Iron Replacement Therapy Research Articles

Iron Deficiency Anemia in the Elderly: Prevalence and Endoscopic Evaluation of the Gastrointestinal Tract in Outpatients

Iron deficiency anemia (IDA), mostly due to chronic occult bleeding from the gastrointestinal tract, is a common problem in the elderly. This study aimed to determine the prevalence of IDA in the elderly and to investigate the gastrointestinal tract in elderly patients with IDA. 1,388 patients over 65 years were prospectively evaluated for IDA in our outpatient clinic. IDA was defined if decreased hemoglobin concentrations (<13 g/dl for men and <12 g/dl for women) were associated with low serum ferritin levels (<15 ng/ml in men and <9 ng/ml in women). We evaluated the gastrointestinal system of all patients with IDA by upper gastrointestinal endoscopy and colonoscopy regardless of fecal occult blood loss. The prevalence of anemia was found to be 25% (n = 347) in our study population, and 30.5% (n = 106) of these patients with anemia had iron deficiency. Upper gastrointestinal endoscopy and colonoscopy were performed in 96 patients with IDA. Fifty-eight upper gastrointestinal system lesions (55 patients, 57.3%) and 27 colonic lesions (26 patients, 27.1%) were detected. We diagnosed gastrointestinal malignancy in 15 (15.6%) elderly patients with IDA (8 colon, 1 esophageal and 6 gastric cancers). IDA is a common problem in elderly patients; consequently, before iron replacement therapy, patients should be thoroughly investigated regarding a possible association with gastrointestinal malignancy.

PLUMMER‐VINSON SYNDROME: A REPORT OF THREE CASES

SUMMARYPlummer‐Vinson syndrome is characterised by dysphagia, anaemia, glossitis and oesophageal web. We report our findings in three patients with membranes in the upper oesophagus. All patients underwent endoscopic dilatation and iron replacement therapy, with good results. We review the literature of this syndrome.

Iron deficiency and cognition

Iron deficiency is the most prevalent nutritional disorder in the world. One of the most worrying consequences of iron deficiency in children is the alteration of behaviour and cognitive performance. In iron-deficient children, striking behavioural changes are observed, such as reduced attention span, reduced emotional responsiveness and low scores on tests of intelligence. Animal studies on nutritional iron deficiency show effects on learning ability that parallel the human studies. Despite the obvious confounding impact of socioeconomic factors, there is a wealth of clinical, biochemical and neuropathological research that shows that iron deficiency can exert a direct deleterious effect on learning and the brain, and that this can occur with normal haemoglobin levels. Nutritional iron replacement therapy readily corrects haematological iron status in iron-deficient children within 2-3 weeks, but behavioural problems persist for several months or years. This resi stance to iron-replacement therapy and its long-term consequences on learning are not quite understood. A recent study in infants showed that the cognitive deficits in iron deficiency was reversed with iron supplementation. This finding provides evidence that in some settings cognitive deficits are not always permanent. Although further research is required to address these issues, several studies support the theory that iron sufficiency throughout the course of brain development is critical to normal brain iron and behavioural outcome.

Iron-deficiency anemia

One of the most common causes of iron-deficiency anemia (IDA) in men and postmenopausal women in the United States is gastrointestinal blood loss, and therefore IDA is a frequent reason for referral to a gastroenterologist. It is important to begin the workup with confirmation of the diagnosis of IDA and to exclude other causes of anemia, including nongastrointestinal sources of blood loss. We review the mechanisms and regulation of iron absorption, storage, and iron loss, an understanding of which can be particularly useful in evaluating patients with concomitant chronic inflammatory diseases, end-stage renal disease, and patients receiving erythropoietin during chemotherapy. A major component of the evaluation of IDA is gastrointestinal investigation, usually beginning with bidirectional endoscopy, including colonoscopy and esophagogastroduodenoscopy. If patients have a negative lower and upper gastrointestinal evaluation, examination of the small bowel with enteroscopy and/or capsule endoscopy must be considered. The standard treatment of IDA requires correction of the underlying abnormality and oral iron replacement therapy, but in certain cases will require parenteral iron replacement. We will review the physiology, differential diagnosis, and evaluation of IDA, including the appropriate gastrointestinal evaluation of this disease process, along with a concise review of iron replacement therapy.

Anemia in patients with coronary artery disease.

