Ret-Y a measure of reticulocyte size: a sensitive indicator of iron deficiency anemia

In this study the size of reticulocytes was measured, reticulocyte-Y (Ret-Y), to distinguish iron deficiency anemia from the anemia of chronic disease using a Sysmex XE2100 cell counter. We evaluated this parameter prospectively in 100 patients seen for the evaluation of anemia. A clinical diagnosis of iron deficiency anemia or anemia of chronic disease was made on the basis of a complete blood count, examination of the peripheral smear, and serum ferritin along with a history and physical examination. We analyzed the sensitivity and specificity of the Ret-Y in relationship to the clinical diagnosis. We also measured serum transferrin receptor levels to use as the gold standard laboratory test for iron deficiency against which we compared the Ret-Y. In 40 normal individuals with normal serum ferritin and transferrin receptor levels the mean Ret-Y was 1874 +/- 178 (1 SD). The mean Ret-Y in the anemia of chronic disease group (n=62) was 1722 +/- 162, not significantly different from normal. The mean Ret-Y value among iron-deficient patients (n=38), was 1407 +/- 136 (P <0.01 vs. the anemia of chronic disease group's Ret-Y value). Receiver operator curves showed that Ret-Y correlated closely to the serum transferrin receptor and was superior to the mean corpuscular volume, and ferritin level, in differentiating the type of anemia. The Ret-Y parameter has the highest overall sensitivity and specificity of the panel of tests routinely used in differentiating iron deficiency anemia from anemia of chronic disease.     

Soluble transferrin receptor and soluble transferrin receptor/log ferritin index in diagnosis of iron deficiency anemia in pediatric inflammatory bowel disease

Background

There is no single reliable marker of iron homeostasis in inflammatory bowel disease.

Clinical importance of determining levels of circulating transferrin receptors in blood

Circulating serum transferrin receptor level was measured using mouse monoclonal antibody against transferrin receptor (Orion Diagnostica, Finland) in 126 patients with various disorders of erythropoiesis and the results were compared to those obtained form control group consisted of 30 healthy volunteers with normal iron stores. Serum transferrin receptor level was significantly elevated in patients with iron deficiency and in all patients with hyperplastic erythropoiesis (hereditary spherocytosis, immune hemolytic anemia, beta thalassemia, myelodysplasia). Measurement of circulating serum transferrin receptor level was a sensitive indicator of iron depletion as well as a helpful parameter in differential diagnosis between iron deficiency and anemia of chronic disease where circulating transferrin receptor level was not elevated. Index transferrin receptor/ferritin calculated as a ratio of circulating serum transferrin receptor level to log serum ferritin level was a more sensitive parameter than measurement of serum transferrin receptor not only for determination of patients with anemia of chronic disease, but also for discrimination of patients with elevated serum transferrin receptor level due to true iron deficiency from those with high serum transferrin receptor level caused by relative iron deficiency in hyperplastic erythropoiesis.     

Serum transferrin receptors in detection of iron deficiency in pregnancy

 A prospective hospital-based study was conducted to evaluate the efficacy of serum transferrin receptors in the detection of iron deficiency in pregnant women. The iron status of 100 pregnant women with single uncomplicated term pregnancies in the first stage of labor was established using standard laboratory measures. These included complete hemogram, red cell indices, serum iron, percent transferrin saturation, and serum ferritin. In addition, serum transferrin receptor (STFR) was estimated. The results of 81 women with complete laboratory profiles were analyzed. Thirty-five (43.2%) women were anemic (hemoglobin <11 g/dl). Hemoglobin (Hb) showed a significant correlation with MCH, MCHC, serum iron, and percent transferrin saturation, suggesting that the anemia was likely to be due to iron deficiency. The mean STFR level was 18.05±9.9 mg/l in the anemic women and was significantly raised (p<0.001) compared with that of the nonanemic women. STFR correlated significantly with Hb (p<0.001), MCH (p<0.05), MCHC (p<0.01), serum iron (p<0.01), and percent transferrin saturation (p<0.01) and also showed a highly significant correlation with the degree of anemia. Serum ferritin in these women did not correlate with Hb, and only 54.4% of the women had levels <12 ng/ml, which does not reflect the true prevalence of iron deficiency. Serum transferrin receptor estimation is thus a useful measure for detecting iron deficiency in pregnancy. Received: August 26, 1998 / Accepted: March 30, 1999     

