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Patients with cyanosis as a result of congenital heart disease and/or pulmonary hypertension (PH) given intravenous (IV) ferrous carboxymaltose experienced significant improvements in average hemoglobin, hematocrit, ferritin, and transferrin saturation, according to the results of a study published in the International Journal of Cardiology.
Patients (n=142) who presented with cyanosis resulting from congenital heart disease and/or pulmonary hypertension at a single center were treated with a slow IV infusion of ferrous carboxymaltose during a period of 60 minutes. Patients were monitored for an additional hour after treatment for adverse events.
Average hemoglobin, hematocrit, ferritin, and transferrin saturation were evaluated before and after treatment and compared.
Of the study participants, congenital heart disease was present in 59.2% of the population. In addition, Eisenmenger syndrome was present in 48.8% of patients with congenital heart disease. After iron supplementation, significant improvements in hemoglobin concentration, hematocrit, mean corpuscular volume, ferritin, and transferrin saturation were observed during the 100-day follow-up. However, not all patients achieved normal iron levels, with 45.7% having transferrin saturation <20% and 66.0% having low ferritin or low transferrin saturation.
The study authors wrote, “In our study, IV iron carboxymaltose administration appeared to be safe for treating iron deficiency in cyanotic patients with [congenital heart disease] and/or PH, providing measures are taken to minimise the risk of air embolism and that patients are monitored for minor allergic reactions around infusion.”
However, they also stressed the need for efficacy studies, adding, “Further randomised studies are needed to confirm the safety and efficacy of IV iron administration in this setting.”
Reference
Blanche C, Alonso-Gonzalez R, Uribarri A, et al. Use of intravenous iron in cyanotic patients with congenital heart disease and/or pulmonary hypertension [published online May 19, 2018]. Int J Cardiol. doi:10.1016/j.ijcard.2018.05.062