The pathophysiology of impaired hemodynamic and nonhemodynamic responses to anemia in patients with coronary artery disease is discussed. In animals, experimentally induced coronary artery disease significantly inhibits the hemodynamic response to surgical blood loss; anecdotal evidence in humans corroborates these findings. Erythropoietic response to surgical blood loss may also be blunted in patients with coronary artery disease. Regardless of whether anemia is the result of a preexisting condition or surgical blood loss, its presence worsens outcomes in patients with coronary artery disease who undergo cardiac surgery. The combination of coronary artery disease and anemia has resulted in acute myocardial infarction as well. Finally, anemia after noncardiac surgery is associated with an increased risk of myocardial ischemia, potentially creating a cycle in which blood loss and myocardial ischemia exacerbate each other. Oral iron replacement therapy after elective cardiac surgery increases adverse events without significantly improving hematocrit and hemoglobin levels or iron stores. Allogeneic blood transfusions are less than ideal, and autologous blood transfusion with erythropoietin administration is only possible before elective procedures. New procedures and medications have reduced the blood loss associated with percutaneous coronary intervention, and minimization of blood loss during percutaneous coronary intervention has potentially major clinical and economic implications.

Iron status in anemic pregnant women.

A descriptive study at a tertiary care center was carried out to assess the prevalence of iron status in anemic pregnant women and to determine the appropriate iron supplement. Eligible subjects were pregnant women with a hemoglobin concentration <11 g/dL. Pregnant women who received antenatal vitamin and/or iron supplements before blood testing and women with an underlying chronic disease were excluded. Hemoglobinopathy was defined by hemoglobin typing other than HbA2A, percentage of HbA2 >4%, and HbF >1.1%. We diagnosed iron deficiency and iron depletion if their serum ferritin were <12 and 20 ng/mL, respectively, whereas anemia from undetermined causes was defined by hemoglobin typing, namely: A2A, HbA2 <4% and HbF <1.1%, and serum ferritin >20 ng/mL. Among the 137 anemic pregnant women recruited, 67 (49.8%) had HbA2A, 47(34.3%) HbEA, 15 (10.9%) HbEE, 3 (2.2%) HbCSA2A, 2 (1.5%) HbCSEA, 1 (0.7%) HbCSA2A Bart's, 1 (0.7%) HbEA Bart's, and 1 (0.7%) beta-thalassemia. Among the 67 women with normal hemoglobin (HbA2A), 14 (20.9%) had iron deficiency, and 12 (17.9%) iron depletion. Among the 70 women with hemoglobinopathy, 6 (8.6%) had iron deficiency, and 10 (14.3%) iron depletion. Anemic pregnant women with hemoglobinopathy could also be iron deficient so will need iron supplementation, as other pregnant women do, and some iron replacement therapy.

Retrospective review of the role of intravenous iron replacement therapy in treatment of anemia in patients with inflammatory bowel disease

Retrospective review of the role of intravenous iron replacement therapy in treatment of anemia in patients with inflammatory bowel disease

Intravenous Iron Replacement with Sodium Ferric Gluconate Complex in Sucrose for Iron Deficiency Anemia in Adults

Background: When oral iron replacement therapy is ineffective, IV or IM iron dextran products have been used successfully in many patients. However, adverse events, including urticaria, anaphylaxis, and death, sometimes are associated with the use of these products. Objective: The aim of this study was to assess the efficacy and tolerability of sodium ferric gluconate complex (SFGC) in sucrose in the treatment of adults with iron deficiency anemia. Methods: This was a single-center, open-label, uncontrolled study. Consecutive adults in need of IV iron replacement who experienced severe reactions to generic IV iron dextran and who had previously failed to respond to oral iron products were treated with a single dose of IV SFGC (312, 375, or 500 mg) infused over 2 hours. A second dose of SFGC could be administered 6 to 8 weeks later, if needed. Results: Six patients (3 men, 3 women; mean [SD] age, 77.0 [10.4] years) were enrolled. All patients received a single-dose infusion of SFGC, and 2 patients received a second dose. No adverse events were observed at the lower doses (312 and 375 mg); however, both patients given the 500-mg dose reported transient nausea, and 1 had pruritus and the other had transient hypertension. Conclusion: The results of this study show that SFGC is a satisfactory alternative when IV iron replacement is needed by adults with iron deficiency anemia.

High serum transferrin receptor level in anemia of chronic disorders indicates coexistent iron deficiency.

