Efficacy of a Low-Dose Intravenous Iron Sucrose Regimen in Peritoneal Dialysis Patients

2002 ◽  
Vol 22 (1) ◽  
pp. 60-66 ◽  
Author(s):  
Elisabeth Dittrich ◽  
Martin Schillinger ◽  
Gere Sunder–Plassmann ◽  
Walter H. Hörl ◽  
Andreas Vychytil

Objective Sufficient iron substitution leads to a decrease in the required recombinant human erythropoietin (rHuEPO) dose and/or an increased hematocrit in dialysis patients. Intravenous (IV) application of larger doses of iron sucrose may be associated with hyperferritinemia, appearance of catalytically free iron, and impaired phagocyte function. Therefore, we investigated the effectiveness of a low-dose IV iron regimen in peritoneal dialysis (PD) patients. Patients and Interventions Forty-five PD patients were followed over a period of 1 year. Serum ferritin, serum transferrin saturation, and hemoglobin were measured monthly. In cases of absolute iron deficiency (serum ferritin < 100 μg/L), 50 mg iron sucrose was given IV every second week. In cases of functional iron deficiency (ferritin ≥ 100 μg/L and transferrin saturation < 20%) and in iron repleted patients (ferritin ≥ 100 μg/L and transferrin saturation ≥ 20%), 50 mg IV iron sucrose was applied monthly. Iron therapy was stopped in cases of acute infection (until complete recovery) and when serum ferritin level was ≥ 600 μg/L. Results To analyze the influence of iron substitution on erythropoiesis and rHuEPO requirements, the EPO resistance index (ERI; quotient of rHuEPO dose in units/kilogram/week and hemoglobin in grams per deciliter) was calculated every 3 months. The ERI decreased significantly during the course of the study in the whole patient group ( p = 0.009) as well as in the subgroup of 21 patients with absolute iron deficiency ( p = 0.01). A nonsignificant decrease in the ERI was observed within the group of 14 iron repleted patients ( p = 0.5). There was no significant change in the ERI in 10 patients with functional iron deficiency ( p = 0.6). Conclusion The low-dose IV iron regimen used in this study substantially decreased rHuEPO requirements in patients with absolute iron deficiency and was effective in maintaining iron stores in iron repleted patients. However, in the absence of significant hyperparathyroidism, aluminum toxicity, or inadequate dialysis, it did not improve the ERI in patients with functional iron deficiency.

2019 ◽  
Vol 7 (2) ◽  
pp. 10-16
Author(s):  
Aditya Mahaseth ◽  
Jay Narayan Shah ◽  
Bikash Nepal ◽  
Biplave Karki ◽  
Jeet Ghimire ◽  
...  

Background and Objectives: Iron Deficiency is the commonest nutritional deficiency worldwide, affecting more than one-third of the population, its association with Heart Failure with or without anemia is of growing interest. As iron supplementation improves prognosis in patients with Heart Failure, Iron Deficiency is an attractive therapeutic target – a hypothesis that has recently been tested in clinical studies. This study is designed to estimate the prevalence and pattern of iron deficiency (ID) in heart failure (HF) with reduced ejection fraction patients with or without anemia. Material and methods: It was a single center hospital based cross sectional observational study. A total of 60 male and female patients with diagnosis of heart failure based on the Framingham Criteria, who gave consent for the study were included. They underwent laboratory evaluation including hemoglobin concentration, serum iron, transferrin saturation percentage, serum ferritin, total iron binding capacity. Serum ferritin <100 μg/l was used to diagnose absolute ID. Functional ID was defined as a serum ferritin level of 100–300 μg/l and a transferrin saturation of <20 %. Anemia was defined as hemoglobin (Hb) <13 g/dl for males and <12 g/dl for females, based on World Health Organization definition. Results: Using the above definitions iron deficiency was found in 28 (46.67%) patients. 36.67% patients had absolute iron deficiency and 10% patients had functional iron deficiency. Females had a higher non statistically significant iron deficiency than males 63.16% vs 39.02%. 15 patients (48.38%) with iron deficiency did not have anemia, and 11 (35.5%) of those patients had absolute iron deficiency. Conclusion: Iron deficiency is prevalent in patients with heart failure and reduced ejection fraction irrespective of anemia and hemoglobin levels. Many of those patients can have functional iron deficiency. Measurement of iron status should be a routine during workup of heart failure patients and further studies are needed to determine the prognostic value of iron status measurement and the influences of treatment of iron deficiency in heart failure patients. Many such trials are now underway.  