Biochemical expression of heterozygous hereditary hemochromatosis

Background: Hereditary hemochromatosis (HH) is a common autosomal recessive disease caused by an iron overload. Two mutations (C282Y and H63D) on the responsible HFE gene have been described. HH heterozygotes may have a slight iron overload that does not cause clinical disease. Compound heterozygosity may be associated with higher iron stores than C282Y heterozygosity. We studied biochemical iron parameters in HH C282Y and compound heterozygotes without a clinically significant iron overload. Methods: Data on hemoglobin, hematocrit, mean corpuscular volume, serum ferritin, serum iron, transferrin, and transferrin saturation were obtained from 40 C282 wild type controls (irrespective of H63D genotype), 61 C282Y heterozygotes, and 18 compound (C282Y/H63D) heterozygotes without clinical iron overload disease. Results: Serum ferritin levels were significantly higher in female HH heterozygotes, particularly in compound heterozygotes, than in normal women. In male heterozygotes, no difference in serum ferritin was found. We found higher mean serum iron and transferrin saturation levels in male and female HH heterozygotes than in normal controls, the highest in the group of compound heterozygotes. Conclusions: Mean serum ferritin (only in women), serum iron, and transferrin saturation are highest in compound heterozygotes and lowest in controls. C282Y heterozygotes seem to be an intermediate group between compound heterozygotes and the normal population.     

Anemia in Crohn's disease

Intestinal blood loss as well as chronic inflammation are regarded as the most important mechanisms in the pathogenesis of anemia in Crohn's disease. In addition, cytokines such as interleukin-6 can suppress erythropoietin production. This study was performed to investigate the importance of iron status, inflammatory activity, and endogenous erythropoietin concentrations for the development of anemia in Crohn's disease. In 49 consecutive patients with Crohn's disease, hemoglobin, inflammatory activity (Crohn's disease activity index, C-reactive protein, α₁-acid glycoprotein), iron status (serum iron, transferrin, transferrin saturation, ferritin), and serum erythropoietin levels were studied. Anemic (Hb<12.0 g/dl;N=16) vs nonanemic patients (Hb≥12 g/dl;N=33) showed reduced iron compartments (eg, ferritin 28.7±12.9 µg/liter vs 63.2±15.0 µg/liter, transferrin saturation 6.2±1.4% vs 11.5±1.3%,P<0.01) but no differences in inflammatory activity. An inverse correlation between erythropoietin and hemoglobin concentrations was found (r=-0.62;P<0.001), but the increase in erythropoietin levels was inadequate to the degree of anemia. There was no correlation between erythropoietin and interleukin-6 serum levels. Four of five anemic patients with hemoglobin below 10.5 g/dl and erythropoietin levels within the normal range were treated with parenteral iron (200 mg iron saccharate in 250 ml NaCl, weekly, intravenously). Two of them additionally received recombinant human erythropoietin (150 units/kg, 3× weekly, subcutaneously). After five weeks all patients had a marked increase in hemoglobin. However, the mean increase in erythropoietin-treated patients was 5.0 g/dl compared to 2.0 g/dl in the patients with iron therapy only. No side effects were seen. Our data demonstrate that inadequate erythropoietin production and iron deficiency are pathogenetic factors of anemia in Crohn's disease. The therapeutic management using recombinant human erythropoietin and parenteral iron is reasonable and effective.     

Bone marrow iron distribution,hepcidin, and ferroportin expression in renal anemia

Abstract

Objectives

The hepcidin–ferroportin system is involved in both conditions associated with iron-restricted erythropoiesis in renal anemia: iron deficiency and anemia of chronic disorders. As serum hepcidin could aid diagnosis, we investigated its relationships with bone marrow iron distribution, hepcidin–ferroportin expression in bone marrow cells, and peripheral iron indices in non-dialysis chronic kidney disease (CKD) patients.

Methods

Fifty-four epoetin and iron naive CKD patients entered this prospective, observational study. According to bone marrow iron distribution (iliac crest biopsy, Perls' stain), 26 had iron deficiency anemia, 21 anemia of chronic disorders and 7 had normal iron stores. Medullar hepcidin and ferroportin expression (immunofluorescence (IF), semiquantitative scales) and serum hepcidin (Hep25 – ELISA) were the main studied parameters.

Results

Low hepcidin and high ferroportin expression by erythroblast and macrophage were seen in iron deficiency anemia, while the opposites were true in anemia of chronic disorders. In regression analysis, higher Hep25 and ferritin predicted hepcidin expression (R²=0.48; P < 0.0001), while lower ferritin and Hep25 - predicted ferroportin expression (R² = 0.29; P = 0.003) by erythroblast; inflammation had no contribution. In ROC analysis, serum hepcidin and ferritin had similar moderate utility in differentiating iron deficiency anemia from anemia of chronic disorders (AUC 0.63 95% CI 0.47–0.79 and 0.76 95% CI 0.61–0.90, respectively).

