TABLE 5.
Contribution of inflammation to population estimates of micronutrient deficiency among children in rural Nepal (n = 1000)1
| Indicator | Cutoff | PRR2 | PAR (95% CI)3 | Population prevalence explained by presence of inflammation4 |
| Retinol, μmol/L | <0.7 | 3.95 | 0.484 (0.319, 0.609) | +4.1% |
| <1.05 | 1.34 | 0.098 (0.060, 0.136) | +5.4% | |
| β-Carotene, μmol/L | <0.09 | 1.27 | 0.081 (0.028, 0.130) | +3.3% |
| PLP, nmol/L | <20 | 1.40 | 0.111 (0.060, 0.160) | +4.8% |
| Folic acid, nmol/L | <13.6 | 2.32 | 0.294 (0.094, 0.450) | +1.8% |
| Ferritin, μg/L | <15 | 0.66 | −0.118 (−0.238, −0.010) | −1.2% |
| TfR, mg/L | >8.3 | 1.38 | 0.107 (0.052, 0.158) | +4.3% |
| Total circulating selenium, μmol/L | <0.89 | 1.24 | 0.070 (0.035, 0.104) | +4.2% |
| Any deficiency | ≥1 | 1.06 | 0.019 (0.008, 0.030) | +1.7% |
| Multiple deficiencies | ≥2 | 1.24 | 0.070 (0.038, 0.099) | +4.6% |
Limited to micronutrient indicators in plasma where significant differences in prevalence of deficiency by inflammatory status occurred, from Table 4. PAR, population attributable risk; PLP, pyridoxal-5′-phosphate; PRR, prevalence rate ratio; TfR, transferrin receptor.
Calculated as the prevalence of deficiency among children with inflammation divided by the prevalence in children without inflammation, from Table 4.
Calculated as Pe(PRR−1)/(Pe(PRR−1)+1), where Pe is the proportion of the population exposed to inflammation (0.316) (39, 40). 95% CIs were calculated as lower limit = 1−exp(ln(1−PAR)+1.96s); upper limit = 1−exp(ln(1−PAR)−1.96s), where “s” is calculated as the square root of [b+(a+d)PAR]/nc, and b = number with inflammation but no deficiency, a = number with inflammation and deficiency, d = number with no inflammation or deficiency, n = total number of participants, c = children with deficiency but no inflammation, according to Fleiss (40).