhood severe malarial anemia and not an exclusive consequence of hemolysis

2018 ◽  
Vol 8 (1) ◽  
Author(s):  
Samuel Eneọjọ Abah ◽  
Florence Burté ◽  
Sandrine Marquet ◽  
Biobele J. Brown ◽  
Francis Akinkunmi ◽  
...  
Keyword(s):  
Risk Factor ◽  
Severe Malarial Anemia ◽  
Life Threatening ◽  
Plasma Haptoglobin ◽  
Malarial Anemia

scholarly journals Developing a novel risk prediction model for severe malarial anemia

2017 ◽  
Vol 2 ◽  
Author(s):  
E. B. Brickley ◽  
E. Kabyemela ◽  
J. D. Kurtis ◽  
M. Fried ◽  
A. M. Wood ◽  
...  
Keyword(s):  
Prediction Model ◽  
Prediction Models ◽  
Blood Levels ◽  
Transmission Season ◽  
Severe Malarial Anemia ◽  
Screening Programs ◽  
Life Threatening ◽  
Larger Sample ◽  
Related Mortality ◽  
Malarial Anemia

AbstractAs a pilot study to investigate whether personalized medicine approaches could have value for the reduction of malaria-related mortality in young children, we evaluated questionnaire and biomarker data collected from the Mother Offspring Malaria Study Project birth cohort (Muheza, Tanzania, 2002–2006) at the time of delivery as potential prognostic markers for pediatric severe malarial anemia. Severe malarial anemia, defined here as aPlasmodium falciparuminfection accompanied by hemoglobin levels below 50 g/L, is a key manifestation of life-threatening malaria in high transmission regions. For this study sample, a prediction model incorporating cord blood levels of interleukin-1β provided the strongest discrimination of severe malarial anemia risk with a C-index of 0.77 (95% CI 0.70–0.84), whereas a pragmatic model based on sex, gravidity, transmission season at delivery, and bed net possession yielded a more modest C-index of 0.63 (95% CI 0.54–0.71). Although additional studies, ideally incorporating larger sample sizes and higher event per predictor ratios, are needed to externally validate these prediction models, the findings provide proof of concept that risk score-based screening programs could be developed to avert severe malaria cases in early childhood.

scholarly journals Severe malarial anemia of low parasite burden in rodent models results from accelerated clearance of uninfected erythrocytes

Blood ◽  
2006 ◽  
Vol 107 (3) ◽  
pp. 1192-1199 ◽  
Author(s):  
Krystal J. Evans ◽  
Diana S. Hansen ◽  
Nico van Rooijen ◽  
Lynn A. Buckingham ◽  
Louis Schofield
Keyword(s):  
Parasite Burden ◽  
Rodent Models ◽  
Phagocytic Cells ◽  
Severe Malarial Anemia ◽  
Blood Compartment ◽  
Circulating Cells ◽  
Life Threatening ◽  
Patent Infection ◽  
Malarial Anemia

AbstractSevere malarial anemia (SMA) is the most frequent life-threatening complication of malaria and may contribute to the majority of malarial deaths worldwide. To explore the mechanisms of pathogenesis, we developed a novel murine model of SMA in which parasitemias peaked around 1.0% of circulating red blood cells (RBCs) and yet hemoglobin levels fell to 47% to 56% of baseline. The severity of anemia was independent of the level of peak or cumulative parasitemia, but was linked kinetically to the duration of patent infection. In vivo biotinylation analysis of the circulating blood compartment revealed that anemia arose from accelerated RBC turnover. Labeled RBCs were reduced to 1% of circulating cells by 8 days after labeling, indicating that the entire blood compartment had been turned over in approximately one week. The survival rate of freshly transfused RBCs was also markedly reduced in SMA animals, but was not altered when RBCs from SMA donors were transferred into naive recipients, suggesting few functional modifications to target RBCs. Anemia was significantly alleviated by depletion of either phagocytic cells or CD4+ T lymphocytes. This study demonstrates that immunologic mechanisms may contribute to SMA by promoting the accelerated turnover of uninfected RBCs.

scholarly journals Suppression of a Novel Hematopoietic Mediator in Children with Severe Malarial Anemia

