Intravenous Iron Administration Research Articles

Iron homeostasis, recycling and vulnerability in the stressed kidney: A neglected dimension of iron-deficient heart failure.

The available evidence suggests that the kidney may contribute importantly to the development of an iron deficiency state in patients with heart failure and may be injured by therapeutic efforts to achieve iron repletion. The exceptional workload of the proximal renal tubule requires substantial quantities of iron for ATP synthesis, which it derives from Fe3+ bound to transferrin in the bloodstream. Following ferrireduction, Fe2+ is conveyed by divalent transporters (e.g. DMT1) out of the endosome of the proximal renal tubule, and highly reactive Fe2+ can be directed to the mitochondria, sequestered safely in a ferritin nanocage or exported through the actions of hepcidin-inhibitable ferroportin. The actions of ferroportin, together with transferrin endocytosis and DMT1-mediated transport, play a key role in the recycling of iron from the tubular fluid into the bloodstream and preventing the loss of filtered iron in the urine. Activation of endogenous neurohormonal systems and proinflammatory signalling in heart failure decrease megalin-mediated uptake and DMT1 expression, and increase hepcidin-mediated suppression of ferroportin, promoting the loss of iron in the urine and contributing to the development of an iron deficiency state. Furthermore, the failure of ferroportin-mediated efflux at the basolateral membrane heightens the susceptibility of the renal tubules to cytosolic excesses of Fe2+, causing lipid peroxidation and synchronized cell death (ferroptosis) through the iron-dependent free radical theft of electrons from lipids in the cell membrane. Ferroptosis is a central mechanism to most disorders that can cause acute and chronic kidney disease. Short-term bolus administration of intravenous iron can cause oxidative stress and is accompanied by markers of renal injury. Experimentally, long-term maintenance of an iron-replete state is accompanied by accelerated loss of nephrons, oxidative stress, inflammation and fibrosis. Intravenous iron therapy increases glomerular filtration rate rapidly in patients with heart failure (perhaps because of a haemodynamic effect) but not in patients with chronic kidney disease, and the effects of intravenous iron on the progression of renal dysfunction in the long-term trials - AFFIRM-AHF, IRONMAN and HEART-FID - have not yet been reported. Given the potential role of dysregulated renal iron homeostasis in the pathogenesis of iron deficiency and the known vulnerability of the kidney to intravenous iron, the appropriate level of iron repletion with respect to the risk of acute and chronic kidney injury in patients with heart failure requires further study.

Administration of intravenous iron by a hospital at home service

Administration of intravenous iron by a hospital at home service

Iron Deficiency Related to Obesity.

There is a direct correlation between being overweight and iron deficiency. Physiological changes occur in obese adipose cells that contribute to the development of iron deficiency (ID) and iron deficiency anemia (IDA). These changes disrupt the normal iron metabolic checks and balances. Furthermore, bariatric surgery can lead to long-term ID and IDA. Oral iron supplementation may not be effective for many of these patients. Intravenous iron infusions can significantly increase the quality of life for individuals experiencing this condition but are also associated with potentially serious complications. Adequate knowledge about intravenous (IV) iron administration can greatly increase the safety of this beneficial therapy. This review article explains the relationship between obesity, ID/IDA, bariatric surgery and the safe administration of IV iron.

Expert consensus guidelines: Intravenous iron uses, formulations, administration, and management of reactions.

Intravenous iron has become an essential component for the treatment of iron deficiency and iron deficiency anemia. Individuals administering Intravenous iron should have knowledge in intravenous iron administration, including a pre-infusion assessment to evaluate infusion reaction risks, pre- and post-infusion monitoring, identification of and management of infusion reactions, accurate documentation of these reactions, laboratory monitoring and recognition and management of treatment-emergent hypophosphatemia. This comprehensive consensus provides step-by-step guidance and tools for practitioners to promote safe delivery of intravenous iron, recognition, and management of infusion reactions and treatment-emergent hypophosphatemia.