Blood ◽  
2004 ◽  
Vol 104 (11) ◽  
pp. 1435-1435
Author(s):  
David Bowen ◽  
Ann Hyslop ◽  
Norene Keenan ◽  
Michael Groves ◽  
Dominic Culligan ◽  
...  

Abstract Recombinant Erythropoietin (+/− G-CSF) is an effective therapy for the anaemia of selected patients with MDS. Validated response prediction models are available, but response rates are only 60% in the “high” predicted response group. Furthermore, half of the total cost of one year’s therapy for a cohort of patients selected for intermediate / high predicted response, is incurred within the initial 12-week therapeutic trial (Cassadeval et al, Blood 2004,104;321). Our hypothesis was that the erythroid response to a single bolus of EPO + G-CSF (Part 1) may predict for sustained response to a therapeutic trial (Part 2). 21 MDS patients (<10% blasts) were randomised in Part 1 to receive either a single s.c. bolus of EPO 18 000 units (NeoRecormon) plus G-CSF (Lenograstim) 263 mcg (n=10), or two vials s.c. placebo (n=11). Serum EPO, haemoglobin concentration and reticulocytes (Sysmex SE9000) were assayed daily from Days 1–8. 20 patients proceeded to Part 2 and received an 8 week therapeutic trial of s.c. EPO 9000 units thrice weekly (tiw), weeks 1–4, escalating to 18 000 units tiw weeks 5–8 if no response, plus titrated s.c. G-CSF tiw. Responders were changed to once weekly (qw) EPO dosing from weeks 12–20 at the total weekly responding dose. 6 patients had erythroid response by study response criteria and 7 by IWG criteria (2HI-E major, 5 HI-E minor). 4/7 RARS patients responded. Incremental change in absolute reticulocyte counts between Day 1 and Day 8 of Part 1 discriminated responders (median increment = 40x109/l, range 31–81, n=6), who received bolus EPO/G-CSF, from non-responders who also received bolus EPO/GSCF (median increment = 1.5x109/l, range −14 to 6, n=4) and from patients receiving placebo (median increment = 5x109/l, range −21 to 18, n=11)(ANOVA P=.002). An incremental increase of >30x109/l was 100% predictive of subsequent response. In patients with erythroid response in Part 2, haemoglobin concentration at qw EPO either did not change compared to tiw dosing (P>.05, n=5), or increased (P=.002, n=1). Serum ferritin, transferrin saturation, CHr (Bayer Advia) and serum transferrin receptor (TfR)concentrations were assayed weekly. Two patients became biochemically iron deficient during weeks 1–8, both of whom had baseline serum ferritin <100mg/l. No iron supplementation was given, and one patient still had an erythroid response. No clear evidence for functional iron deficiency was seen in patients with serum ferritin >100 mg/l. Serum non-transferrin bound iron concentration correlated closely with transferrin saturation both at baseline (n=21 patients), and on treatment (n=4 responders and 4 non-responders). In Part 2, neither ΔHb, nor ΔTfR at weeks 1 or 2 predicted response. No baseline erythroid parameters differed between responders and non-responders. New observations: 1. Absolute reticulocyte increment at Day 8 post s.c. bolus EPO/G-CSF predicts for therapeutic response in this small study, 2. Once weekly EPO is as effective as thrice weekly EPO in similar doses, 3. Functional iron deficiency may impair response in MDS patients with iron-limited erythropoiesis.


