Women of childbearing age are at risk of Fe deficiency if insufficient dietary Fe is available to replace menstrual and other Fe losses. Haem Fe represents 10 -15 % of dietary Fe intake in meat-rich diets but may contribute 40 % of the total absorbed Fe. The aim of the present study was to determine the relative effects of type of diet and menstrual Fe loss on Fe status in women. Ninety healthy premenopausal women were recruited according to their habitual diet: red meat, poultry/fish or lacto-ovo-vegetarian. Intake of Fe was determined by analysing 7 d duplicate diets, and menstrual Fe loss was measured using the alkaline haematin method. A substantial proportion of women (60 % red meat, 40 % lacto-ovo-vegetarian, 20 % poultry/fish) had low Fe stores (serum ferritin ,10 mg/l), but the median serum ferritin concentration was significantly lower in the red meat group (6·8 mg/l (interquartile range 3·3, 16·25)) than in the poultry/fish group (17·5 mg/l (interquartile range 11·3, 22·4) (P,0·01). The mean and standard deviation of dietary Fe intake were significantly different between the groups (P¼ 0·025); the red meat group had a significantly lower intake (10·9 (SD 4·3) mg/d) than the lacto-ovo-vegetarians (14·5 (SD 5·5) mg/d), whereas that of the poultry/fish group (12·8 (SD 5·1) mg/d) was not significantly different from the other groups. There was no relationship between total Fe intake and Fe status, but menstrual Fe loss (P¼ 0·001) and dietary group (P¼ 0·040) were significant predictors of Fe status: poultry/fish diets were associated with higher Fe stores than lacto-ovo-vegetarian diets. Identifying individuals with high menstrual losses should be a key component of strategies to prevent Fe deficiency.

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59 patients with active pulmonary tuberculosis were evaluated in terms of haematological indices, iron‐related measurements and markers of inflammation. The variables evaluated included the Hb, mean cell volume (MCV), serum iron, total iron‐binding capacity, percentage saturation, serum ferritin, erythrocyte sedimentation rate (ESR) and C‐reactive protein. In addition, marrow iron stores were assessed both histologically and chemically. Among the changes noted was a raised S‐Ferritin, which appeared in part to be a component of the acute phase response, since it correlated with C‐reactive protein concentration (r 0.59, p < 0.0001). In addition, there was a good correlation between the S‐Ferritin and the concentrations of non‐haem iron in the marrow, as assessed chemically on trephine biopsies (r 0.78, p < 0.0001) and histologically on aspirated and biopsy material (rs 0.78, p < 0.0001 and rs 0.68, p < 0.0001, respectively). Furthermore, the quantitative relationship between the S‐Ferritin and the chemical concentrations of non‐haem iron in the marrow was similar to that found previously in a heterogeneous group of subjects without infections. While the present findings confirm that iron is diverted into reticuloendothelial stores in active pulmonary tuberculosis, no evidence was found to suggest that the anaemia which was present in 45 of the 59 patients was secondary to iron‐deficient erythropoiesis; the percentage saturations in the 2 groups were 30.3 and 31.1 respectively. In a final analysis, the present findings were compared with previous ones obtained in a group of patients with Hodgkin's disease. The degree of rise in the S‐Ferritin for a given marrow non‐haem iron concentration was significantly less in the patients with tuberculosis (p < 0.0001).

Two patients with acute blastic transformation of chronic myeloid leukemia (CML) associated with strikingly elevated platelet counts showed abnormalities of chromosome 3q in addition to the standard Philadelphia (Ph1) chromosome translocation. The first patient had an inversion of chromosome 3 (q21q26) cytologically identical to an inversion 3 previously reported in de novo acute megakaryoblastic leukemia, and the second patient showed a translocation between chromosome 3q and the chromosome 9 homologue not involved in the Ph1 translocation, [t(3;9)(q21;q34)]. Previous studies had incriminated either 3q21 or 3q26 as the locus for a regulatory thrombopoietic gene, but the current study suggests that 3q21 is the relevant site.