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In a cohort of term infants (n=91), followed from birth to 12 months, iron intake was examined by 24-h food records, and iron status by blood samples (haemoglobin (Hb)), mean corpuscular volume (MCV), serum values for iron, ferritin and transferrin, and erythrocyte protoporphyrin) at 2, 6 and 9 months. At 9 months of age, 5% had anaemia (Hb<105 g/l), but none had developed iron deficiency according to strict definitions used in this study (serum ferritin < 13 micrograms/l and transferrin saturation < 10%). Infants with high serum ferritin, serum transferrin and erythrocyte protoporphyrin values at one blood sampling also had high values at the following sample (tracking, r=0.45-0.80), suggesting that iron stores at delivery are an important determinant of iron stores during late infancy. Factors related to changes in serum ferritin were investigated by multiple linear regression. From 2 to 6 months, serum ferritin was negatively associated with knee-heel growth velocity (p=0.006) and positively with intake of infant formula (p=0.04). From 6 to 9 months it was negatively associated with intake of bread (p=0.001), and there was a trend for a positive association with intake of meat (p=0.07) and fish (p=0.08) and for a negative association with intake of cow's milk (p=0.07). In conclusion, those with a high growth velocity and a dietary pattern with a high intake of bread and a low intake of meat and fish had lower ferritin values and thereby an increased risk of depleting their iron stores later during infancy., Professor Gösta Samuelson samlade trycksaker; 174

Farmakologi

Udgivelsesdato: 1994-Apr, Iron status, including serum (S-) ferritin and hemoglobin (Hb) was assessed in a population survey of 469 old subjects (70 years of age; 254 men, 215 women); 7.9% of the participants had abnormal laboratory tests indicating diseases which might be connected with inappropriately high S-ferritin levels. Men had a median S-ferritin of 114 micrograms/L, 5-95 percentile 28-373 micrograms/L; 2.4% had values < 15 micrograms/L (i.e., depleted iron stores), 3.5% values from 15-30 micrograms/L (i.e., small iron stores), and 94.1% values > 30 micrograms/L (e.g., replete iron stores); 74.4% had values from 61-300 micrograms/L, and 8.7% values > 300 micrograms/L. Median Hb was 142 g/L (8.8 mmol/L), 5-95 percentile 124-158 g/L (7.7-9.8 mmol/L); Hb values < 129 g/L (8.0 mmol/L) were observed in 7.5%. Iron deficiency anemia (i.e., S-ferritin < 15 micrograms/L and Hb < 129 g/L) was seen in 0.39% of the men. Women had lower S-ferritin than men (p < 0.0001), median 81 micrograms/L, 5-95 percentile 20-273 micrograms/L; 3.3% had values < 15 micrograms/L, 9.3% values from 15-30 micrograms/L, and 87.4% values > 30 micrograms/L; 63.2% had values from 61-300 micrograms/L, and 3.7% values > 300 micrograms/L. Hb was lower in women than in men (p < 0.0001), median 132 g/L (8.2 mmol/L), 5-95 percentile 118-145 g/L (7.3-9.0 mmol/L); Hb values < 121 g/L (7.5 mmol/L) were seen in 6.5%. None of the women had iron deficiency anemia (i.e., S-ferritin < 15 micrograms/L and Hb < 121 g/L).

Udgivelsesdato: 1991-null, The distribution of HLA class II (DR, DQ, and DP) antigens was studied in 41 patients with symptomatic sarcoidosis (SA) and ethnically matched healthy controls. HLA-DR, -DQw1 and -DQw3 typings were performed with alloantisera in the conventional microcytotoxic test, whereas -DP typings were done using primed lymphocyte typing. The frequencies of DRw6 were 41.5% in SA patients and 17.9% in controls (relative risk, RR = 3.2, p = 0.00087, p less than 0.05 when corrected). DR3 was decreased to 14.6% in SA patients compared to 25.9% in controls (RR = 0.49, p = 0.07, i.e., not statistically significant). The decreased frequency of DR3 was only seen in patients with severe, long-standing disease. In contrast, the DRw6 increase was most pronounced in patients with severe disease (RR = 6.4; p = 0.003). There were no statistically significant deviations in the frequencies of DQ and DP alleles between patients and controls. In conclusion, our data suggest that DRW6 confers susceptibility and DR3 resistance to severe, long-standing disease.