Conclusions

Thus, in anemic epoetin naive non-dialysis CKD patients, hepcidin and ferroportin expression by erythroblast and macrophage are closely related to bone marrow iron distribution. Although the hepcidin–ferroportin system seems regulated by ferritin-driven Hep25, serum hepcidin and peripheral iron indices are of little help in describing bone marrow iron status.     

Prevalence of abnormal iron studies in heterozygotes for hereditary hemochromatosis: An analysis of 255 heterozygotes

Iron studies were compared in 434 patients from 80 hemochromatosis families classified as putative homozygotes, heterozygotes, and normal by HLA typing. There were 28 of 255 (11%) heterozygotes with an elevated serum ferritin and 22 of 255 (8.6%) with an elevated transferrin saturation. Serum ferritin (140 ± 10.2 μg/liter; mean ± standard error) was greater in heterozygotes than in normal subjects (87 ± 8.5 μg/liter; P < .05, Mann Whitney test). Transferrin saturation was greater in heterozygotes (38% ± 0.88%) than in normal patients (29% ± 1.1%; P < .0001). Mean hepatic iron concentration was 54 ± 6 μmol/g (n = 17), and the hepatic iron index was <2 in these patients. Most heterozygotes for hemochromatosis have a normal serum ferritin and transferrin saturation. Heterorygotes with minor elevations in serum ferritin or transferrin saturation do not have significant iron overload as assessed by hepatic iron concentration. © 1994 Wiley-Liss, Inc.     

Changes in Hepcidin and Reticulocyte Hemoglobin Equivalent Levels in Response to Continuous Erythropoietin Receptor Activator Administration in Hemodialysis Patients: A Randomized Study

Inadequate iron availability limits the response to erythropoiesis‐stimulating agents (ESA) and hepcidin is a key regulator of iron metabolism. However, there is little information concerning time‐dependent changes in hepcidin in response to the change of accelerated iron demand due to ESA‐induced erythropoiesis. In this study, iron‐related parameters, including hepcidin levels, were explored in comparison to patients receiving continuous erythropoietin receptor activator (CERA) and epoetin beta (EPO) treatment. Ninety‐four patients were randomized to receive monthly CERA (N = 47) or EPO three times/week (N = 47). After the titration period, hemoglobin levels and iron‐related parameters were examined. Data for 71 patients were evaluated (CERA, N = 34; EPO, N = 37). Compared with EPO treatment, CERA treatment caused significant decreases within 1 week in hepcidin (?93.5 ± 46.9 vs. ?1.3 ± 38.3 ng/mL, P < 0.01), reticulocyte hemoglobin equivalent (Ret‐He) (?4.03 ± 2.64 vs. ?1.13 ± 1.41 pg, P < 0.01), ferritin (?58.9 ± 30.5 vs. ?12.2 ± 23.8 ng/mL, P < 0.01) and transferrin saturation (?13.2 ± 9.1 vs. 1.0 ± 11.9%, P < 0.01) and significant increases within 2 weeks in the levels of hemoglobin (0.42 ± 0.38 vs. ?0.02 ± 0.48 g/dL, P < 0.01). In conclusion, hepcidin, Ret‐He, ferritin and transferrin saturation levels decreased within 1 week and hemoglobin increased within 2 weeks after CERA administration. Time course of iron‐related parameters including hepcidin demonstrated accelerated iron utilization appropriately according to ESA‐induced erythropoiesis.     

Value of Soluble Transferrin Receptors and sTfR/log Ferritin in the Diagnosis of Iron Deficiency Accompanied by Acute Infection

There are many causes of anemia; the most common of these are acute and chronic infections, iron deficiency, or both. Identifying the cause is a very important step in management of anemia. So, we evaluated the usefulness of soluble transferrin receptor (sTfR) and of the sTfR/log ferritin in the diagnosis of iron deficiency anemia accompanied by acute infection. This study was conducted on 131 children aged 2–11 years old from those who attended the pediatric outpatient clinics in Menoufia university hospital. Hematological indices, iron balance and sTfR were evaluated and the sTfR/log F was calculated for each examined child. From the examined children four groups were distinguished: Group I (control): included 34 healthy children with normal iron status (66.7% males, age 4.2 ± 1.2). Group II (IDA): included 38 children diagnosed as iron deficiency anemia (47.4% males, age 4.9 ± 1.6). Group III (IDA + infection): included 26 children with infectious disease (upper respiratory tract infection, otitis media, pneumonia, stomatitis, and urinary tract infection) and anemia meeting criteria of IDA (50% males, age 4.2 ± 0.7). Group IV (anemia + infection): included 33 children with infectious anemia without iron deficiency (56.2% males, age 5.06 ± 1.4). It was proved that sTfR and sTfR/log Ferritin were significantly higher in children with anemia due to iron deficiency, and in those with infection + iron deficiency, versus those with infectious anemia or in healthy children. The use of sTfR and sTfR/log ferritin improves the diagnosis of IDA in pediatric patients, especially in the presence of coexisting acute infection.     

