Effect of a mild infection on serum ferritin concentration—clinical and epidemiological implications

Abstract

Objectives: To study the distribution of serum ferritin concentration in adolescent boys and girls with and without a preceding mild infection. Design: The prevalence of iron de®ciency was studied in two representative samples. The ®rst sample from 1990 comprised 207 boys and 220 girls. The second sample from 1994 included 620 boys and 624 girls. In total 1675 adolescents, 15±16 y old, 827 boys and 844 girls were studied. Results: A signi®cant shift of serum ferritin concentration towards higher values was observed in those who reported an upper respiratory infection with fever during the preceding month (P`0.001). Signi®cant differences were found between serum ferritin values in healthy, not infected adolescents and serum ferritin values in those with ongoing infection, both in boys and girls in the two materials (P`0.01), and in those with a mild infection during the preceding three weeks. Conclusions:The prevalence of recent infection should be included as information when trying to assess the prevalence of iron de®ciency on the basis of serum ferritin measurements and when examining relationships between iron status and composition of the diet. The ®ndings imply that differences in prevalence of iron de®ciency between different studies might partly be explained by differences in prevalence of simple respiratory infections. The diagnostic sensitivity of the serum ferritin assay for iron de®ciency, using conventional reference limits, decreases for subjects with recent such infections; similarly, there will be a decrease in the diagnostic speci®city for haemochromatosis. Sponsorship: Swedish Medical Research Council (project B9519X-04721-20B) and Swedish Dairy Association, Stockholm. Descriptors: serum ferritin concentration; mild infection; adolescents; prevalence of iron de®ciency; diagnostic sensitivity and speci®cityairon de®ciency; iron overload

Consequences of iron depletion on health in menstruating women

“…Indeed, inflammatory or infectious events may induce high ferritin concentrations, and subjects with such high values may represent a particularly unhealthy population (Hallberg, 1995;Hulthen et al, 1998). Another limitation of our study is the low number of anemic women, 41, which is in accordance with the literature (Fogelholm et al, 1993;CDC, 1998;Galan et al, 1998) but did not enable separate analyses of the same health variables.…”

“…We then excluded women who were known to be postmenopausal (n ¼ 51) and those over 51 y of age for whom the menopausal status was unknown (n ¼ 86), since natural menopause rarely occurs before this age (Collaborative Group on Hormonal Factors in Breast Cancer, 1997). We finally excluded women with either a baseline or a 2 y ferritin concentration above 80 mg/l (n ¼ 43) in order to minimize the risk of including iron-depleted subjects who had high ferritin concentrations as a consequence of infectious or inflammatory conditions (Hallberg, 1995;Hulthen et al, 1998).…”

Determinants and characteristics of mean corpuscular volume and hemoglobin concentration in white HFE C282Y homozygotes in the hemochromatosis and iron overload screening study

“…Altogether, these observations suggest that multiple factors influence MCV and Hb in C282Y homozygotes. TfSat and SF reflect body iron stores, and also liver disease, inflammation, other tissue injury, and infection [16][17][18][19]. These observations imply that normal or elevated TfSat and SF in some subjects may be insensitive or confounded measures of the availability of iron for hemoglobin synthesis.…”

Capturing the onset of the common cold and its effects on iron absorption

“…The underlying mechanisms are reduced iron absorption from the intestinal lumen, impaired release of recycled iron from macrophages and increased iron uptake by reticuloendothelial cells. The rise in the serum ferritin concentration (S-ferritin) that occurs during inflammation and infection, is also well-known (Elin et al, 1977;Birgegard et al, 1978;Hulthen et al, 1998;Eskeland et al, 2002). The mediator responsible for the altered iron kinetics induced by infection/inflammation appears to be hepcidin, a recently discovered peptide synthesized in the liver in response to interleukin-6 (IL-6) (Kemna et al, 2005;Roy and Andrews, 2005).…”

“…Although the increase in S-ferritin remains for several weeks after recovery from infection (Hulthen et al, 1998;Eskeland et al, 2002), it also seems to be the slowest of the iron markers to respond (Birgegard et al, 1978;Eskeland et al, 2002). Despite this knowledge, the exact duration and the time course of this infection-induced alteration in iron kinetics has not been clearly established.…”