Erythrocyte destruction in<i>Plasmodium falciparum</i>malaria: an investigation of intravascular haemolysis

Devakul, Kanjika; Harinasuta, T; Kanakakorn, K

doi:10.1080/00034983.1969.11686632

Cited by 8 publications

(4 citation statements)

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“…A total of nine articles mentioned infection-induced haemolysis. 24–32 The types of infections reported were typhoid fever, 24 29 31 dengue infection, 25 27 28 falciparum malaria 26 and viral hepatitis. 30 One of the major complications described among patients with typhoid fever or dengue infection who also had G6PDd was acute haemolysis.…”

Section: Resultsmentioning

confidence: 99%

Systematic review of the clinical manifestations of glucose-6-phosphate dehydrogenase deficiency in the Greater Mekong Subregion: implications for malaria elimination and beyond

et al. 2017

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IntroductionTo achieve malaria elimination in the Greater Mekong Subregion (GMS) by 2030, proper case management is necessary. 8-aminoquinolines, such as primaquine, are the only available medicines effective in preventing relapse of the hypnozoite stage of Plasmodium vivax, as well as the onward transmission of Plasmodium falciparum. However, primaquine can cause haemolysis in individuals who have glucose-6-phosphate dehydrogenase deficiency (G6PDd). We conducted a systematic review on the reported clinical manifestations of G6PDd to provide a comprehensive overview of the situation in the GMS.MethodsThe protocol for this systematic review was registered on PROSPERO: International prospective register of systematic reviews (CRD42016043146). We searched the PubMed/MEDLINE, CINAHL, and Web of Science databases for published articles describing the clinical manifestations of G6PDd in the GMS. We included articles of all study designs from inception until 31 July 2016, reporting the clinical manifestations of G6PDd. We then performed a narrative synthesis of these articles.ResultsWe included 56 articles in this review, 45 of which were from Thailand. Haemolysis in G6PD-deficient individuals was caused not only by primaquine but also by other medicines and infections. Other clinical manifestations of G6PDd that were found were favism, neonatal jaundice and chronic non-spherocytic haemolytic anaemia. G6PDd also influenced the clinical presentations of genetic disorders and infections, such as thalassemia and typhoid fever.ConclusionAs G6PDd also affects the clinical presentations of other infections, the benefits of G6PD testing and proper record keeping transcend those of malaria case management. Therefore, healthcare workers at the community level should be made familiar with complications resulting from G6PDd as these complications extend beyond the scope of malaria.

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Section: Resultsmentioning

confidence: 99%

Systematic review of the clinical manifestations of glucose-6-phosphate dehydrogenase deficiency in the Greater Mekong Subregion: implications for malaria elimination and beyond

et al. 2017

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“…Both levels de-plasma Hb levels have been recorded in adults with Z? clined over 72 h. The autologous IgG eluted from 4 falciparum malaria (DEVAKUL et al, 1969). The total malaria patients with major haemolysis was blotted on amount of Hb liberated into plasma over time is not to membrane proteins containing aggregated band 3 easily determined, however, since the plasma Hb conisolated from zinc/BS3-treated RBCs.…”

Section: Increases In Bound C3c Occurred With Median Levelsmentioning

confidence: 99%

“…Intravascular destruction of infected RBCs occurs at merogony (DEVAKUL et al, 1969), and extravascular phagocytosis of infected RBCs is caused by macrophages in the spleen, liver and bone-marrow (AIKAWA et al, 1980;SEED & KREIER, 1980). Uninfected RBCs have a shortened life-span in malaria (PHILLIPS et al, 1986;L~OAREESUWAN et al, 1987) and, irrespective of how they are selected for removal, it has been generally acknowledged that their elimination occurs by ~erythrophagdcytosis (CLARK & CHAUDHRI.…”

