<div style="text-align:justify;"> <strong>Introduction</strong><strong>: </strong>Iron deficiency (ID) is often present (32% - 65%) in patients with heart failure (HF). Oral iro...<div style="text-align:justify;"> <strong>Introduction</strong><strong>: </strong>Iron deficiency (ID) is often present (32% - 65%) in patients with heart failure (HF). Oral iron absorption in patients with HF is generally poor. This is the reason why oral treatment is not recommended. <b>Aim</b><b>: </b>To test whether oral iron succinate significantly increases iron deposits in non-anaaemic patients with HF. <span "=""></span><b>Methods</b><b>: </b><span "="">ID was defined as ferritin < 100 μg/L or 100 - 299 μg/L with transferrin saturation (TSAT) < 20%. Forty-two patients were screened. Ferrous succinate was administered as one tablet (100 mg, including 32.48 mg Fe<sup>2+ </sup>plus 100 mg succinate) in the morning and one tablet at bedtime for at least 3 months. Hemoglobin, CRP, ferritin, iron, TSAT, and hepcidin were analyzed before starting treatment, at 6 weeks, and at 3 months end of study (EOS). </span><span "=""></span><b>Results</b><b>: </b>Five women and 15 men were included in the study. The level of ferritin increased significantly from baseline to 6 weeks (47 to 78 μg/L, p = 0.009) and baseline to EOS (47 to 85 μg/L, p = 0.001). TSAT increased significantly from baseline to 6 weeks (20% to 27%, p = 0.046) and baseline to EOS (20% to 25%, p = 0.043). Hepcidin increased significantly from baseline to 6 weeks (2.5 nmol/L to 4.8 nmol/L, p = 0.006) and baseline to EOS (2.5 to 4.2 nmol/L, p = 0.02)<span "="">. <b>Conclusion</b></span><b>: </b><span "="">Oral iron succinate significantly increased iron uptake, almost doubling the ferritin levels and increasing the TSAT, in patients with HF. Our findings challenge the opinion that <a name="_Hlk27389187"></a>oral iron treatment cannot significantly increase iron deposits in non-anemic patients with ID and HF.</span> </div>展开更多
文摘<div style="text-align:justify;"> <strong>Introduction</strong><strong>: </strong>Iron deficiency (ID) is often present (32% - 65%) in patients with heart failure (HF). Oral iron absorption in patients with HF is generally poor. This is the reason why oral treatment is not recommended. <b>Aim</b><b>: </b>To test whether oral iron succinate significantly increases iron deposits in non-anaaemic patients with HF. <span "=""></span><b>Methods</b><b>: </b><span "="">ID was defined as ferritin < 100 μg/L or 100 - 299 μg/L with transferrin saturation (TSAT) < 20%. Forty-two patients were screened. Ferrous succinate was administered as one tablet (100 mg, including 32.48 mg Fe<sup>2+ </sup>plus 100 mg succinate) in the morning and one tablet at bedtime for at least 3 months. Hemoglobin, CRP, ferritin, iron, TSAT, and hepcidin were analyzed before starting treatment, at 6 weeks, and at 3 months end of study (EOS). </span><span "=""></span><b>Results</b><b>: </b>Five women and 15 men were included in the study. The level of ferritin increased significantly from baseline to 6 weeks (47 to 78 μg/L, p = 0.009) and baseline to EOS (47 to 85 μg/L, p = 0.001). TSAT increased significantly from baseline to 6 weeks (20% to 27%, p = 0.046) and baseline to EOS (20% to 25%, p = 0.043). Hepcidin increased significantly from baseline to 6 weeks (2.5 nmol/L to 4.8 nmol/L, p = 0.006) and baseline to EOS (2.5 to 4.2 nmol/L, p = 0.02)<span "="">. <b>Conclusion</b></span><b>: </b><span "="">Oral iron succinate significantly increased iron uptake, almost doubling the ferritin levels and increasing the TSAT, in patients with HF. Our findings challenge the opinion that <a name="_Hlk27389187"></a>oral iron treatment cannot significantly increase iron deposits in non-anemic patients with ID and HF.</span> </div>