Patients with chronic inflammatory conditions including chronic kidney disease (CKD) and heart failure (HF) are undertreated with iron-deficiency anemia (IDA). Progressive inflammation and reduced iron transport associated with CKD and HF may reduce the efficacy of oral iron therapy. Oral ferric citrate improves anemia markers in CKD, but its effects in patients with CKD and concomitant HF have not been described. Patients with CKD not on dialysis and IDA from a phase 2 and 3 trial were treated with ferric citrate (n = 190) or placebo (n = 188); patients with HF were identified from medical histories. Hemoglobin response was defined as a ≥10.0-g/L increase in hemoglobin. Changes in hemoglobin, transferrin saturation, ferritin, and serum phosphate from baseline to week 12 and the incidence of adverse events potentially related to HF were evaluated. HF was reported in 22% (n = 81) of patients. The proportion of patients with hemoglobin response to ferric citrate treatment did not significantly differ in patients with and without HF (43% vs 49%, respectively; p = 0.47); changes from baseline in hemoglobin, iron parameters, and serum phosphate were similar. Adverse events potentially related to HF were noted more frequently in patients with HF (ferric citrate, 23%; placebo, 17%) versus those without HF (ferric citrate, 12%; placebo, 11%). In conclusion, these results indicate a potential role for ferric citrate in the treatment of IDA in patients with CKD not on dialysis and concomitant HF.
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http://dx.doi.org/10.1016/j.amjcard.2018.04.062 | DOI Listing |
J Hazard Mater
December 2024
State Key Laboratory of Biogeology and Environmental Geology, School of Environmental Studies, China University of Geosciences, Wuhan 430078, China. Electronic address:
Petroleum hydrocarbon contamination, such as n-alkanes, poses a significant global threat to ecosystems and human health. Microbial remediation emerges as a promising strategy for addressing this issue through both aerobic and anaerobic processes. Notably, the majority of anaerobic hydrocarbon degraders identified to date are Gram-negative bacteria.
View Article and Find Full Text PDFInt J Hematol
December 2024
Department of Hematology, Juntendo University Graduate School of Medicine, 2-1-1, Hongo, Bunkyo-Ku, Tokyo, 113-8421, Japan.
We investigated the cost-effectiveness of treating iron deficiency anemia (IDA) with ferric citrate hydrate (FC) in Japan. We employed four treatment strategies: switching from sodium ferrous citrate (SF) to FC at (1) 500 mg (approximately 120 mg of iron) per day or (2) 1000 mg (approximately 240 mg of iron) per day in patients with SF-induced nausea/vomiting, or starting treatment with FC at (3) 500 mg/day or (4) 1000 mg/day. We evaluated the cost-effectiveness of these strategies compared with SF 100 mg (100 mg of iron) per day.
View Article and Find Full Text PDFCefiderocol (FDC), a siderophore-cephalosporin conjugate, is the newest option for treating infection with carbapenem-resistant gram-negative bacteria. We identified a novel mechanism contributing to decreased FDC susceptibility in Klebsiella pneumoniae clinical isolates. The mechanism involves 2 coresident plasmids: pKpQIL, carrying variants of bla carbapenemase gene, and pKPN, carrying the ferric citrate transport (FEC) system.
View Article and Find Full Text PDFMolecules
November 2024
BioMedical Research Centre, Norwich Medical School, University of East Anglia, Norwich NR4 7TJ, UK.
Salinomycin and its derivatives display promising anti-proliferating activity against bloodstream forms of . The mechanism of trypanocidal action of these compounds is due to their ionophoretic activity inducing an influx of sodium cations followed by osmotic water uptake, leading to massive swelling of bloodstream-form trypanosomes. Generally, higher trypanocidal activities of salinomycin derivatives are associated with higher cell swelling activities.
View Article and Find Full Text PDFQJM
December 2024
National Heart and Lung Institute, Imperial College London, London, UK.
Background: Disease biomarkers are often identified long after initiating pathologies, hampering mechanistic understanding and development of preventative strategies. We hypothesised that aberrant cellular responses to normally-encountered stresses may be relevant to later disease states.
Aim: To model two under-explored acute cellular stresses for blood-exposed cells, and cross-reference to known biomarkers of disease.
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