2009 ◽  
Vol 77 (9) ◽  
pp. 3864-3871 ◽  
Author(s):  
Christopher C. Keller ◽  
Collins Ouma ◽  
Yamo Ouma ◽  
Gordon A. Awandare ◽  
Gregory C. Davenport ◽  
...  
Keyword(s):  
Growth Factor ◽  
Mononuclear Cells ◽  
Dependent Manner ◽  
Peripheral Blood Mononuclear ◽  
Severe Malarial Anemia ◽  
Lectin Domain ◽  
Stem Cell Growth Factor ◽  
Reticulocyte Production ◽  
Pediatric Morbidity ◽  
Malarial Anemia

ABSTRACT In areas of holoendemic Plasmodium falciparum transmission, severe malarial anemia (SMA) is a leading cause of pediatric morbidity and mortality. Although many soluble mediators regulate erythropoiesis, it is unclear how these factors contribute to development of SMA. Investigation of novel genes dysregulated in response to malarial pigment (hemozoin [PfHz]) revealed that stem cell growth factor (SCGF; also called C-type lectin domain family member 11A [CLEC11A]), a hematopoietic growth factor important for development of erythroid and myeloid progenitors, was one of the most differentially expressed genes. Additional experiments with cultured peripheral blood mononuclear cells (PBMCs) demonstrated that PfHz decreased SCGF/CLEC11A transcriptional expression in a time-dependent manner. Circulating SCGF levels were then determined for Kenyan children (n = 90; aged 3 to 36 months) presenting at a rural hospital with various severities of malarial anemia. SCGF levels in circulation (P = 0.001) and in cultured PBMCs (P = 0.004) were suppressed in children with SMA. Circulating SCGF also correlated positively with hemoglobin levels (r = 0.241; P = 0.022) and the reticulocyte production index (RPI) (r = 0.280; P = 0.029). In addition, SCGF was decreased in children with reduced erythropoiesis (RPI of <2) (P < 0.001) and in children with elevated levels of naturally acquired monocytic PfHz (P = 0.019). Thus, phagocytosis of PfHz promotes a decrease in SCGF gene products, which may contribute to reduced erythropoiesis in children with SMA.

scholarly journals Lack of mortality in 22 children with sickle cell anemia and severe malarial anemia

2017 ◽  
Vol 65 (1) ◽  
pp. e26745 ◽  
Author(s):  
Robert O. Opoka ◽  
Paul Bangirana ◽  
Richard Idro ◽  
Estela Shabani ◽  
Ruth Namazzi ◽  
...  
Keyword(s):  
Sickle Cell ◽  
Sickle Cell Anemia ◽  
Severe Malarial Anemia ◽  
Malarial Anemia

scholarly journals Circulatory hepcidin is associated with the anti-inflammatory response but not with iron or anemic status in childhood malaria

Blood ◽  
2013 ◽  
Vol 121 (15) ◽  
pp. 3016-3022 ◽  
Author(s):  
Florence Burté ◽  
Biobele J. Brown ◽  
Adebola E. Orimadegun ◽  
Wasiu A. Ajetunmobi ◽  
Nathaniel K. Afolabi ◽  
...  
Keyword(s):  
Inflammatory Response ◽  
Cerebral Malaria ◽  
Severe Malaria ◽  
Severe Malarial Anemia ◽  
Key Points ◽  
Mild Malaria ◽  
Anti Inflammatory ◽  
Childhood Malaria ◽  
Malarial Anemia

Key Points Hepcidin rises more dramatically in mild malaria than in severe malaria. Hepcidin levels are linked to inflammation, not anemia, in severe malarial anemia and cerebral malaria.

scholarly journals Severe Malarial Anemia: Innate Immunity and Pathogenesis

2011 ◽  
Vol 7 (9) ◽  
pp. 1427-1442 ◽  
Author(s):  
Douglas J. Perkins ◽  
Tom Were ◽  
Gregory C. Davenport ◽  
Prakasha Kempaiah ◽  
James B. Hittner ◽  
...  
Keyword(s):  
Innate Immunity ◽  
Severe Malarial Anemia ◽  
Malarial Anemia
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