Newborn phosphocalcic metabolism after intravenous iron administration during pregnancy

Objective Iron deficiency anemia is a very common health problem during pregnancy and intravenous (IV) iron substitution has become part of routine management. However, recent studies have raised concerns about the association of IV iron infusion and the development of secondary transitory hypophosphatemia (HP) in adults, including pregnant women. We aimed to evaluate the impact of IV iron administration during pregnancy on the phosphocalcic metabolism of newborns. Methods A prospective, single-center, observational study was performed from December 2022 to May 2023 at the maternity facility of Geneva University Hospitals. We included women treated with either IV or oral iron during pregnancy. At delivery, a maternal blood sample was collected to assess hemoglobin, hematocrit, and levels of ferritin, phosphate and calcium, as well as an umbilical cord blood sample to assess levels of phosphate and calcium. Univariate and multivariate analyses were performed to evaluate the contribution of IV iron substitution on cord blood phosphatemia and calcemia, considering potential confounding factors. Neonatal HP was defined as a phosphate level <1.3 mmol/L. Results Forty-three pregnant women were included in our study. Among these, 22 were treated with ferric carboxymaltose and 21 with oral iron. There were three cases of maternal HP in the IV iron group (13.6%) and one (4.8%) in the control group (p value for the difference= .607). We observed one case (4.5%) of neonatal HP in the IV iron group and no cases in the control group. Median cord blood phosphatemia and calcemia were 1.7 mmol/L vs. 1.71 mmol/L and 2.67 mmol/L vs. 2.64 mmol/L in the IV iron and oral groups, respectively. After adjustment, IV iron administration had no impact on cord blood phosphate (p= .919) and calcium (p= .891) levels. Conclusion No impact of IV iron administration during pregnancy was observed on the newborn phosphocalcic metabolism.

E-Iron: An Asynchronous Telemedicine Referral Platform for Management of Anemic Pregnant Patients and the Expediting of Treatment with Intravenous Iron

Introduction: Intravenous iron (IVI) is a valuable but underused strategy in the management of iron deficiency anemia in pregnancy, a common condition linked to adverse maternal and neonatal outcomes. At our institution and elsewhere, administration of IVI has historically entailed referral to hematology, a frequently slow and labor-intensive process, that commonly results in significant delays, thus undermining the usefulness of this intervention. E-Iron is a specialized e-consult protocol operational at our institution, built into the EPIC EMR, and designed to facilitate ‘electronic’ referral of patients requiring IVI. Using a template-based design, e-IRON assists referring providers with the gathering and electronic submission of key clinical information required to determine eligibility for IVI. Following submission, a hematologist reviews the request within 3 days. If IVI is deemed appropriate, it is promptly scheduled, as is a face-to-face appointment if deemed necessary. Where IVI is not deemed appropriate, guidance as to alternate management is provided. We have previously shown that e-IRON, by dispensing with the need for a face-to-face hematology visit, simplifies the process of referral for IVI across a broad range of indications, and significantly accelerates the administration of IVI when appropriate. Here we report on the characteristics and selected outcomes of a cohort of anemic pregnant women referred to the e-IRON program over an 18-month period. Results: From July 2021 until December 2022, 239 patients were referred. Of these, 18 were excluded from our analysis due to absence of follow up data. The vast majority (84%) of referrals occurred in the 3rd trimester, the median number of days prior to estimated date of delivery being 47, (average 54.7 days) IV iron was approved for 149 patients (67% of total referred). Of these, 132 patients (89%) received infusion, which occurred a median of 13 days (IQR: 9.4 - 17.5) after the e-IRON consult was placed. Reasons for non-administration included “no shows” (60%) and intervening delivery (33%). Treatment consisted of ‘single dose infusion’ in 88% of infused patients, either using iron dextran 1g, - the Georgetown regimen - (68%), or iron carboxymaltose 750 mgs (19%). No significant complications relating to infusions were reported. IVI was not approved where deemed to be without utility (63%), notably, if the patient was not iron deficient, if the request was too close to delivery, or if anemia was mild. In such cases consideration for IVI during admission for delivery was recommended to expedite post-delivery Hb recovery. IVI was not approved if laboratory studies were not current (11%) or if failure of oral iron was not demonstrated (26%). In the latter group of 19 patients a trial of oral iron was recommended, deemed successful in 10, but in whom 7 ultimately proceeded to IVI. A face-to-face hematology consultation was recommended in 7 patients (3%). 36 patients in the cohort (16%) had a history of bariatric surgery. IVI was approved in 89% of this group, versus 63% in patients without this history. Effects of the intervention are shown in Table 1, with a notable decrease in the proportion of anemic women at time of delivery, most marked in the group who received IVI. The improvement in Hb was greater the earlier IVI was administered. Transfusions occurred exclusively in the context of post-partum hemorrhage, and predominantly with surgical delivery (Table 2). Rates in the cohort were higher than in a historical control (12.2% vs 5.2%). This was attributed to selection bias; e-IRON referrals occurring in a higher pregnancy risk cohort. Conclusions: E-IRON represents a successful implementation of an electronic, asynchronous, telemedicine protocol, that facilitates rapid triage and treatment of anemic pregnant patients requiring IVI. We have shown that the earlier infusion is administered, the greater the increment in Hb, which underscores the value of a protocol that minimizes the time interval between referral and infusion. The speed of IVI administration since implementation of e-IRON is unprecedented at our institution. We believe the model is easily replicated, and can be readily implemented in any other health system that utilizes an integrated EMR, providing similar benefit to an at-risk patient demographic, with a common clinical problem that is habitually neglected or undertreated.

