Ceived and designed the experiments: XZ. Performed the experiments: TH. Analyzed

Ceived and designed the experiments: XZ. Performed the experiments: TH. Analyzed the data: XZ TH. Contributed reagents/materials/analysis tools: XZ. Wrote the paper: TH XZ.
Iron deficiency (ID) is the most common and widespread nutrient deficiency, affecting approximately two billion people worldwide and resulting in over 500 million cases of anaemia [1,2]. In sub-Saharan Africa, the Licochalcone A web prevalence of iron-deficiency anaemia (IDA) is estimated around 60 [1,2], with 40 to 50 of children under five years of age in developing countries being iron deficient [3]. ID has been estimated to cause around 800,000 deaths and 35,057,000 disability adjusted life years lost annually [2], with the greatest toll in South-East Asia and Africa [1,4]. By six months of age there is a physiological depletion of the iron stores that were accumulated by the foetus in the last months of pregnancy. If the infant’s diet does not provide enough iron, there is a significant risk to develop IDA. This physiological iron deficiency is often exacerbated by the early introduction of weaning foods [4], that frequently contain iron absorption inhibitors [5]. Iron deficiency may also be worsened by intestinalchronic blood loss from intestinal parasitic infections [3,6]. All these determinants are frequent in developing countries, leading to a prevalence of ID that may reach more than 30 by 12 months of age [7]. Because IDA tends to develop slowly, adaptation occurs and the disease can go unrecognized for long periods, yet having an important impact on the children’s physical and cognitive development [8]. The controversy around the risk-benefit ratio of giving iron supplements to individuals exposed to malaria is still unresolved [9,10]. While a recent Cochrane review on this issue concluded that “iron supplementation does not adversely affect children living in malaria-endemic areas and should not be withheld from them” [11], the current WHO guidelines on iron supplementation to children exposed to malaria and high prevalence of infections recommend “against universal iron supplementation for children under the age of two years living in malaria-endemic areas” [12,13]. Moreover, screening to identify iron-deficient children isIron Deficiency Tubastatin A custom synthesis Diagnosis and InfectionsTable 1. Demographic and clinical characteristics of the study participants.Table 2. Proportion of children classified as iron deficient using internationally accepted cut-off values of iron markers.Characteristics Age (months)* Gender Male Female Fever Wasted (WAZ,22) Stunted (HAZ,22) (n = 179) Haemoglobin* Degree of anaemia Moderate Severe Very severe Inflammation (n = 176) P. falciparum (n = 170) Clinical Malaria (n = 170) HIV (n = 164) Parvovirus B19 Epstein-Barr virus Bacteraemia (n = 173) a-Thalassaemia (n = 41) Bone marrow iron content Absent Diminished Normal IncreasedResult 22.06 (13.67) 102 (57 ) 78 (43 ) 163 (91 ) 88 (49 ) 56 (31 ) 7.73 (1.97) 119 (66 ) 45 (25 ) 16 (9 ) 155 (88 ) 74 (44 ) 73 (43 ) 40 (24 ) 15 (8 ) 56 (31 ) 13 (8 ) 32 (78 ) 54 (30 ) 90 (50 ) 14 (8 ) 22 (12 ) Iron marker Ferritin (ng/ml) Ferritin (ng/ml) by CRP CRP,1 mg/dl CRP 1 mg/dl Ferritin (ng/ml) by age 3? months .5 months sTfR (mg/l) TfR-F index TfR-F index by CRP CRP,1 mg/dl CRP 1 mg/dl Plasma iron (mg/dl) Transferrin (g/l) Transferrin saturation ( ) TIBC (mg/l) MCHC (g/dl)* MCV (fl) by age ,2 years 2 years Obs. 173 173 21 152 173 6 167 163 163 163 1407003 17 146 176 176 176 176 173 174 110 64 70?1 73?9 #1.5 #0.8 22?50 2.0?.85 16?5.Ceived and designed the experiments: XZ. Performed the experiments: TH. Analyzed the data: XZ TH. Contributed reagents/materials/analysis tools: XZ. Wrote the paper: TH XZ.
Iron deficiency (ID) is the most common and widespread nutrient deficiency, affecting approximately two billion people worldwide and resulting in over 500 million cases of anaemia [1,2]. In sub-Saharan Africa, the prevalence of iron-deficiency anaemia (IDA) is estimated around 60 [1,2], with 40 to 50 of children under five years of age in developing countries being iron deficient [3]. ID has been estimated to cause around 800,000 deaths and 35,057,000 disability adjusted life years lost annually [2], with the greatest toll in South-East Asia and Africa [1,4]. By six months of age there is a physiological depletion of the iron stores that were accumulated by the foetus in the last months of pregnancy. If the infant’s diet does not provide enough iron, there is a significant risk to develop IDA. This physiological iron deficiency is often exacerbated by the early introduction of weaning foods [4], that frequently contain iron absorption inhibitors [5]. Iron deficiency may also be worsened by intestinalchronic blood loss from intestinal parasitic infections [3,6]. All these determinants are frequent in developing countries, leading to a prevalence of ID that may reach more than 30 by 12 months of age [7]. Because IDA tends to develop slowly, adaptation occurs and the disease can go unrecognized for long periods, yet having an important impact on the children’s physical and cognitive development [8]. The controversy around the risk-benefit ratio of giving iron supplements to individuals exposed to malaria is still unresolved [9,10]. While a recent Cochrane review on this issue concluded that “iron supplementation does not adversely affect children living in malaria-endemic areas and should not be withheld from them” [11], the current WHO guidelines on iron supplementation to children exposed to malaria and high prevalence of infections recommend “against universal iron supplementation for children under the age of two years living in malaria-endemic areas” [12,13]. Moreover, screening to identify iron-deficient children isIron Deficiency Diagnosis and InfectionsTable 1. Demographic and clinical characteristics of the study participants.Table 2. Proportion of children classified as iron deficient using internationally accepted cut-off values of iron markers.Characteristics Age (months)* Gender Male Female Fever Wasted (WAZ,22) Stunted (HAZ,22) (n = 179) Haemoglobin* Degree of anaemia Moderate Severe Very severe Inflammation (n = 176) P. falciparum (n = 170) Clinical Malaria (n = 170) HIV (n = 164) Parvovirus B19 Epstein-Barr virus Bacteraemia (n = 173) a-Thalassaemia (n = 41) Bone marrow iron content Absent Diminished Normal IncreasedResult 22.06 (13.67) 102 (57 ) 78 (43 ) 163 (91 ) 88 (49 ) 56 (31 ) 7.73 (1.97) 119 (66 ) 45 (25 ) 16 (9 ) 155 (88 ) 74 (44 ) 73 (43 ) 40 (24 ) 15 (8 ) 56 (31 ) 13 (8 ) 32 (78 ) 54 (30 ) 90 (50 ) 14 (8 ) 22 (12 ) Iron marker Ferritin (ng/ml) Ferritin (ng/ml) by CRP CRP,1 mg/dl CRP 1 mg/dl Ferritin (ng/ml) by age 3? months .5 months sTfR (mg/l) TfR-F index TfR-F index by CRP CRP,1 mg/dl CRP 1 mg/dl Plasma iron (mg/dl) Transferrin (g/l) Transferrin saturation ( ) TIBC (mg/l) MCHC (g/dl)* MCV (fl) by age ,2 years 2 years Obs. 173 173 21 152 173 6 167 163 163 163 1407003 17 146 176 176 176 176 173 174 110 64 70?1 73?9 #1.5 #0.8 22?50 2.0?.85 16?5.

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