Section: Introductionmentioning

confidence: 99%

Acute haemolysis in childhood falciparum malaria

Ekvall

Arese

Turrini

et al. 2001

Transactions of the Royal Society of Tropical Medicine and Hygi

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Acute haemolysis associated with clinical episodes of high-level Plasmodium falciparum parasitaemia was studied in 20 children from an holoendemic area (coastal Tanzania). The change in blood haemoglobin (Hb) concentration ranged from -46 to g/L during the 72-h observation period and was linearly related to maximum parasitaemia. Balance studies between loss of blood Hb, increase in plasma Hb and appearance of Hb in the urine indicated that extravascular clearance of red cells was the predominant mode of erythrocyte clearance. Most subjects, however, showed minor signs of intravascular haemolysis. The plasma Hb was << 1% of blood Hb and haemoglobinuria was detected in 14/20 children but the excretion of Hb in urine was < 0.5% of total Hb loss. Haemoglobinuria was, however, a marker of severe haemolysis, since the maximum blood Hb loss in children without haemoglobinuria was 10 g/L. Erythrocyte-bound opsonins known to induce erythrophagocytosis, i.e., complement C3c fragments and autologous IgG, were increased in all patients. In the patients with major haemolysis, the changes correlated to the haemolysis over time. Hence, a similar mechanism for predominantly extravascular erythrocyte clearance may be operative in acute malarial anaemia, normal erythrocyte senescence and other forms of acute haemolysis.

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“…Most studies of IVH in malaria have focussed on the influence of glucose 6-phosphate dehydrogenase (G6PD) [ 10 - 12 ], and the role played by antimalarial drugs such as chloroquine [ 13 , 14 ]. Mechanical trauma from a damaged endothelium, complement fixation and activation on the RBC surface, and infectious agents may cause direct membrane degradation and cell destruction [ 4 ].…”

Section: Introductionmentioning

confidence: 99%

Complement activation in Ghanaian children with severe Plasmodium falciparum malaria

Helegbe

Goka

Kurtzhals

et al. 2007

Malar J

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BackgroundSevere anaemia (SA), intravascular haemolysis (IVH) and respiratory distress (RD) are severe forms of Plasmodium falciparum malaria, with RD reported to be of prognostic importance in African children with malarial anaemia. Complement factors have been implicated in the mechanism leading to excess anaemia in acute P. falciparum infection.MethodsThe direct Coombs test (DCT) and flow cytometry were used to investigate the mean levels of RBC-bound complement fragments (C3d and C3bαβ) and the regulatory proteins [complement receptor 1 (CD35) and decay accelerating factor (CD55)] in children with discrete clinical forms of P. falciparum malaria. The relationship between the findings and clinical parameters including coma, haemoglobin (Hb) levels and RD were investigated.ResultsOf the 484 samples tested, 131(27%) were positive in DCT, out of which 115/131 (87.8%) were positive for C3d alone while 16/131 (12.2%) were positive for either IgG alone or both. 67.4% of the study population were below 5 years of age and DCT positivity was more common in this age group relative to children who were 5 years or older (Odds ratio, OR = 3.8; 95%CI, 2.2–6.7, p < 0.001). DCT correlated significantly with RD (β = -304, p = 0.006), but multiple regression analysis revealed that, Hb (β = -0.341, p = 0.012) and coma (β = -0.256, p = 0.034) were stronger predictors of RD than DCT (β = 0.228, p = 0.061). DCT was also not associated with IVH, p = 0.19, while spleen size was inversely correlated with Hb (r = -402, p = 0.001). Flow cytometry showed similar mean fluorescent intensity (MFI) values of CD35, CD55 and C3bαβ levels on the surfaces of RBC in patients and asymptomatic controls (AC). However, binding of C3bαβ correlated significantly with CD35 or CD55 (p < 0.001).ConclusionThese results suggest that complement activation contributed to anaemia in acute childhood P. falciparum malaria, possibly through induction of erythrophagocytosis and haemolysis. In contrast to other studies, this study did not find association between levels of the complement regulatory proteins, CD35 and CD55 and malarial anaemia. These findings suggest that complement activation could also be involved in the pathogenesis of RD but larger studies are needed to confirm this finding.

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Erythrocyte destruction inPlasmodium falciparummalaria: an investigation of intravascular haemolysis

Cited by 8 publications

References 3 publications

Systematic review of the clinical manifestations of glucose-6-phosphate dehydrogenase deficiency in the Greater Mekong Subregion: implications for malaria elimination and beyond

Systematic review of the clinical manifestations of glucose-6-phosphate dehydrogenase deficiency in the Greater Mekong Subregion: implications for malaria elimination and beyond

Acute haemolysis in childhood falciparum malaria

Complement activation in Ghanaian children with severe Plasmodium falciparum malaria

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