The Impact of Iron Deficiency Anemia on Cerebrovascular Physiology, Brain Structure, and Cognitive Function in Otherwise Healthy Women

Introduction: Moderate iron deficiency anemia(IDA), defined as a hemoglobin below 11 g/dl, occurs in 1.5% of the United States population and is overrepresented in minority populations. IDA is known to cause permanent structural and function damage in children, but IDA's cognitive and neurovascular phenotype in adults is poorly characterized. We performed brain MRI and cognitive testing in 34 otherwise healthy women with IDA to determine whether oxygen delivery and metabolism are preserved as well as the association of IDA with brain volumes and cognitive function. Methods: We recruited potential blood donors from four hospital-based donor centers, Children's Hospital Los Angeles, University of California Los Angeles, Cedar's Sinai, and City of Hope, whose point-of-care hemoglobin values were less than 10.5 g/dl. We also recruited individuals from the community using social media advertisements, with anemia documented by screening hemoglobin assessment. All participants were free from inflammatory, infectious, or malignant diseases that may impact blood counts and iron metabolism. IDA was confirmed by laboratory assessment of CBC, reticulocyte count, iron indices, methyl malonic acid, hemoglobin electrophoresis, homocysteine, and high-sensitivity C-reactive protein. Patients underwent a four-hour neurocognitive assessment consisting of subsets from the Weschler Abbreviated Scale of Intelligence (WASI-II), the California Verbal Learning Test (CVLT), the Rey Complex Figure Test (RCFT), and the NIH Cognitive Toolkit. MRI was performed on a 3T Philips Achieva using a 32-element head coil. Anatomic imaging consisted of 3D T1, 3D T2, 3D T2*/QSM, and 2D multishell diffusion imaging. Phase contrast and arterial spin labeling measured total and regional brain blood flow, respectively. Cerebral venous oximetry was performed using T2 relaxation under spin tagging. Results: The study population demonstrated a classic IDA phenotype characterized by low ferritin and transferrin saturation, high iron binding capacity, decreased MCV and MCHC, and hypochromic microcytosis on blood smear (not shown). Neurocognitive function was impaired across multiple domains for women having hemoglobin values less than 10.0 g/dl (Figure 1, left), with Cohen's D values ranging from 0.7 - 1.5. Cerebral blood flow (CBF) rose slightly as oxygen content declined (Figure 1, right), but much less than predicted based on historical controls 1,2 leading to impaired brain oxygen delivery. Oxygen extraction fraction was independent of hemoglobin concentration, thus cerebral metabolic rate was also decreased. Grey matter volume was smaller in the right temporal lobe and correlated with 2/3 of the abnormal cognitive indices (in Figure 1, left). White matter volume was decreased in the right cingulate gyrus, corpus callosum, and cerebellum, correlating with the remaining abnormal cognitive indices. Discussion: Our study demonstrates that iron deficiency has serious effects on cognitive performance; individuals with hemoglobin less than 10.0 g/dl scored more than one standard deviation below their peers with milder anemia. Poor cognitive performance was correlated with demonstrable brain shrinkage whose reversibility is unknown. The failure of the brain to upregulate CBF in response to IDA was striking because most patients with chronic anemia preserve cerebral oxygen delivery through compensatory hyperemia 1,2. While both anemia and iron deficiency can impair brain function on their own, it is likely that iron deficiency is the primary contributor to the cognitive and neurovascular effects. We will test this hypothesis in subsequent work by reexamining women with IDA shortly after intravenous iron administration, thus creating a window where the iron deficiency has been corrected but the anemia persists(NCT05929729). We will also determine whether the cerebrovascular, anatomic, and functional deficits are reversible with iron repletion.