Blood ◽  
2010 ◽  
Vol 116 (21) ◽  
pp. 5149-5149
Author(s):  
John Adamson ◽  
Zhu Li ◽  
Paul Miller ◽  
Annamaria Kausz

Abstract Abstract 5149 BACKGROUND Iron deficiency anemia (IDA) is associated with reduced physical functioning, cardiovascular disease, and poor quality of life. The measurement of body iron stores is essential to the management of IDA, and the indices most commonly used to assess iron status are transferrin saturation (TSAT) and serum ferritin. Unfortunately, serum ferritin is not a reliable indicator of iron status, particularly in patients with chronic kidney disease (CKD), because it is an acute phase reactant and may be elevated in patients with iron deficiency in the presence of inflammation. Recent clinical trials have shown that patients with iron indices above a strict definition of iron deficiency (TSAT >15%, serum ferritin >100 ng/mL), do have a significant increase in hemoglobin (Hgb) when treated with iron. These results are consistent with recent changes to the National Cancer Comprehensive Network (NCCN) guidelines, which have expanded the definition of functional iron deficiency (relative iron deficiency) to include a serum ferritin <800 ng/mL; previously, the serum ferritin threshold was <300 ng/mL. Additionally, for patients who meet this expanded definition of functional iron deficiency (TSAT <20%, ferritin <800 ng/mL), it is now recommended that iron replacement therapy be considered in addition to erythropoiesis-stimulating agent (ESA) therapy. Ferumoxytol (Feraheme®) Injection, a novel IV iron therapeutic agent, is indicated for the treatment of IDA in adult patients with CKD. Ferumoxytol is composed of an iron oxide with a unique carbohydrate coating (polyglucose sorbitol carboxymethylether), is isotonic, has a neutral pH, and evidence of lower free iron than other IV irons. Ferumoxytol is administered as two IV injections of 510 mg (17 mL) 3 to 8 days apart for a total cumulative dose of 1.02 g; each IV injection can be administered at a rate up to 1 mL/sec, allowing for administration of a 510 mg dose in less than 1 minute. METHODS Data were combined from 2 identically designed and executed Phase III randomized, active-controlled, open-label studies conducted in 606 patients with CKD stages 1–5 not on dialysis. Patients were randomly assigned in a 3:1 ratio to receive a course of either 1.02 g IV ferumoxytol (n=453) administered as 2 doses of 510 mg each within 5±3 days or 200 mg of oral elemental iron (n=153) daily for 21 days. The main IDA inclusion criteria included a Hgb ≤11.0 g/dL, TSAT ≤30%, and serum ferritin ≤600 ng/mL. The mean baseline Hgb was approximately 10 g/dL, and ESAs were use by approximately 40% of patients. To further evaluate the relationship between baseline markers of iron stores and response to iron therapy, data from these trials were summarized by baseline TSAT and serum ferritin levels. RESULTS Overall, results from these two pooled trials show that ferumoxytol resulted in a statistically significant greater mean increase in Hgb relative to oral iron. When evaluated across the baseline iron indices examined, statistically significant (p<0.05) increases in Hgb at Day 35 were observed following ferumoxytol administration, even for subjects with baseline iron indices above levels traditionally used to define iron deficiency. Additionally, at each level of baseline iron indices, ferumoxytol produced a larger change in Hgb relative to oral iron. These data suggest that patients with CKD not on dialysis with a wide range of iron indices at baseline respond to IV iron therapy with an increase in Hgb. Additionally, ferumoxytol consistently resulted in larger increases in Hgb relative to oral iron across all levels of baseline iron indices examined. Disclosures: Adamson: VA Medical Center MC 111E: Honoraria, Membership on an entity's Board of Directors or advisory committees. Li:AMAG Pharmaceuticals, Inc.: Employment. Miller:AMAG Pharmaceuticals, Inc.: Employment. Kausz:AMAG Pharmaceuticals, Inc.: Employment.