Blood transferrin receptor (TR) level is largely determined by the quantum of erythropoiesis and by intracellular iron content of the cells of the erythroid lineage. Hence, a high serum TR level has been found to be useful in distinguishing iron deficiency anemia (IDA) from anemia of chronic disorders (ACD). In order to examine its potential role in the diagnosis of concomitant iron deficiency in ACD, we determined serum TR levels in 130 cases of ACD, in 25 cases of IDA, and in 40 normal adults. As expected, all patients of IDA had significantly higher serum TR levels compared to the normal subjects (4.2-19.2 microg/dL vs. 1.3-3.0 microg/dL) (P < 0.002). In 11/25 cases of IDA, the total iron-binding capacity (TIBC) was in the normal range although bone marrow iron store was absent and serum TR levels were high, thereby highlighting the superiority of TR level in the diagnosis of iron deficiency compared to TIBC. Although 54% (70/130) patients of ACD had normal or low serum TR levels (0.9-3.0 microg/dL) as expected, in 46% (60/130) of ACD patients, serum TR levels were high (3.2-11.0 microg/dL). Mean corpuscular volume, red cell distribution width, and transferrin saturation were significantly lower (P < 0.001) in the latter group of patients compared to the former, and these parameters resembled those in IDA patients. Also, serum iron was lower and TIBC was higher in this group of ACD patients compared to those with normal or low serum TR. All these features point to an "IDA-like" profile of ACD patients with high TR and support the possibility of co-existent iron deficiency in this subgroup of ACD patients. In light of these observations it would be prudent to treat ACD patients with high serum TR levels with iron replacement therapy.

A Hematologic “Gold Standard” for Iron-deficient States?1

In this issue of the Journal, Thomas and Thomas (1) provide a novel approach to the diagnosis of iron-deficient states. Traditionally, iron deficiency studies have used various biochemical indicators of iron metabolism to establish the absence or presence of biochemical iron deficiency and to assess the performance of a potentially novel biochemical or hematologic marker. Biochemical indicators have included serum iron, serum transferrin, transferrin saturation, serum ferritin, and serum circulating transferrin receptor (TfR) as well as various ratios of these variables. Hematologic indices that have been used to establish the presence of iron deficiency anemia have included, in addition to hemoglobin (Hb) or hematocrit (Hct), abnormal erythrocytes or reticulocyte indices that identify the presence of hypochromic and microcytic cells. Additional variables that have been investigated include zinc protoporphyrin and erythrocyte ferritin. Studies on the diagnosis of iron-deficient states have been complicated by the absence of a clear reference method to detect biochemical iron deficiency. Iron staining of bone marrow biopsy is widely quoted as a gold standard, but the invasive nature of this procedure severely limits its use. A less invasive standard for iron deficiency is based on the hematologic response to iron replacement therapy: an increase of the reticulocyte count or reticulocyte index after oral or intravenous iron replacement therapy reveals the presence of iron deficiency. The use of biochemical markers to diagnose iron-deficient states is problematic in clinical conditions such as the anemia of chronic disease (ACD). When a disturbed iron metabolism is associated with acute or chronic phase inflammatory responses, serum ferritin and transferrin concentrations are affected and not informative. Biochemical markers are also less effective in diagnosing functional iron deficiency, a transient discrepancy between iron supply and utilization that is mostly seen in individuals treated with recombinant human erythropoietin (r-HuEPO). In their report, Thomas and Thomas …

Folate metabolism in renal failure.

In most patients with chronic kidney disease, provision of sufficient human recombinant erythropoietin (rHuEPO) and iron replacement therapy will effectively correct renal anaemia. Folate deficiency has been implicated as a contributory factor in renal anaemia and hyporesponsiveness to rHuEPO treatment. As such, the necessity of regular folate supplementation has been debated over the last decade. Although folate loss through dialysis is greater than by urinary excretion, these losses are easily balanced by a normal mixed diet containing 60 g protein/day. Thus, unless patients show significant folate depletion, additional supplementation of folic acid does not appear to have a beneficial effect on erythropoiesis or on responsiveness to rHuEPO therapy. However, a diagnosis of folate deficiency should be considered in patients with chronic renal insufficiency and significant elevation in mean cell volume or hypersegmented polymorphonuclear leucocytes; in patients with malnutrition or a history of alcohol abuse, or in patients hyporesponsive to rHuEPO treatment, especially when accompanied by macrocytosis. Measurements of serum folate are not necessarily indicative of tissue folate stores and red blood cell (RBC) folate measures provide a more accurate picture. Low RBC folate concentrations in these patients indicate the need for folate supplementation. Folate supplementation can also reduce elevated levels of homocysteine in dialysis patients, which may contribute to the high cardiovascular morbidity prevalent in these individuals. High-dose folate therapy (5-15 mg/day) has been shown to reduce plasma homocysteine levels by 25-30% and appears to be well tolerated provided the patient has adequate vitamin B(12) stores. Although long-term benefits of this intervention for cardiovascular protection and patient survival have yet to be established, folic acid is considered a relatively non-toxic and well-tolerated vitamin.