Evaluating Trainees' Experiences with Intravenous Iron Use

Background: Iron deficiency (ID) and iron deficiency anemia (IDA) cause significant morbidity. Despite being a disease of high prevalence, affecting people with heart failure, chronic kidney disease, heavy menstrual bleeding, irritable bowel disease, hereditary hemorrhagic telangiectasia (HHT), and bariatric surgery, it has low healthcare priority. The World Health Organization (WHO) estimates 37% of people who are pregnant, and 30% of women 15-49 years of age worldwide are anemic. Fibroids, which are the leading cause of abnormal uterine bleeding, disproportionately impact people of color. ID and IDA cause fatigue, impaired cognitive function, and poor mental health, eroding quality of life and personal productivity. In addition, IDA has been associated with an increase in all-cause mortality is associated with an increased risk of arterial and venous thrombosis. Under-treatment of IDA results in avoidable hospitalizations, emergency room visits, blood transfusions, decreased HRQoL, and loss of personal productivity. Despite the significant impact ID and IDA can have on morbidity, mortality, and quality of life, intravenous iron remains underutilized. No study has been performed to date to assess provider practices, knowledge, and perceptions of intravenous iron use. This qualitative study aims to understand trainees' experiences with intravenous iron use in patients with ID and IDA. Methods: We conducted an inductive reflective thematic analysis of semi-structured qualitative interviews from five focus groups to understand trainees' experiences with and barriers to prescribing intravenous iron in patients with ID and IDA. Internal medicine residents from academic institutions across the country were recruited via snowball sampling. Chief residents from six internal medicine programs were contacted to disseminate sign up links to their residents; programs were chosen for geographic diversity. Results: Twenty-eight internal medicine residents responded and nineteen residents across five institutions participated (PGY levels 1-3). Thematic analysis of trainees' experiences of caring for patients with conditions characterized by iron deficiency resulted in three main themes: education, systemic factors, and practice pattern. Participants identified a wide range of conditions for which they consider administration of oral or intravenous iron. However, they generally expressed uncertainty as to whether evidence-based guidelines exist to guide their decision-making with the exception of intravenous iron administration in heart failure patients. In addition, systemic factors, such as setting, support staff, hospital formularies, order sets, and insurance status often impacted their decision to use intravenous iron. Conclusions: There is a wide variation among residents' practice patterns in regard to their comfort with prescribing intravenous iron. The ease or hesitancy with which they do so is greatly influenced by educational and systemic factors. By gaining a deeper understanding of the experiences of trainees we can lay the foundation to develop evidence-based guidelines and educational initiatives for conditions characterized by ID and IDA. Additionally, by identifying both institutional facilitators and barriers, we can cultivate system-based initiatives to improve access to intravenous iron. To assess this need on a larger scale, our next step involves developing a survey that will be widely distributed via national societies. While cost, insurance status, and need for specialty referral were identified as barriers for intravenous iron use, there was no explicit discussion of how these barriers may contribute to healthcare inequity for underserved populations.