2012 ◽  
Vol 08 (02) ◽  
pp. 74
Author(s):  
Mark Janis ◽  

Anemia is highly prevalent, affecting approximately 40 % of cancer patients, and results in a significant decrease in health-related quality of life while also being associated with shorter cancer survival times. A recent survey of 15,000 cancer patients in Europe found that 39 % were anemic at the time of enrolment. In addition, anemia is a recognized complication of myelosuppressive chemotherapy, and it has been estimated that, in the US, around 1.3 million cancer patients who are not anemic at the time of diagnosis will develop anemia during the course of their disease. The etiology of anemia in cancer patients is variable and often multifactorial, and may be the result of an absolute or a functional iron deficiency. Cancer produces an enhanced inflammatory state within the body—causing hepcidin levels to increase and erythropoietin production to decrease—and results in a reduction in erythropoiesis due to impaired iron transport. This type of anemia is known as functional iron deficiency, where the body has adequate iron stores but there are problems with mobilization and transport of the iron. Absolute iron deficiency is when both iron stores and iron transport are low. The National Comprehensive Cancer Network (NCCN) treatment guidelines for cancer-related anemia recommend intravenous (IV) iron products alone for iron repletion in cancer patients with absolute iron deficiency, and erythropoiesis-stimulating agents (ESAs) in combination with IV iron in cancer patients (currently undergoing palliative chemotherapy) with functional iron deficiency. Although IV iron has been demonstrated to enhance the hematopoietic response to ESA therapy, the use of supplemental iron has not yet been optimized in oncology. Here we discuss the significance of iron deficiency anemia in cancer patients and the need to implement tools to properly diagnose this condition, and we provide an overview of the management strategies and recommendations for patients with iron deficiency anemia as outlined in the NCCN guidelines.


Author(s):  
Satish Kumar

Introduction: Anemia is the commonest major contributing factor in maternal mortality and morbidity in developing countries and according to World Health Organization (WHO) criteria, it contributes to 20% of maternal deaths. Anemia in pregnancy defined as hemoglobin level <11 gm/dl (7.45 mmol/L) and hematocrit less than 33% (WHO). Aim: To compare the efficacy of oral iron ferrous sulphate therapy with intravenous iron sucrose therapy in the treatment of iron deficiency anemia during postpartum period. Material & Methods: This was a prospective randomized comparative clinical trial single center study conducted on 200 postpartum women aged >18 years (after normal delivery or LSCS) within 10 days of delivery with Hb level more or equal to 6 gm/dl but less than 10 gm/dl were included in the study. This was a one year study conducted during 1st December 2018 to 30th November 2019. Results : There was a significant increase in the hemoglobin level in both the groups i.e. in IV iron group, from 8.26 ±1.03gm/dl on day 1 to 11.62±0.94gm/dl on day 45 as compared to oral iron group, from 8.24±1.09gm/dl on day 1 to 11.07±1.14gm/dl on day 45; and serum ferritin level from 41.69±40.45ng/ml on day 1 to 77.34±41.60ng/ml on day 45 in IV iron group as compared to the oral iron group from 22.20±8.82ng/ml on day 1 to 31.72±9.72 ng/ml on day 45. So, there was a rapid increase in both hemoglobin and serum ferritin levels in IV iron group as compared to the oral iron group. Conclusion: Intravenous iron sucrose administration increases the hemoglobin level and serum ferritin more rapidly in compare to the oral intake of ferrous sulphate in women with iron deficiency anemia in postpartum women in our study. Keywords: Iron deficiency anemia, Intravenous iron sucrose, Serum ferritin, Maternal mortality.