Erythropoietin deficiency causes anemia in nephrotic children with normal kidney function

Anemia in persistent nephrotic syndrome (NS) has been described in a few case reports but has not been studied systematically. We present a group of 19 children with NS who developed anemia before the deterioration of kidney function. The aim of our study is to determine whether erythropoietin (EPO) and/or iron deficiency are causative factors and to evaluate the effect of EPO replacement therapy. Serum EPO levels, iron status, and vitamin B12 concentrations were measured in nephrotic patients with anemia (NS-A) and compared with those of nephrotic children with normal hemoglobin (Hb) levels (NS-NHb; n = 13). Two control groups consisted of age-matched patients without kidney disease or hypoxemia with either iron deficiency anemia (IDA; n = 19) or normal Hb concentrations (NHb; n = 16). Most NS-A patients experienced persistent steroid-resistant NS, whereas most NS-NHb children had steroid-responsive NS. Although serum iron, ferritin, and B12 levels were significantly lower in NS-A children, appropriate replacement therapy that resulted in normalization of ferritin and/or cobalamin levels did not lead to correction of the anemia. NS-A patients had greater EPO levels than those without anemia (21.6 ± 3.3 versus 5.5 ± 0.8 IU/L; P < 0.001), but their response to anemia was inappropriately low compared with IDA children (EPO, 94.6 ± 15.1 IU/L) despite similar Hb concentrations. EPO therapy for 4 to 9 months in 6 NS-A children with Hb levels less than 9 g/dL led to resolution of the anemia. In conclusion, anemia is a common feature of persistent NS that develops before the deterioration of kidney function. Depletion of iron stores may contribute to the development of anemia, but iron replacement therapy is ineffective. Nephrotic patients have EPO deficiency with a blunted response to anemia. The EPO deficiency is amenable to EPO therapy, which is recommended for this group of patients.

Incidence of Peritonitis in Chronic Peritoneal Dialysis Patients Infused with Intravenous Iron Dextran

The Dialysis Outcomes Quality Initiative (DOQI) guidelines, published in 1997, emphasize the need for careful monitoring of iron stores and for provision of adequate iron replacement therapy to achieve target goals of hemoglobin concentration in end-stage renal disease (ESRD) patients, especially those treated with recombinant erythropoietin (rHuEPO). Intravenous iron dextran (IVID) therapy, which has long been used in hemodialysis patients, is increasingly being used in chronic peritoneal dialysis (CPD) patients. In 1997, we began using this form of iron therapy for our CPD patients. However, because considerable data exists to show a relationship between iron metabolism and acute infections, we questioned whether IVID infusion placed our patients at greater risk for peritonitis, the leading cause of death and patient drop-out from CPD therapy. To evaluate the relationship between iron and infection, we studied episodes of peritonitis in CPD patients who were infused with IVID. In a retrospective study of adult CPD patients who received IVID during 1998, we investigated the occurrence of peritonitis episodes and the spectrum of causative organisms. Patients with a hemoglobin level of < 12.5 g/dL who also had a ferritin level < 100 ng/mL or a transferrin saturation level < 20% (or both) and who did not respond to oral iron therapy, were administered between 0.5 g and 1.0 g of IVID in an outpatient hospital setting. We calculated the expected and observed number of peritonitis episodes in these patients within 30, 60, and 90 days after infusion of IVID. During the study period, 56 patients received 77 doses of IVID, with 14 patients requiring 2 or more infusions. Of the 77 doses, 71 were given as a 1-g bolus. The IVID was well tolerated by all patients. Within 90 days of IVID administration, 14 patients developed peritonitis: 6 episodes occurred within 30 days, 7 episodes occurred between 31 and 60 days, and 1 episode occurred between 61 and 90 days after the IVID dosing. The peritonitis rate for patients not receiving IVID was 1 episode per 13.7 patient-months. Taking this rate as the "expected" rate, the expected number of episodes of peritonitis for the study population was 5.6 episodes within 30 days, 11.2 episodes within 60 days, and 16.8 episodes within 90 days following IVID administration. The difference between the expected and observed rates of peritonitis in patients who were dosed with IVID was not statistically different. The spectrum of organisms seen in the peritonitis episodes in the study population was not significantly different from that seen in the peritonitis episodes in our CPD unit population. There is evidence that IVID infusion therapy can improve anemia and reduce rHuEPO requirements in CPD patients, usually without adverse reaction and without exposing patients to an increased risk of peritonitis. More research is needed in the area of potential increased risk of infection in ESRD patients who are (1) infused with large doses of IVID, and (2) iron-overloaded.

