IntroductionHeightened awareness in recent years of the adverse consequences of iron deficiency has prompted renewed efforts to reduce the prevalence of this common micronutrient insufficiency. One of the main reasons for the limited success of programs to combat iron deficiency is the continuing uncertainty about the optimal epidemiologic approach for identifying it and for measuring its severity. The inadequacy of anemia surveys is reflected in the wide-ranging estimates by various expert committees of the global prevalence of iron deficiency. In a 1985 World Health Organization (WHO) report, it was estimated that 15% to 20% of the world's population had iron deficiency anemia. 1 Despite the lack of new prevalence data, estimates of the global prevalence of iron deficiency anemia have increased to more than two thirds of the world population. 2 More reliable methods to assess iron status are needed to determine the prevalence of iron deficiency and the impact of iron supplementation and fortification trials.In the present article, a new method is described for assessing iron status based on the quantitative measurement of body iron. The method has been used to examine the iron status in a consensus sample of adult men and women in the United States and of pregnant women in Jamaica. The usefulness of the method has been further evaluated by measuring the absorption of added iron in a supplementation trial in pregnant women and a food fortification trial in anemic women. Materials and methods Estimation of body ironMeasurements of body iron were based on a prior study in which serial measurements of serum ferritin and serum transferrin receptor (sTfR) were obtained during repeated phlebotomies in 14 healthy control subjects. 3 Phlebotomy was discontinued when the baseline hemoglobin concentration in each subject had fallen by 20 g/L and remained so for 3 weeks without further bleeding. The amount of storage iron at baseline was calculated from the amount of hemoglobin iron removed to reduce the serum ferritin concentration to less than 12 g/L. Body iron was then calculated from the hemoglobin iron removed at each bleeding after correction for the absorption of dietary iron. A close linear relationship was demonstrated between the logarithm of the concentrations in micrograms per liter, of serum transferrin receptor/serum ferritin (R/F ratio), and of body iron expressed as milligram per kilogram body weight (Figure 1). The latter is expressed as the iron surplus in stores (positive value) or the iron deficit in tissues (negative value). Body iron was calculated from the R/F ratio as follows: body iron (mg/kg) ϭ Ϫ[log(R/F ratio) Ϫ 2.8229]/0.1207. SurveysData from 3 published studies were used to evaluate quantitative measurements of body iron. The largest data set was a convenience sample collected in the third National Health and Nutrition Examination Survey (NHANES III) in the US population from 1988 to 1994. 4 The sample differed from the full NHANES III sample in that it was not selected to represent the US po...

BACKGROUNDAlthough induction chemotherapy results in remission in many older patients with acute myeloid leukemia (AML), relapse is common and overall survival is poor. METHODSWe conducted a phase 3, randomized, double-blind, placebo-controlled trial of the oral formulation of azacitidine (CC-486, a hypomethylating agent that is not bioequivalent to injectable azacitidine), as maintenance therapy in patients with AML who were in first remission after intensive chemotherapy. Patients who were 55 years of age or older, were in complete remission with or without complete blood count recovery, and were not candidates for hematopoietic stem-cell transplantation were randomly assigned to receive CC-486 (300 mg) or placebo once daily for 14 days per 28-day cycle. The primary end point was overall survival. Secondary end points included relapse-free survival and health-related quality of life. RESULTSA total of 472 patients underwent randomization; 238 were assigned to the CC-486 group and 234 were assigned to the placebo group. The median age was 68 years (range, 55 to 86). Median overall survival from the time of randomization was significantly longer with CC-486 than with placebo (24.7 months and 14.8 months, respectively; P<0.001). Median relapse-free survival was also significantly longer with CC-486 than with placebo (10.2 months and 4.8 months, respectively; P<0.001). Benefits of CC-486 with respect to overall and relapse-free survival were shown in most subgroups defined according to baseline characteristics. The most common adverse events in both groups were grade 1 or 2 gastrointestinal events. Common grade 3 or 4 adverse events were neutropenia (in 41% of patients in the CC-486 group and 24% of patients in the placebo group) and thrombocytopenia (in 22% and 21%, respectively). Overall health-related quality of life was preserved during CC-486 treatment. CONCLUSIONSCC-486 maintenance therapy was associated with significantly longer overall and relapse-free survival than placebo among older patients with AML who were in remission after chemotherapy. Side effects were mainly gastrointestinal symptoms and neutropenia. Quality-of-life measures were maintained throughout treatment.