Maternal malaria status and metabolic profiles in pregnancy and in cord blood: relationships with birth size in Nigerian infants

Ayoola, Oluwagbemiga Oluwole; Whatmore, Andrew; Balogun, Williams; Jarrett, Olatokunbo Olumide; Cruickshank, J.; Clayton, Peter E.

doi:10.1186/1475-2875-11-75

Cited by 30 publications

(37 citation statements)

References 47 publications

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“…A low fetal/placental weight ratio is a marker of placental insufficiency and has been associated with malaria [9], [31], [32] and PM with IV cases had lower fetal/placental weight ratio than uninfected controls (p = 0.036). For a number of amino acids, cord concentration was positively correlated with fetal/placental weight ratio, either among all PM cases or for those with IV (Table 3).…”

Section: Resultsmentioning

confidence: 99%

Plasmodium falciparum Malaria Elicits Inflammatory Responses that Dysregulate Placental Amino Acid Transport

et al. 2013

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Placental malaria (PM) can lead to poor neonatal outcomes, including low birthweight due to fetal growth restriction (FGR), especially when associated with local inflammation (intervillositis or IV). The pathogenesis of PM-associated FGR is largely unknown, but in idiopathic FGR, impaired transplacental amino acid transport, especially through the system A group of amino acid transporters, has been implicated. We hypothesized that PM-associated FGR could result from impairment of transplacental amino acid transport triggered by IV. In a cohort of Malawian women and their infants, the expression and activity of system A (measured by Na+-dependent 14C-MeAIB uptake) were reduced in PM, especially when associated with IV, compared to uninfected placentas. In an in vitro model of PM with IV, placental cells exposed to monocyte/infected erythrocytes conditioned medium showed decreased system A activity. Amino acid concentrations analyzed by reversed phase ultra performance liquid chromatography in paired maternal and cord plasmas revealed specific alterations of amino acid transport by PM, especially with IV. Overall, our data suggest that the fetoplacental unit responds to PM by altering its placental amino acid transport to maintain adequate fetal growth. However, IV more profoundly compromises placental amino acid transport function, leading to FGR. Our study offers the first pathogenetic explanation for FGR in PM.

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Section: Resultsmentioning

confidence: 99%

Plasmodium falciparum Malaria Elicits Inflammatory Responses that Dysregulate Placental Amino Acid Transport

et al. 2013

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“…Parity also affects the risk of malaria as primigravidae are at higher risk than multigravidae,18–20, 23–24 though less in low transmission settings,15 while in epidemic areas, the risk is not affected by parity 25. Most of the available data on malaria relate to the second and third trimesters 12, 19, 26–27. The peak of malaria prevalence seems to occur during the second trimester 28.…”

Section: Introductionmentioning

confidence: 99%

“…Where transmission is stable, such as in most of sub-Saharan Africa, most infections are asymptomatic but increase substantially the risk of anaemia 19,26,30–31. This occurs over a background of physiological anaemia of pregnancy due to increased blood volume.…”

Section: Introductionmentioning

confidence: 99%

“…Malaria increases the risk of low birth weight (LBW),19,23,30,49–51 particularly in primigravidae, and this risk seems to be higher for infections in first or second trimester,23–24,30,49 though in one study this was true also for infections occurring late in pregnancy 49. In high malaria transmission settings, such an effect is due to intrauterine growth retardation (IUGR) rather than pre-term delivery, as most infections are asymptomatic.…”

