In the present paper biomarkers of micronutrient status in childhood and some of the factors influencing them, mainly dietary intake, requirements and inflammation will be examined. On a body-weight basis the micronutrient requirements of children are mostly higher than those of an adult, but most biomarkers of status are not age-related. A major factor that is often overlooked in assessing status is the influence of subclinical inflammation on micronutrient biomarkers. In younger children particularly the immune system is still developing and there is a higher frequency of sickness than in adults. The inflammatory response rapidly influences the concentration in the blood of several important micronutrients such as vitamin A, Fe and Zn, even in the first 24 h, whereas dietary deficiencies can be envisaged as having a more gradual effect on biomarkers of nutritional status. The rapid response to infection may be for protective reasons, i.e. conservation of reserves, or by placing demands on those reserves to mount an effective immune response. However, because there is a high prevalence of disease in many developing countries, an apparently-healthy child may well be at the incubation stage or convalescing when blood is taken for nutritional assessment and the concentration of certain micronutrient biomarkers will not give a true indication of status. Most biomarkers influenced by inflammation are known, but often they are used because they are convenient or cheap and the influence of subclinical inflammation is either ignored or overlooked. The objective of the present paper is to discuss: (1) some of the important micronutrient deficiencies in childhood influenced by inflammation; (2) ways of correcting the interference from inflammation.

Inflammation influences the assessment of nutritional status. For example, inflammation reduces plasma retinol concentrations and vitamin A deficiency is overestimated. Conversely inflammation increases plasma ferritin concentrations and Fe deficiency is underestimated. Blood samples were obtained from 163 free-living HIV-1-infected adults, not on continuous medication, anti-retroviral drugs or micronutrients, not unwell and who had not reached WHO stage IV of HIV/AIDS. We used four markers of inflammation, C-reactive protein (CRP), a1-acid glycoprotein (AGP), a1-antichymotrypsin and erythrocyte sedimentation rate but mainly CRP and AGP were used to separate the subjects into four groups: 'healthy' where both CRP and AGP were normal; 'incubation phase' where CRP was elevated; 'early convalescence' where AGP and CRP were elevated and 'late convalescence' where only AGP was elevated. Correction factors were calculated to remove the influence of inflammation from each biomarker and group where inflammation was present and the data are shown before and after recalculation. The correction increased median plasma retinol concentrations of the whole group from 1·16 to 1·33 mmol/l, comparable with values (mean 1·29 mmol/l) in HIV-negative Kenyan women. Median ferritin concentrations fell by about 50 % in both sexes and the number of women with plasma ferritin concentrations #12 mg/l increased from eleven to twenty. The correction also increased plasma carotenoids and Hb but not a-tocopherol concentrations. We suggest that the method described to remove the influence of inflammation from nutritional biomarkers should be generally applicable in apparently healthy people and prevents discarding valuable data because of mild inflammation. The method does now need to be tested in other populations.

Hemoglobin and ferritin are important biomarkers of iron status but are both altered by inflammation. We used the inflammation biomarkers C-reactive protein (CRP) and alpha1-acid glycoprotein (AGP) to adjust hemoglobin and ferritin concentrations to clarify interpretation of iron status. Apparently healthy adults who tested positive twice for HIV but who had not reached stage IV or clinical AIDS were randomly allocated to receive a food supplement (n = 17 and 21) or the food plus a micronutrient capsule (MN; 10 men and 34 women, respectively) containing 30 mg iron/d. Hemoglobin, ferritin, CRP, and AGP concentrations were measured at baseline and 3 mo and subjects were divided into 4 groups (reference, no inflammation; incubating, raised CRP; early convalescence, raised AGP and CRP; and late convalescence, raised AGP). Correction factors (the ratios of the median for the reference group over each inflammatory group) improved the consistency of the ferritin but not the hemoglobin results. After correction, ferritin (but not hemoglobin) increased in both men (48 microg/L; P = 0.02) and women (12 microg/L; P = 0.04) who received MN but not in the food-only group. However, hemoglobin did improve in subjects who showed no inflammation both at baseline and mo 3 (P = 0.019), but ferritin did not increase in this group. In conclusion, ferritin concentrations were more closely linked to current inflammation than hemoglobin; hence, correction by inflammation biomarkers improved data consistency. However, low hemoglobin concentrations were the consequence of long-term chronic inflammation and improvements in response to MN supplements were only detected in subjects with no inflammation.

Inflammation seems to block any increase in plasma zinc after MN supplement and it is important to identify those without inflammation to determine the effectiveness of a zinc supplementation program.

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