Blood ◽  
2020 ◽  
Vol 136 (Supplement 1) ◽  
pp. 42-43
Author(s):  
Michael Auerbach ◽  
Carlo Brugnara ◽  
Steve Staffa

It is estimated anemia affects over 30% of the world's population, with iron deficiency (ID) the overwhelmingly most common cause. Whether absolute due to blood loss and/or iron sequestration to underlying morbidity, the need for repletion especially in females, is a formidable medical issue. The diagnosis of iron deficient erythropoiesis has been traditionally based on the biochemical parameters ferritin and percent transferrin saturation (TSAT), mean cell volume and hemoglobin (Hb) concentration. In recent years, reticulocyte Hb content has emerged as a parameter helpful in identifying iron deficient erythropoiesis and informing a need, or lack thereof, for replacement. 556 consecutive, non-selected patients referred for diagnosis and/or treatment of anemia were included in this diagnostic study to compare the performance of reticulocyte hemoglobin equivalent (RET-He) versus traditional biochemical markers for diagnosis and treatment of IDA. CBC, serum ferritin, iron and TSAT were performed as clinically indicated. RET-He was measured with a Sysmex XN-450 analyzer on the residual CBC sample. 556 patients were studied at baseline and 150 were subsequently treated with intravenous (IV) iron. 240/556 were seen at follow-up, with 57 treated and 183 not treated with IV iron. At baseline, ret-He, positively correlated with Hb (Spearman correlation (rho)=0.365, P &lt; 0.001), MCV (rho=0.576, P &lt; 0.001), MCH (rho=0.777, P &lt; 0.001), serum iron (rho=0.526, P &lt; 0.001) and TSAT (rho=0.492, P &lt; 0.001). Serum iron, and TSAT (but not serum ferritin or MCV, or absolute reticulocyte count) positively correlated with Hb concentrations. Based on either a serum ferritin &lt;30 ng/ml and/or a TSAT&lt; 20%, 241/556 (43.4%) patients were diagnosed as iron deficient. Anemia was present in 64/241 of the iron deficient patients (26.6%). Despite the limitations of the biochemical markers outlined above, we performed ROC analysis assessing the value of RET-He in identifying iron deficiency as defined by serum ferritin &lt;30 ng/mL or transferrin saturation &lt;20%. ROC analysis demonstrates a reasonable performance for RET-He (AUC= 0.733, 95% CI: 0.692, 0.775), with a cut-off value of &lt;30.7 pg yielding 68.2% sensitivity and 69.7% specificity. Using both Hb and RET-He in a multivariable ROC analysis does not provide an improved AUC, as compared to just using RET-He (AUC=0.605 vs.0.733). IV iron administration was associated with significant increases in Hb, MCV, MCH, RET-He, serum ferritin, iron and TSAT, whereas in the no-IV iron cohort, there was a small reduction in RET-He and small increases in MCV and MCH, with no significant variations in Hb and in the other parameters. Serum ferritin was below 30 ng/mL in 18/57 (32%) of the patients requiring IV iron and in 19/183 (10.4%) of those not requiring iron at visit 1. These values changed to 4/57 (7%) (P=0.002) and 23/183 (13%) (P=0.623) at visit 2, respectively. Regression analysis for Hb response following IV iron showed that baseline RET-He values are predictive of Hb response, with every unitary increase in RET-He corresponding to a blunting of the Hb change by -0.19 g/dl (95% CI: -0.27, -0.11; P &lt; 0.001). Changes in RE-He associated with IV iron administration are also predictive of the Hb response, with every additional unit increase in RET-He corresponding to a 0.21 g/dL increase in Hb (95% CI: 0.13, 0.28; P &lt; 0.009). ROC analysis for the capability to predict Hb response among the 57 patients receiving IV iron shows that a value of baseline RET-He &lt; 28.5 pg together with a baseline Hb value &lt; 10.3 g/dL provide the highest Youden's index for predicting Hb response &gt; 1.0 g/dl, with sensitivity of 84% and specificity of 78%. The Figure presents data for the 21/57 patients who had RET-He &lt; 28.5 pg and Hb &lt; 10.3 g/dL vs the 36/57 who did not. The present data show that an abnormally low ret-He value (&lt; 28.5 pg) identifies patients who will respond to iron replacement, obviating delays to obtain standard iron parameters. Baseline and changes in ret-He also associate with Hb response. Given the enormous prevalence of ID in the general population the use of the ret-He, which is available with the CBC on the autoanalyzer, informs need for iron replacement, or lack thereof, represents an increase in convenience for patient and physician, decreases costs, streamlines care and represents an improvement in the treatment paradigm of one of the commonest maladies on the planet. Figure 1 Disclosures Auerbach: AMAG: Research Funding; Sysmex: Research Funding. Brugnara:American Journal of Hematology: Other; Sysmex America Inc.: Consultancy.