Factor V Leiden mutation carriership and venous thromboembolism in polycythemia vera and essential thrombocythemia

The aim of the present study is to evaluate in an elderly hospitalized population the diagnostic value of the serum transferrin receptor (sTfR) in distinguishing IDA (iron deficiency anemia) from ACD (anemia of chronic disease) as compared to conventional laboratory tests of iron metabolism, especially serum ferritin. In a prospective study, 34 patients with IDA and 38 patients with ACD (a chronic disorder in 23 and an acute infection in 15) were evaluated using iron status tests including serum transferrin receptor assay. The iron stores were assessed by bone marrow examination. sTfR levels were elevated (>28.1 nmol/L) in 68% of the IDA patients but also in 43% of the patients with ACD-chronic inflammation and 33% with ACD-acute infection. Serum ferritin was the best test to differentiate IDA from ACD patients. We conclude that serum ferritin is a more sensitive and specific parameter than the sTfR assay to predict the bone marrow iron status in an elderly anemic population.     

Evaluation of derived Coulter red blood cell parameters for the assessment of iron deficiency in adults with congenital heart disease

Introduction: The aim of our study was to evaluate derived red blood cell parameters in determining the presence of iron depletion and iron‐deficient erythropoiesis, as states that precede iron deficiency anemia, in adults with congenital heart disease. Methods: Eighty‐eight adults who were diagnosed with congenital heart disease were divided into two groups (cyanotic and acyanotic). In both groups, congenital heart disease patients were then divided into three subgroups: with iron depletion, with iron‐deficient erythropoiesis, and a control group. The following parameters were measured: complete blood count, reticulocytes, ferritin, soluble transferrin receptor, haptoglobin, lactate dehydrogenase, and calculated parameters: low hemoglobin density (LHD), red cell size factor (RSF), and microcytic anemia factor (MAF). Results: Discriminant analysis indicated statistically significant differences in the first discriminant function: Function 1 – body iron, LHD, MAF, sTfR, and RSF (P < 0.001) in patients with acyanotic congenital heart disease and significant differences in both discriminant functions in patients with cyanotic congenital heart disease: Function 1 – body iron, soluble transferrin receptor, LHD, RSF, MAF, lactate dehydrogenase, and haptoglobin (P = 0.008) and Function 2 – reticulocytes (#), immature reticulocyte fraction and reticulocytes (%) (P = 0.049). Conclusions: Beside parameters that describe iron metabolism dynamics (body iron and soluble transferrin receptor), LHD, indicator of hypochromia, have the highest potential to differentiate and classify iron deficiency in patients with congenital heart disease.     

HFE Gene Mutations, Serum Ferritin Level, Transferrin Saturation, and Their Clinical Correlates in a Korean Population

The aim of this study was to investigate HFE gene mutations, blood iron indices, and their clinical correlates in a Korean population. In 484 prospectively enrolled health-check examinees, HFE gene mutations and iron indices with clinical and laboratory variables were analyzed. Although neither the C282Y nor S65C gene mutation were found, the H63D heterozygote was detected in 41 subjects (8.5%). The mean serum ferritin and transferrin saturation (TS) were 136.2 ± 129.8 μg/dl and 39.2 ± 15.7%, respectively. The H63D genotype was not significantly associated with iron indices. High serum ferritin was associated with old age, the male gender, high body mass index (BMI), and the presence of nonalcoholic fatty liver disease (NAFLD). High TS was associated with the male gender and alcohol drinking. HFE gene mutation is rare; however, TS seems to be higher in Koreans compared to Caucasians or other ethnic groups. Serum ferritin reflects iron store as well as the presence of NAFLD.     

