An 8-week course of 45 mg of carbonyl iron daily reduces iron deficiency in female whole blood donors aged 18 to 45 years: results of a prospective randomized controlled trial.

BACKGROUND: Blood donation is known to contribute to iron deficiency in regular blood donors. This study investigated the safety and efficacy of postdonation iron replacement to mitigate iron deficiency in blood donors. STUDY DESIGN AND METHODS: A total of 282 female whole blood donors aged 18 to 45 were prospectively randomized in a double-blinded placebo controlled trial to receive an 8-week postdonation course of carbonyl iron (45 mg daily) or placebo. The primary endpoint was prevalence of iron deficiency (ferritin < 15 ng/mL) at 12 weeks postdonation. Secondary endpoints were eligibility to donate based on capillary hemoglobin (Hb) and incidence of gastrointestinal (GI) complaints. RESULTS: Ferritin levels at Week 12 were significantly higher in donors receiving carbonyl iron (17.0 ± 10.9 ng/mL) compared with those receiving placebo (10.6 ± 8.4 ng/mL; p < 0.001). The proportion of iron-deficient donors was significantly lower in the carbonyl iron group (51.9%) compared to the placebo (80.5%; p < 0.001). The mean Hb level in the carbonyl iron group (134.6 ± 8.7 g/L) was significantly higher than in the placebo arm (130.0 ± 9.9 g/L; p < 0.001), significantly improving eligibility to donate at Week 12. Significantly more donors receiving carbonyl iron had at least one GI side effect (p < 0.001). Importantly, 86.7% of donors receiving carbonyl iron indicated that they would take iron on an ongoing basis. CONCLUSION: An 8-week postdonation course of 45 mg of carbonyl iron significantly reduced iron deficiency and was well tolerated in female whole blood donors. Postdonation iron replacement may have a role in a broader strategy to optimize donor iron status.

Iron status and dietary iron intake of female blood donors.

BACKGROUND: The aim was to assess iron status and dietary iron intake in a sample of premenopausal female regular and new blood donors. STUDY DESIGN AND METHODS: Premenopausal women blood donors were invited to participate. Blood samples were analyzed for serum ferritin and hemoglobin. An iron checklist assessed dietary iron intake. Donors were classified as regular donors or new donors. RESULTS: Twenty-one new donors (mean [SD] age, 28.6 [6.0] years; body mass index [BMI], 25.6 [4.5] kg/m(2) ) and 172 regular donors (mean age, 29.4 [5.5] years; BMI, 24.7 [3.8] kg/m(2) ) participated. Fifty percent of regular donors and 24% of new donors had depleted iron stores (serum ferritin <15 µg/L; difference p = 0.036). Dietary iron intake was higher in regular donors (mean [SE], 12.6 [0.7] mg/day) compared to new donors (9.9 [0.4] mg/day; p = 0.006). Eighty-five percent of regular donors and 79% of new donors met the estimated average requirement for iron. CONCLUSIONS: Despite the fact that most of these donors had an adequate dietary iron intake, more than half of the blood donors had depleted iron stores. Increasing dietary iron intake through supplements and/or dietary means is expected to be necessary to maintain adequate iron status in this group.

A prospective trial assessing the safety and efficacy of collecting up to 840 mL of plasma in conjunction with saline infusion during plasmapheresis.

BACKGROUND: The demand for plasma for manufacturing intravenous immunoglobulin and other plasma derivatives is increasing. A prospective study was conducted to determine whether up to 840 mL of plasma could be safely and effectively collected in conjunction with saline infusion during plasmapheresis. STUDY DESIGN AND METHODS: Ninety-one plasma donors were enrolled in a modified 3 × 3 crossover study to assess the equivalence of three plasma collection methods: 750 mL of plasma with no saline (control, Method 1), 840 mL of plasma with a 250-mL saline infusion during and at the end of the donation (Method 2), and 800 mL of plasma with a 500-mL saline infusion at the end of the donation (Method 3). The primary efficacy endpoint was the total protein concentration of the collected plasma. Secondary efficacy endpoints were immunoglobulin (Ig)G and Factor (F)VIII plasma concentration and donors' acceptance of the new procedures. Safety was determined from the adverse event (AE) rate. RESULTS: The total protein, IgG, and FVIII concentrations in plasma collected under Methods 2 and 3 were significantly lower than those in plasma collected under Method 1 (p < 0.0001). These variables were also significantly lower in plasma collected under Method 2 compared to Method 3. During the study, 75 AEs were recorded, 73 of which were mild to moderate. Significantly more donors (31%) preferred Method 2 compared to Method 3 (p = 0.006). CONCLUSIONS: Saline infusion during plasmapheresis led to hemodilution of plasma proteins. However, the benefits to donor safety and satisfaction are compelling reasons to implement saline infusion during plasmapheresis.

Understanding decision and enabling factors influencing clinical trial participation in Australia: a view point.

Understanding patient decision making with respect to clinical trial participation has the potential to improve both the efficiency of recruitment for clinical trials and their management. In this mini-review we consider 3 key factors influencing clinical trial recruitment outcomes that include; 1) patient personal characteristics, 2) enabling factors that involve patient centered attitudes or circumstances, and 3) aversion. These factors are explored across both Australian rural and urban settings and contrasted to reported outcomes from research across other countries. Australia has the lowest number of publications on rural clinical trial participation when compared to rural research in America and Canada. Across Australian urban areas where all 3 factors have been studied, trends are similar to those reported in other developed countries. In conclusion we suggest that trial participation could be improved if participants are better informed about a trial as this is a valuable factor to enable recruitment.

Mechanism for the inhibition of transglutaminase 2 by cystamine.

Cystamine is neuroprotective in a number of models of neurodegeneration. The therapeutic benefit of cystamine has been attributed, in part, to its inhibition of transglutaminase activity. Cystamine [beta-mercaptoethanolamine (MEA) disulfide] is reduced within cells to MEA which is largely responsible for the in vivo effects of its disulfide precursor. In the current study, the amine group of MEA was shown to act as a transglutaminase (TG) substrate resulting in the formation of N(beta)-(gamma-l-glutamyl)-MEA bonds. The formation of such bonds would compete with the generation of other TG-catalyzed reactions that may contribute to neurodegeneration such as polyamination, protein cross-linking, deamination and the covalent attachment of ceramide to proteins. The demonstration that cystamine-derived MEA can form N(beta)-(gamma-l-glutamyl)-MEA bonds offers a unique tool for identifying the TG substrates that occur in diseased brains in vivo. Structure-function studies also indicated that the mercapto group of MEA significantly influences the substrate behavior of this compound. These structure-function studies also identified the following hierarchy of physico-chemical characteristics: hydrophobicity > S as the group VIII atom > distance separating the N and group VIII atom, as the major determinants contributing to the substrate behavior for low-molecular weight amine substrates of TG 2.