2020 ◽  
Vol 7 ◽  
pp. 205435812093339
Author(s):  
Paweena Susantitaphong ◽  
Monchai Siribumrungwong ◽  
Kullaya Takkavatakarn ◽  
Kamonrat Chongthanakorn ◽  
Songkiat Lieusuwan ◽  
...  

Background: There is no consensus on intravenous (IV) iron supplement dose, schedule, and serum ferritin target in functional iron deficiency anemia to maintain optimum target levels of iron stores by several guidelines. Objective: To examine the effect of IV iron supplementation to different targets of serum ferritin on erythropoietin dose and inflammatory markers in chronic hemodialysis (HD) patients with functional iron deficiency anemia. Design: A multicenter, randomized, open-label study. Setting: In a developing country, Thailand. Patients: Chronic HD patients with functional iron deficiency anemia. Measurements: Erythropoietin resistance index, high-sensitivity C-reactive protein, and fibroblast growth factor 23. Methods: Two hundred adult chronic HD patients with transferrin saturation less than 30% and serum ferritin of 200 to 400 ng/mL were randomized 1:1 to maintain serum ferritin 200 to 400 ng/mL (low-serum ferritin group, N = 100) or 600 to 700 ng/mL (high-serum ferritin group, N = 100). During a 6-week titration period, participants randomized to the high-serum ferritin group initially received 600 mg IV iron (100 mg every week), while the participants in the low-serum ferritin group did not receive IV iron. During the 6-month follow-up period, the dose of IV iron was adjusted by protocol. Results: The mean dose of IV iron was 108.3 ± 28.2 mg/month in the low-serum ferritin group and 192.3 ± 36.2 mg/month in the high-serum ferritin group. The mean serum ferritin was 367.0 ± 224.9 ng/mL in the low ferritin group and 619.6 ± 265.2 ng/mL in the high ferritin group. The erythropoietin resistance index was significantly decreased in the high-serum ferritin group compared to the low-serum ferritin group after receiving IV iron in the 6-week titration period (mean difference: −113.43 ± 189.14 vs 41.08 ± 207.38 unit/week/g/dL; P < .001) and 3-month follow-up period (mean differences: −88.88 ± 234.43 vs −10.48 ± 217.75 unit/week/g/dL; P = .02). Limitations: Short follow-up period. Conclusion: Maintaining a serum ferritin level of 600 to 700 ng/mL by IV iron administration of approximately 200 mg per month as a maintenance protocol can decrease erythropoietin dose requirements in chronic HD patients with functional iron deficiency anemia. Trials registration: The study was registered with the Thai Clinical Trials Registry TCTR20180903003.