Intravenous iron administration in patients with heart failure alters endothelial homeostasis with early release of endothelial microvesicles and subsequent mobilization of endothelial progenitor cell

Abstract Background Intravenous iron supplementation is an established therapy for patients with heart failure (HF) with reduced ejection fraction (LV-EF&amp;lt;50%) and iron deficiency, resulting in reduced risk of HF hospitalization. Since iron may induce oxidative stress, inflammation and apoptosis in endothelial cells, concerns persist regarding potential adverse vascular effects of iron therapy. To evaluate endothelial health following ferric carboxymaltose (FCM) administration, we assessed the profile of circulating endothelial microvesicles (EMVs) and endothelial progenitor cells (EPCs) in a cohort of 23 HF patients using flow cytometry. Results Compared to healthy control subjects (HC; n=15), baseline levels of CD31+/CD41- EMVs were significantly higher and EMVs featured a more apoptotic phenotype in HF patients. Following administration of 1000mg FCM, EMV levels showed an early but transient increase (Fig. 1) and displayed an altered phenotype profile with dominant augmentation of EMVs expressing the inducible markers CD62E and CD54, indicating endothelial activation and injury. Levels of circulating vasoregenerative CD45lowCD34+KDR+ EPCs were lower in HF patients and FCM application resulted in an early decrease of EPCs followed by substantial mobilization into the circulation after one week (Fig. 2). Levels of EMVs and EPCs returned to baseline values within two and four weeks, respectively. Compared to HF patients with preserved renal function, the EMV/EPC ratio was higher in HF patients whereas EPC mobilization was diminished with additional chronic kidney disease, suggesting impaired vascular repair capacity. In vitro experiments with cultured endothelial cells revealed that FCM at therapeutic concentrations dose-dependently promotes endothelial apoptosis, increases expression of adhesion molecules and CXCL12, and triggers the generation of EMVs. Conclusion Intravenous iron supplementation with FCM in HF patients provokes a biphasic response with early release of CD62E+ and CD54+ enriched EMVs and subsequent mobilization of EPCs, suggesting temporary aggravation of endothelial dysfunction upon FCM supplementation and consecutive engagement of a vascular defense program.

Intravenous Iron for Heart Failure: Updated Systematic Review and Meta-Analysis.

While the administration of intravenous (IV) iron to those with heart failure has been implicated to be associated with a possible reduction in hospitalizations and improvement in symptoms, a recent large multicenter trial only showed modest benefits in reducing hospitalization, necessitating the updated systematic review. We conducted a systematic review and meta-analysis, searching the MEDLINE and EMBASE database until January 9, 2023. Outcomes included total heart failure hospitalizations, first heart failure hospitalization, six-minute walk test (6MWT) distance, and incidence of infection. There were 13 studies with 3410 participants (1,790 with IV iron). Pooled analysis that reported the incidence of cardiovascular death showed that patients with IV iron did not have significantly lower odds of cardiovascular death or first heart failure hospitalization. In contrast, those who received IV iron had significantly lower total heart failure hospitalization (pooled odds ratio (OR) 0.63, 95% confidence interval (CI) 0.44-0.90, I2 59.0%, P = .017) and a composite of cardiovascular death and first heart failure hospitalization (pooled OR 0.55, 95% CI 0.47-0.64, I2 0%, P = .656). While the efficacy is modest, IV iron therapy could be associated with reduced hospitalization for heart failure without significant adverse events.

Intravenous iron administration before cardiac surgery reduces red blood cell transfusion in patients without anaemia