Thrombopoietic Cytokines in Patients with Iron Deficiency Anemia with or without Thrombocytosis

Iron deficiency anemia is a cause of reactive thrombocytosis. A moderate increase in platelet numbers is common but sometimes counts may exceed 1,000 × 10⁹/l. The mechanisms causing reactive thrombocytosis are unclear. In this study, we evaluated 15 women with iron deficiency anemia and thrombocytosis (platelets >450 × 10⁹/l) and 16 women with iron deficiency anemia with normal platelet counts. Serum samples were taken before oral iron replacement therapy, after 1 and 3 months and at the end of replacement therapy. Thrombopoietin, erythropoietin (EPO), leukemia inhibitory factor, interleukin-6 and interleukin-11 levels were assayed. There was no change in the levels of thrombopoietic cytokines except for EPO. The correlation between high EPO levels and high platelet counts may suggest that EPO increases platelet counts, but the same EPO level changes can also be demonstrated in women with iron deficiency anemia but normal initial platelet counts. The fact that the levels of other cytokines remained unchanged during treatment suggests that either these cytokines have no effect on reactive thrombocytosis or the change in platelet counts in our patients is in a narrow range and is thus not affected by the cytokine levels.

Hypotransferrinemia of chronically hemodialyzed patients.

Increasingly, the iron needs of hemodialysis patients receiving erythropoietin are being met by infusions of intravenous iron guided by laboratory tests to measure body iron availability. The interpretation of assays based on ferritin and transferrin must take into account the effect of inflammation on both proteins and malnutrition on the latter. In our chronic hemodialysis population, hypotransferrinemia was present in greater than 90% of the patients. Using statistical methods and laboratory studies, we sought to identify the principal reasons for the high prevalence of hypotransferrinemia. We observed that transferrin levels were disproportionately low relative to albumin and prealbumin and correlated inversely with ferritin levels. There was no correlation between transferrin and the soluble transferrin receptor. After the infusion of 900 mg of iron, transferrin saturation increased and total transferrin decreased so that unsaturated iron bonding capacity decreased as well. Ferritin concentrations increased significantly after iron loading. Attempts to demonstrate activation of the patients' antioxidant mechanisms associated with iron infusion were negative. We concluded that the low transferrin may be principally the result of diminished synthesis related to the chronic inflammatory status of hemodialysis patients, which favors production of ferritin, but iron and nutritional status may also influence the blood transferrin concentration. These factors make interpretation of transferrin-dependent assessment of body iron stores unreliable and can result in inadequate or overly aggressive iron-replacement therapy.

Reversal of iron deficiency anemia after Helicobacter pylori eradication in patients with asymptomatic gastritis.

Iron deficiency anemia is the most common form of anemia worldwide. Recent studies have suggested an association between Helicobacter pylori infection and iron deficiency. To investigate the effects of eradicating H. pylori with combination antibiotic therapy on iron deficiency anemia in patients with H. pylori-associated gastritis. Case series. University hospital. 30 patients with a long history of iron deficiency anemia in whom H. pylori-associated gastritis was the only pathologic gastrointestinal finding detected. Eradication therapy with two antibiotics and discontinuation of iron replacement therapy. Complete blood count, ferritin levels, and gastroscopy with biopsy to evaluate H. pylori status. At 6 months, 75% of patients had recovered from anemia (P<0.001), ferritin values increased from 5.7+/-0.7 microg/L to 24.5+/-5.2 microg/L (95% CI, 8.85 to 29.97). After 12 months, 91.7% of patients had recovered from anemia. Cure of H. pylori infection is associated with reversal of iron dependence and recovery from iron deficiency anemia.