2008 ◽  
Vol 28 (2) ◽  
pp. 149-154 ◽  
Author(s):  
Han Li ◽  
Shi-Xiang Wang

Objective To explore the safety and efficacy of intravenous (IV) iron sucrose in maintenance peritoneal dialysis (PD). Design Randomized, controlled, parallel-group single-center trial. Setting Blood Purification Center of Chaoyang, Beijing Capital University of Medical Science, China. Methods 46 patients on PD were involved in this trial. 26 patients received IV iron sucrose (200 mg iron) once per week for 4 weeks then once every other week for a further 4 weeks. The other 20 patients received oral ferrous succinate, 200 mg three times per day, for 8 weeks. Hemoglobin, hematocrit, serum ferritin (SF) level, and transferrin saturation (TSAT) were assessed at baseline and then again after 2, 4, and 8 weeks of treatment. Results There were no differences between the IV and oral groups in terms of sex, age, duration of PD, mean dialysate dosage per day, erythropoietin dosage per week, or hematological parameters at baseline. After 4 and 8 weeks of treatment, mean Hb and Hct were significantly increased in the IV group and were also significantly higher than those in the oral group. Levels of SF and TSAT were also significantly increased in the IV group, and significantly higher than in the oral group. After 8 weeks, the response rate in the IV group was 94.8%, which was significantly higher than that in the oral group. The mean erythropoietin dose was significantly lower in the IV group than in the oral group. Hb, Hct, SF, and TSAT levels were maintained between 4 and 8 weeks in the IV group despite the decrease in dose frequency. There were no adverse events with IV iron. Eight patients in the oral group had adverse gastrointestinal effects. Conclusion IV iron sucrose is safe in PD patients. It increases Hb levels and serum iron parameters more effectively than oral iron; it is well tolerated and can permit reductions in the required dose of erythropoietin.


Blood ◽  
2021 ◽  
Vol 138 (Supplement 1) ◽  
pp. 3077-3077
Author(s):  
Lia Phillips ◽  
Marc Richmond ◽  
Cindy Neunert ◽  
Gary M. Brittenham

Abstract Introduction: The overall aim of our study was to determine if iron deficiency has harmful effects on cardiac function in children with chronic heart failure. Heart failure in children is a complex, heterogeneous disorder leading to a final common pathway of cardiomyocyte dysfunction and attrition. Cellular, animal, and human studies have shown that iron deficiency causes cardiomyocyte dysfunction that can be reversed with iron treatment. Cellular studies of human iron-deficient cardiomyocytes have shown that supplemental iron restores impaired contractility and relaxation. Animal studies have found that cardiomyocyte-specific deletions or alterations of critical iron proteins (transferrin receptor 1, hepcidin, ferroportin) produce cardiomyocyte iron deficiency (without anemia) and result in ultimately fatal cardiac dysfunction that can be rescued with intravenous (IV) iron. Over half of adults with chronic heart failure are iron deficient. Meta-analysis of small randomized clinical trials has shown that IV iron significantly reduces recurrent hospitalization, cardiovascular mortality, and all-cause mortality in iron deficient adults with heart failure. European Society of Cardiology, American College of Cardiology and American Heart Association guidelines recommend consideration of IV iron therapy for adult iron-deficient patients with heart failure. The prevalence and consequences of iron deficiency in children with heart failure have not been established. Previously, two small retrospective studies of children with heart failure have reported that 56% to 96% were iron deficient, with increased morbidity and mortality. The goals of our study of children with heart failure were to determine (i) how often iron status is assessed, (ii) the prevalence of iron deficiency, and (iii) the effects of iron deficiency on cardiac function in patients with cardiomyopathy. Methods: We retrospectively reviewed electronic medical records to identify pediatric patients ages 1-21 years old seen at Columbia University Irving Medical Center Pediatric Heart Failure clinic with absolute iron deficiency during 2010-2020. Heart failure was defined as presence of symptoms or systolic dysfunction by echocardiography. Patients were excluded with a history of heart transplant, isolated diastolic failure, or renal failure requiring dialysis. In adults with heart failure, a transferrin saturation &lt;20% has a sensitivity of 94% and a specificity of 84% in identifying absolute iron deficiency, as determined from a bone marrow aspirate, and iron stores were present in 100% of patients with a transferrin saturation ≥30% (Circ Heart Fail. 2018;11:e0045). In children with heart failure, we used these criteria to define absolute iron deficiency as a transferrin saturation &lt;20% and iron sufficiency as a transferrin saturation ≥30%. Patients with an intermediate transferrin saturation are likely a mixture of absolute and functional iron deficiency, and of iron sufficiency and were excluded from our analysis of cardiomyopathy. Cardiac ejection fraction was evaluated by an echocardiogram performed within 3 months of measurement of transferrin saturation. Results: Of 579 patients with heart failure, only 159 (27%) had any type of laboratory iron studies. Of patients with iron studies, 81 (51%) were evaluated as outpatients; 49% as inpatients. The cause of heart failure was cardiomyopathy (52%), congenital heart disease (34%), acute myocarditis (6%), and other (8%). In the 82 patients with heart failure due to cardiomyopathy, 39 (48%) were iron deficient and 16 (20%) iron sufficient. In the iron deficient children with cardiomyopathy, the left ventricular ejection fraction was lower than in the iron sufficient patients (median 21% vs. 37%; p=0.03 (Mann-Whitney); Figure). The groups did not differ significantly with respect to hemoglobin (Figure), sex, age, or New York Heart Association class. Conclusion: We report a clinically important decrease in cardiac ejection fraction in children with heart failure due to cardiomyopathy who have absolute iron deficiency. Potentially, iron treatment could safely and effectively reverse the harmful effect of iron deficiency on heart function and prospective randomized trials of oral and intravenous iron therapy are urgently needed. Measurement of iron status should routinely be included in the evaluation of children with heart failure. Figure 1 Figure 1. Disclosures Neunert: Novartis: Research Funding.