BackgroundReducing the need for blood transfusion among patients undergoing cardiac surgery FLA reduce postoperative complications and mortality. Our study aimed to assess the effects of administering preoperative i.v. ferric carboxymaltose on postoperative red cell transfusion requirements in patients without anaemia undergoing on-pump cardiac surgery. MethodsThis double-blind, randomised, placebo-controlled trial was conducted between October 2016 and November 2019, with a follow-up period of up to 6 weeks after surgery. Patients without anaemia who underwent on-pump cardiac surgery were included as participants and administered i.v. iron in the form of ferric carboxymaltose or placebo once, 24–72 h before surgery. The primary outcome was the number of red cell units transfused during the first four postoperative days, and the secondary outcome measures were blood haemoglobin concentrations at 4 days and 6 weeks after surgery. ResultsThe 200 patients included were randomly assigned to the ferric carboxymaltose (n=102) and placebo (n=98) groups. By postoperative Day 4, a significantly lower mean number of red cell units were transfused in the ferric carboxymaltose than in the placebo group, 0.3 (0.8) vs 1.6 (4.4), respectively; P=0.007. The mean haemoglobin concentrations on postoperative Day 4 were 9.7 (1) g dl−1 and 9.3 (1) g dl−1, respectively (P=0.03). Corresponding values at 6 weeks after surgery were 12.6 (1.4) g dl−1 and 11.8 (1.5) g dl−1, respectively (P=0.012). ConclusionsIn patients without anaemia undergoing on-pump cardiac surgery, treatment with a single dose of 1000 mg ferric carboxymaltose i.v. 1–3 days before surgery significantly reduced the need for red cell transfusions and increased the postoperative haemoglobin concentration. Clinical trial registrationNCT02939794.

Intravenous iron administration in Home Hospitalization Units: Good practice recommendations

Intravenous iron administration in Home Hospitalization Units: Good practice recommendations

Iron deficiency in myocardial ischaemia: molecular mechanisms and therapeutic perspectives.

Systemic iron deficiency (SID), even in the absence of anaemia, worsens the prognosis and increases mortality in heart failure (HF). Recent clinical-epidemiological studies, however, have shown that a myocardial iron deficiency (MID) is frequently present in cases of severe HF, even in the absence of SID and without anaemia. In addition, experimental studies have shown a poor correlation between the state of systemic and myocardial iron. MID in animal models leads to severe mitochondrial dysfunction, alterations of mitophagy, and mitochondrial biogenesis, with profound alterations in cardiac mechanics and the occurrence of a fatal cardiomyopathy, all effects prevented by intravenous administration of iron. This shifts the focus to the myocardial state of iron, in the absence of anaemia, as an important factor in prognostic worsening and mortality in HF. There is now epidemiological evidence that SID worsens prognosis and mortality also in patients with acute and chronic coronary heart disease and experimental evidence that MID aggravates acute myocardial ischaemia as well as post-ischaemic remodelling. Intravenous administration of ferric carboxymaltose (FCM) or ferric dextrane improves post-ischaemic adverse remodelling. We here review such evidence, propose that MID worsens ischaemia/reperfusion injury, and discuss possible molecular mechanisms, such as chronic hyperactivation of HIF1-α, exacerbation of cytosolic and mitochondrial calcium overload, amplified increase of mitochondrial [NADH]/[NAD+] ratio, and depletion of energy status and NAD+ content with inhibition of sirtuin 1-3 activity. Such evidence now portrays iron metabolism as a core factor not only in HF but also in myocardial ischaemia.

Incidence of Hypophosphatemia After Intravenous Administration of Iron: A Matching-Adjusted Indirect Comparison of Data from Japanese Randomized Controlled Trials.

Intravenous (IV) administration of iron is considered a safe and efficacious treatment for iron deficiency anemia (IDA), recommended in patients requiring rapid replenishment of iron, or intolerant or unresponsive to oral administration of iron. Recent randomized controlled trials (RCTs) have shown high incidence of hypophosphatemia after administration of two IV iron preparations: saccharated ferric oxide (SFO) and ferric carboxymaltose (FCM). The present study aimed to conduct matching-adjusted indirect comparison (MAIC) of hypophosphatemia incidence with these iron formulations and ferric derisomaltose (FDI) based on data from head-to-head RCTs conducted in Japan. A MAIC of hypophosphatemia incidence was conducted on the basis of data from two head-to-head RCTs. The relative odds of hypophosphatemia with FDI versus SFO were obtained from patient-level data from a recent RCT and adjusted for cumulative iron dose, while parametric models of serum phosphate levels from a separate RCT were used to estimate the relative odds of hypophosphatemia with FCM with SFO. An anchored MAIC was then conducted comparing FDI with FCM. The adjusted odds of experiencing hypophosphatemia were significantly lower with FDI than SFO [odds ratio (OR) of 0.02; 95%confidence interval(CI) 0.01-0.05]. The parametric models of serum phosphate from the RCT comparing FCM with SFO provided an estimated OR of 1.17 for the incidence of hypophosphatemia with FCM versus SFO. Combining the two estimates in the MAIC showed that the odds of experiencing hypophosphatemia would be 52.5 (95%CI 27.7-99.4) times higher with FCM than FDI in patients with IDA associated with heavy menstrual bleeding in Japan. Direct comparison of patient-level data and a MAIC from two RCTs in Japanese patients with heavy menstrual bleeding indicated that hypophosphatemia is less frequent in patients treated with FDI than those with FCM or SFO. Results are in agreement with RCTs comparing FDI and FCM in patients with various etiologies conducted in the USA and Europe.

