Dual therapy with oral sucrosomial iron (SI) on top of ferric carboxymaltose (FCM) for iron deficiency anemia (IDA) after cardiac surgery (CS): final results

Background FCM, the gold standard for IDA, can bypass uptake through the reticuloendothelial system, increasing the risk of oxidative stress and cardiomyocyte toxicity [1]. Oral SI compared to FCM, after CS, was able to induce a similar improvement in key hematological parameters (HP) and a reduction in ferritin (F) release [1]. This study reports the final results to evaluate whether dual therapy can mitigate the increase in F and C-reactive protein (CRP). Methods 104 consecutive IDA patients (mean age 71,3 ± 8.9 y), with normal ventricular function (EF: 54.5±6.3), admitted in Cardiac Rehabilitation after CS were all treated with FCM (group A) and a part (group B, n 52) also with SI. The study design included a single dose of 1000 mg of FCM at T1 (at 8-10 days from CS) and after a dose of 60 mg of SI per day from T1 to T2 (the day of discharge) until T3, 15 days after. Measures of efficacy included changes from baseline in HP and CRP. Results the data are shown in the Table. The statistical analysis was conducted with the Mann Whitney test (non-parametric). The HP increased significantly, with no differences between the two groups. However, the levels of hemoglobin (Hb), Transferrin Saturation (TSAT) and iron (I) were significantly lower at T1 in group B with a greater Δ increase (for Hb (g/dl) 2.59 and 2.27, for TSAT (%) 11.54 and 10.20, I (µg/dl) 37.6 (B) vs. 37.71 (A), respectively in the FCM + SI vs. FCM alone group). F at T1 was also significantly higher in group B. At T3 its level was lower in the dual therapy group with a statistically lower ΔF increase (121,77±347,88 (B) vs. 420,30±521,06 (A) ng/ml, p.0005) Therefore a 20% increase in F in group B vs. 87% in group A. Likewise, CRP was significantly higher at baseline in group B, with no difference at T3, but with a significantly higher ΔCRP decrease for the dual therapy (-4.22±4.94 (B) vs. -2.44±3.14 (A), p.031). See the Figure for the time course of F and CRP Conclusions After CS, an inflammatory state is present. FCM, while rapidly correcting HP, also increases blood iron levels by stimulating its deposition in the form of F and activating macrophages through the release of cytokines, which can exacerbate inflammation. SI appears to mitigate the increase in F and CRP by stimulating the reticuloendothelial pathway, thus reducing oxidative stress on the myocardium. Although dual therapy has not induced significant improvement in other HP, lower baseline levels of I, Hb, and TSAT indicate the possibility of more rapid resolution of IDA.