Effects of iron deficiency anemia on hemoglobin A1c in type 1 diabetes mellitus.

The relationship between hemoglobin A1c (HbA1c) and iron status in type 1 diabetes mellitus (DM) has not been adequately studied. In this prospective investigation, we aimed to determine the effect of iron deficiency on HbA1c in diabetic patients who also had insufficient iron stores. Thirty-seven patients with type 1 DM were included in the study. Eleven of them were also iron deficient (ID) and the remaining 26 were iron-sufficient (IS). Two non-diabetic control groups were selected for the ID and IS groups. All patients with ID were treated with iron at 6 mg/kg per day for 3 months. Glycemia in diabetic patients was monitored at home before breakfast and supper by a glycometer. Hemoglobin A1c was measured in all subjects at the beginning and the end of the study. Patients with ID DM had higher levels of HbA1c than those in the control group (P < 0.001). There were no significant differences in the weekly average glucose concentration of the patients with ID DM before and after iron supplementation. In contrast, HbA1c decreased from a mean of 10.1 +/- 2.7% to a mean of 8.2 +/- 3.1% (P < 0.05). Additionally, HbA1c in ID non-diabetic patients decreased from a mean of 7.6 +/- 2.6% to 6.2 +/- 1.4% after iron therapy (P < 0.05). We conclude that among type 1 DM patients with similar level of glycemia, iron deficiency anemia is associated with higher concentrations of HbA1c. In addition, iron replacement therapy leads to a drop in HbA1c in both diabetic and non-diabetic patients. The iron status of the patient must be considered during the interpretation of HbA1c concentrations in type 1 DM.

Sodium ferric gluconate complex in sucrose: safer intravenous iron therapy than iron dextrans.

Use of recombinant human erythropoietin in patients with end-stage renal disease has highlighted iron deficiency as the major cause of resistant anemia. The current mainstay of intravenous (i.v.) iron replacement therapy, iron dextran, has been shown in prior studies to have a risk of serious life-threatening anaphylaxis of just under 1 per 100 patients exposed. The current study assessed the safety profile of an alternative i.v. iron, sodium ferric gluconate complex in sucrose (Ferrlecit), as compared with iron dextrans. Sodium ferric gluconate complex in sucrose, a unique chemical preparation, has been in use since 1959, principally in Europe, at a rate of approximately 2.7 million i.v. doses per year (1992 to 1996) in Germany and Italy alone. For iron dextran, usage in the United States was comparable--principally renal hemodialysis--and estimated from market sources at 3.0 million doses per year (1995). From 1976 to 1996, there were 74 allergic adverse events reported for sodium ferric gluconate complex in sucrose to the World Health Organization (WHO), German Health Bureau, and the manufacturer (all combined). For the years 1992 to 1996, sodium ferric gluconate complex in sucrose had an allergy event reporting rate of 3.3 allergy episodes per million doses per year compared with a similar rate of 8.7 reported allergy events per million doses per year for iron dextran in the United States in 1995. Case fatalities for sodium ferric gluconate complex in sucrose and iron dextran within these reports were then compared. For sodium ferric gluconate complex in sucrose, there were no reports of deaths over the entire period (1976 to 1996). However, for iron dextrans, there were 31 fatalities among 196 allergy/anaphylaxis cases reported in the United States between 1976 and 1996, yielding a case-fatality rate of 15.8%. These data show that sodium ferric gluconate complex in sucrose, when compared with iron dextrans in comparably sized patient usage populations with similar total rates of reporting of allergic events, has a significantly lower reported mortality rate (P < 0.001). Thus, the data justify usage of sodium ferric gluconate complex in sucrose as the safer iron replacement therapeutic agent.

Beneficial effects of iron therapy in renal failure patients on hemodialysis

Iron deficiency is a common problem in patients treated with hemodialysis. If not detected and treated appropriately, the effectiveness of recombinant human erythropoietin therapy is compromised. Much has been learned in recent years with respect to iron therapy for hemodialysis patients. A series of studies have clearly defined the efficacy of intravenous iron compounds, and recently released clinical practice guidelines have set the appropriate clinical context for the use of these agents. The purpose of this article is to examine the beneficial effects of iron replacement therapy for hemodialysis patients.

Decrease Serum Erythropoietin Level Induced by Iron Replacement Therapy in Patients with Iron Deficiency Anemia

Decrease Serum Erythropoietin Level Induced by Iron Replacement Therapy in Patients with Iron Deficiency Anemia