Effect of Preoperative Intravenous Iron for Anemic Patients on Outcomes after Cardiac Surgery: A Systematic Review

Abstract Background Iron-deficiency anemia is a global health problem and a common medical condition seen in everyday clinical practice and especially with patients going through cardiac surgery. The most rapid and effective method of correcting anemia is by transfusion of red blood cells. However, blood transfusion itself is not without risk. Treatment of perioperative anemia using iron replacement therapy is, in contrast to blood transfusion, a safe, cheap, and relatively convenient therapy Aim of the Work This study aims to perform a systematic review regarding the effect of preoperative intravenous iron therapy on the need for perioperative blood transfusion and the incidence of major morbidity in anemic patients undergoing cardiac surgery. Search Methodology The review was conducted according to the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) guidelines, and articles were identified by searching PubMed, Web of Science, EMBASE, COCHRANE Database of systematic reviews (CDSR), Scopus, and Web of Science. Quality of the studies was assessed using the Cochrane Risk of Bias Tool 2 (ROB-2) and Risk of Bias in Non-randomized Studies tool (ROBANS). The primary outcomes are change in hemoglobin and hematocrit after cardiac surgery and perioperative need for blood transfusion, while secondary outcomes are postoperative length of hospital stay and incidence of major adverse outcomes. Results Of the articles reviewed a total of six randomized controlled trials (RCT) and seven non-randomized observational studies (NRSI) were included in the review. Across studies, 1,732 patients were enrolled. The quality of the RCTs was mostly high, while the quality of the NRSTs was low, primarily due to issues related to blinding of assessors. Two studies showed higher hemoglobin with iron therapy, and only one study showed significant differences in multiple outcomes such as transfusion and morbidity. Hospital stay was reported in 4 studies and averaged 9 days. Conclusion Our results showed benefits of preoperative intravenous iron administration in reducing the likelihood of allogeneic blood transfusion and providing a modest increase a modest increase in hemoglobin concentration in anemic patients undergoing caridac surgery.

Cardiorenal syndrome and iron supplementation-more benefits than risks: a narrative review.

Intravenous iron administration has emerged as a crucial intervention for managing patients with cardiorenal syndrome (CRS) and iron deficiency, with or without the presence of anemia. Multiple studies have demonstrated the benefits of intravenous iron supplementation in improving anemia, symptoms, and functional capacity in patients with HF and iron deficiency. Furthermore, iron supplementation has been associated with a reduction in hospitalizations for HF exacerbation and the improvement of patients' quality of life and clinical outcomes. In addition to its effects on HF management, emerging evidence suggests a potential positive impact on kidney function in patients with CRS. Studies have shown an increase in estimated glomerular filtration rate and improvements in renal function markers in patients receiving intravenous iron therapy, highlighting the potential of this intervention in patients with CRS. This paper reviews the existing literature on the impact of intravenous iron therapy in these patient populations and explores its effects on various clinical outcomes. Future research endeavors are eagerly awaited to further improve our understanding of its clinical implications and optimize patient outcomes.

Administración de hierro intravenoso en unidades de hospitalización a domicilio: recomendaciones de buenas prácticas

Administración de hierro intravenoso en unidades de hospitalización a domicilio: recomendaciones de buenas prácticas

Optimizing diagnosis and treatment of iron deficiency and iron deficiency anemia in women and girls of reproductive age: Clinical opinion.