2017 ◽  
Vol 1 (2) ◽  
pp. 31-35
Author(s):  
Shaheen Anjum ◽  
Nidhi Garg ◽  
Sri Beriwal ◽  
Anjum Parvez

ABSTRACT Objective To compare an accelerated high-dose (500 mg) vs low-dose (200 mg) regimen of intravenous iron sucrose in a cohort of iron-deficient anemic antenatal patients in terms of efficacy, safety, and compliance. Materials and methods In a prospective hospital-based study, antenatal and postnatal women with anemia attending Jawaharlal Nehru Medical College and Hospital, Aligarh, India, between December 2010 and December 2012 were enrolled. The inclusion criteria were all outpatient and admitted anemic antenatal women ≤ 36 weeks gestation and postnatal women with hemoglobin (Hb) below 10 gm/dL, or serum ferritin ≤ 30 μg/L or transferrin saturation ≤ 40% irrespective of prior oral iron therapy. Patients were excluded from the study if they were hemodynamically unstable, actively bleeding, having fever, or were nauseated or vomiting. Participants were assigned to control and study groups according to simple random sampling. Intravenous iron sucrose group I (500 mg)/group II (200 mg) was infused after test dose on alternate days for the calculated total dose in the study population. Blood and iron indices were measured at baseline and after 2 weeks of administration of last dose. The primary outcome of the study was to assess the rise in Hb and safety of high-dose intravenous iron sucrose. Results There was a statistically significant increase in Hb level in patients receiving either regimen, with larger mean increase in group I (2.7 ± 0.4) compared with group II (2.25 ± 6.39). Serum iron and serum ferritin also increased in both fortnightly (p < 0.001). Blood transfusion was avoided by 90.1% in severely anemic cases with Hb < 7. Hospital stay was reduced by 50% in group I. Conclusion The accelerated regimen of high-dose (500 mg) intravenous iron sucrose in anemic antenatal patients appears to be safe and effective in correcting anemia, restoring iron stores, and avoiding blood transfusion. How to cite this article Anjum S, Garg N, Beriwal S, Parvez A. High-dose Accelerated vs Low-dose Frequent Regime of Iron Sucrose Therapy in Antenatal and Postnatal Women with Iron Deficiency. World J Anemia 2017;1(2):31-35.


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