Section: Introductionmentioning

confidence: 99%

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Malaria in Pregnancy

Takem¹,

D’Alessandro

2013

Mediterr J Hematol Infect Dis

133

102

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Pregnant women have a higher risk of malaria compared to non-pregnant women. This review provides an update on knowledge acquired since 2000 on P. falciparum and P.vivax infections in pregnancy. Maternal risk factors for malaria in pregnancy (MiP) include low maternal age, low parity, and low gestational age. The main effects of MIP include maternal anaemia, low birth weight (LBW), preterm delivery and increased infant and maternal mortality.P. falciparum infected erythrocytes sequester in the placenta by expressing surface antigens, mainly variant surface antigen (VAR2CSA), that bind to specific receptors, mainly chondroitin sulphate A. In stable transmission settings, the higher malaria risk in primigravidae can be explained by the non-recognition of these surface antigens by the immune system. Recently, placental sequestration has been described also for P.vivax infections. The mechanism of preterm delivery and intrauterine growth retardation is not completely understood, but fever (preterm delivery), anaemia, and high cytokines levels have been implicated.Clinical suspicion of MiP should be confirmed by parasitological diagnosis. The sensitivity of microscopy, with placenta histology as the gold standard, is 60% and 45% for peripheral and placental falciparum infections in African women, respectively. Compared to microscopy, RDTs have a lower sensitivity though when the quality of microscopy is low RDTs may be more reliable. Insecticide treated nets (ITN) and intermittent preventive treatment in pregnancy (IPTp) are recommended for the prevention of MiP in stable transmission settings. ITNs have been shown to reduce malaria infection and adverse pregnancy outcomes by 28–47%. Although resistance is a concern, SP has been shown to be equivalent to MQ and AQ for IPTp. For the treatment of uncomplicated malaria during the first trimester, quinine plus clindamycin for 7 days is the first line treatment and artesunate plus clindamycin for 7 days is indicated if this treatment fails; in the 2nd and 3rd trimester first line treatment is an artemisinin-based combination therapy (ACT) known to be effective in the region or artesunate and clindamycin for 7 days or quinine and clindamycin. For severe malaria, in the second and third trimester parenteral artesunate is preferred over quinine. In the first trimester, both artesunate and quinine (parenteral) may be considered as options. Nevertheless, treatment should not be delayed and should be started immediately with the most readily available drug.

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“…Controversial data are reported concerning total cholesterol and triglyceride levels during plasmodial infection; hypocholesterolemia and hypercholesterolemia are reported during the acute phase of the infection; hypertriglyceridemia is often described during the first two weeks of the infection (Parola et al, 2004;Ayoola et al, 2012). However, very few studies have examined the in vivo relationships between the levels of these lipids and the factors implicated in the pathophysiology of clinical malaria.…”

Section: Introductionmentioning

confidence: 99%

Altered total cholesterol and triglyceride levels during the course of Plasmodium falciparum infection in children

Bouyou-Akotet¹,

Mboumba²,

Guiyedi³

et al. 2014

J. Parasitol. Vector Biol.

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Changes of lipid parameter concentrations are observed in patients suffering from malaria. However, there are few data on their evolution during the course of the infection and their relationship with the infection parameters. The levels of triglycerides (TG) and total cholesterol (TC) were measured during and after uncomplicated Plasmodium falciparum malaria in 122 children. The relationship with the antimalarial drug treatment, the parasite density and haemoglobin levels was also assessed. Mean TG levels were high before the treatment (1.9 ± 1.2 mmol/L) and at day 3 post-treatment (2.3 ± 1.3 mmol/L), then subsequently decreased to reach normal level from day 7. A negative correlation was found between haemoglobin (Hb) levels and TG (rho = -0.47; p < 0.01); previous high parasitaemia at inclusion was associated with a subsequent increase of TG levels after treatment administration. The majority of patients with hypertriglyceridemia were anaemic at day 3 (n = 20/20) and at day 7 (n = 18/19). Only 5 (4.1%) patients had hypertriglyceridemia at day 28. A trend toward a negative correlation between TC levels and parasite density was observed (rho = -0.18; p = 0.05). Mean TC concentration was significantly lower at day 0 when all the patients were parasitaemic (3.0 ± 1.0 mmol/L) compared to day 3 (3.7 ± 1.2 mmol/L) (p = 0.01). Mean CT was low during the first week and at day 28, 71 (58.2%) children still had a subnormal CT levels. No relationship was found with the type of antimalarial drug. Transient hypertriglyceridemia and hypocholesterolemia are observed during the course of P. falciparum infection. High TG levels seem to be related to the malaria related haemolysis.

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Maternal malaria status and metabolic profiles in pregnancy and in cord blood: relationships with birth size in Nigerian infants

Cited by 30 publications

References 47 publications

Plasmodium falciparum Malaria Elicits Inflammatory Responses that Dysregulate Placental Amino Acid Transport

Plasmodium falciparum Malaria Elicits Inflammatory Responses that Dysregulate Placental Amino Acid Transport

Malaria in Pregnancy

Altered total cholesterol and triglyceride levels during the course of Plasmodium falciparum infection in children

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