Iron deficiency (ID) is the world's most common disorder and one of the top five causes of years lived with disability. Whereas low serum ferritin is diagnostic of ID, ferritin-an acute phase reactant-may be elevated in inflammatory states and the first trimester of pregnancy even if ID exists. Consequently, in early pregnancy or chronic inflammation, percent transferrin saturation (TSAT) measurement is the best indicator of iron status. Unfortunately, current guidelines do not recommend routine screening for ID in either pregnant or nonpregnant women in the absence of anemia. This circumstance should be urgently reviewed based on available data. While oral formulations have long been the standard for iron replacement therapy and are widely available and inexpensive, oral iron is frequently associated with adverse gastrointestinal effects for the majority-a major reason for poor adherence, inadequate repletion, and persisting ID symptoms and sequellae. Although safe intravenous iron administration was introduced in the mid-1950s, formulations with cores binding the elemental iron more tightly became available in the 2000s, allowing complete and safe replacement, even in a single setting. Prospectively acquired neonatology evidence reports oral iron's failure to reach the developing fetus when the mother is iron deficient. Consequently, while oral iron remains frontline in the first trimester because of insufficient safety data for intravenous iron, the author recommends that the intravenous route should be the gold standard for second-trimester ID when hemoglobin concentrations are less than 10.5 g/dL and for all iron-deficient women in their third trimester.

Iron infusion - step by step

In many general medical practices, iron infusions are still regarded as the treatment of choice for iron deficiency. However, they are only very rarely indicated and are often prescribed without a medical basis. This article shows the correct procedure for intravenous iron administration if it is really indicated.

Cardiopulmonary exercise testing before and after intravenous iron in preoperative patients: a prospective clinical study

BackgroundAnemia is associated with impaired physical performance and adverse perioperative outcomes. Iron-deficiency anemia is increasingly treated with intravenous iron before elective surgery. We explored the relationship between exercise capacity, anemia, and total hemoglobin mass (tHb-mass) and the response to intravenous iron in anemic patients prior to surgery.MethodsA prospective clinical study was undertaken in patients having routine cardiopulmonary exercise testing (CPET) with a hemoglobin concentration ([Hb]) < 130 g.l−1 and iron deficiency/depletion. Patients underwent CPET and tHb-mass measurements before and a minimum of 14 days after receiving intravenous (i.v.) Ferric derisomaltose (Monofer®) at the baseline visit. Comparative analysis of hematological and CPET variables was performed pre and post-iron treatment.ResultsTwenty-six subjects were recruited, of whom 6 withdrew prior to study completion. The remaining 20 (9 [45%] male; mean ± SD age 68 ± 10 years) were assessed 25 ± 7 days between baseline and the final visit. Following i.v. iron, increases were seen in [Hb] (mean ± SD) from 109 ± 14 to 116 ± 12 g l−1 (mean rise 6.4% or 7.3 g l−1, p = < 0.0001, 95% CI 4.5–10.1); tHb-mass from 497 ± 134 to 546 ± 139 g (mean rise 9.3% or 49 g, p = < 0.0001, 95% CI 29.4–69.2). Oxygen consumption at anerobic threshold (dot{text{V}} O2 AT) did not change (9.1 ± 1.7 to 9.8 ± 2.5 ml kg−1 min−1, p = 0.09, 95% CI − 0.13 − 1.3). Peak oxygen consumption (dot{text{V}} O2 peak) increased from 15.2 ± 4.1 to 16 ± 4.4 ml.kg.−1 min−1, p = 0.02, 95% CI 0.2–1.8) and peak work rate increased from 93 [67–112] watts to 96 [68–122] watts (p = 0.02, 95% CI 1.3–10.8).ConclusionPreoperative administration of intravenous iron to iron-deficient/deplete anemic patients is associated with increases in [Hb], tHb-mass, peak oxygen consumption, and peak work rate. Further appropriately powered prospective studies are required to ascertain whether improvements in tHb-mass and performance in turn lead to reductions in perioperative morbidity.Trial registrationClinicalTrials.gov identifier: NCT 033 46213.