Defective iron supply for erythropoiesis and adequate endogenous erythropoietin production in the anemia associated with systemic-onset juvenile chronic arthritis

Systemic-onset juvenile chronic arthritis (SoJCA) is associated with high levels of circulating interleukin-6 (IL-6) and is frequently complicated by severe microcytic anemia whose pathogenesis is unclear. Therefore, we studied 20 consecutive SoJCA patients with hemoglobin (Hb) levels <12 g/dL, evaluating erythroid progenitor proliferation, endogenous erythropoietin production, body iron status, and iron supply for erythropoiesis. Hb concentrations ranged from 6.5 to 11.9 g/dL. Hb level was directly related to mean corpuscular volume (r = .82, P < .001) and inversely related to circulating transferrin receptor (r = - .81, P < .001) suggesting that the severity of anemia was directly proportional to the degree of iron-deficient erythropoiesis. Serum ferritin ranged from 18 to 1,660 microgram/L and was unrelated to Hb level. Bone marrow iron stores wore markedly reduced in the three children investigated, and they also showed increased serum transferrin receptor and normal-to-high serum ferritin. All 20 patients had elevated IL-6 levels and normal in vitro growth of erythroid progenitors. Endogenous erythropoietin (epo) production was appropriate for the degree of anemia as judged by both the observed to predicted log (serum epo) ratio 10.95 +/- 0.12) and a comparison of the serum epo- Hb regression found in these subjects with that of thalassemia patients. Multiple regression analysis showed that serum transferrin receptor was the parameter most closely related to hemoglobin concentration: variation in circulating transferrin receptor explained 61% of the variation in Hb level (P < .001). In 10 severely anemic patients, amelioration of anemia following intravenous iron administration resulted in normalization of serum transferrin receptor. Defective iron supply to the erythron rather than blunted epo production is the major cause of the microcytic anemia associated with SoJCA. A true body-iron deficiency caused by decreased iron absorption likely complicates long-lasting inflammation in the most anemic children, and this can be recognized by high serum transferrin receptor levels. Although oral iron is of no benefit, intravenous iron saccharate is a safe and effective means for improving iron availability for erythropoiesis and correcting this anemia. Thus, while chronically high endogenous IL-6 levels do not appear to blunt epo production, they are probably responsible for the observed abnormalities in iron metabolism. Anemia of chronic disease encompasses a variety of anemic conditions whose peculiar features may specifically correlate with the type of cytokine(s) predominantly released.     

Serum transferrin receptor in hereditary hemochromatosis and African siderosis

The present investigation evaluated the serum transferrin receptor concentration in subjects with nontransfusional iron overload who were identified in two separate studies on the basis of a serum ferritin level above 400 μg/L. Subjects with preciinical hereditary hemochromatosis were evaluated in the first study and those with the African form of iron overload in the second. in the first study, hereditary hemochromatosis was identified in 14 white men on the basis of a persistent elevation in transferrin saturation above 55%. The serum receptor concentration was elevated above the upper cut-off of 8.5 mg/L in two of the subjects, but the mean receptor of 6.1 ± 1.4 mg/L (mean ± 2 SE) did not differ significantly from the normal mean for this assay of 5.6 ± 0.3 mg/L. In the same study, 60 control subjects with secondary iron overload were identified on the basis of a serum ferritin persistently above 400 μg/L, with a normal serum C-reactive protein concentration but with a transferrin saturation <55%. Three of these subjects had an elevated serum receptor concentration but the mean value of 5.5 ± 0.4 mg/L did not differ from normals nor from subjects with hemochromatosis. In the second study, 49 black Africans with iron overload were divided into those with or without an elevated transferrin saturation. The mean serum receptor concentration of 5.0 ± 0.8 mg/L and 4.5 ± 0.4 mg/L, respectively, did not differ statistically. It was concluded that there is no evidence of generalized dysreguiation of the transferrin receptor in hemochromatosis or African siderosis. © 1994 Wiley-Liss, Inc.     

Monitoring oral iron therapy with protoporphyrin/heme ratios in pregnant women

 Assessment of the efficacy of iron therapy has usually been done in populations/patients by monitoring changes in hemoglobin concentration, serum iron, percent transferrin saturation, and serum ferritin. In this study the protoporphyrin heme (P/H) ratio (a measure of free erythrocyte protoporphyrin) was measured before and after iron therapy in three groups of pregnant women, who received 60 mg (group A), 120 mg (group B), and 240 mg (group C) of elemental iron with folic acid (0.5 mg) per day for a period of 12 weeks, to evaluate its efficacy to monitor iron therapy. The three groups were comparable regarding the initial mean Hb concentration and serum ferritin levels. The initial mean P/H ratios were markedly elevated in all three groups and were different in the three groups, being highest in group A (113.2±92.6), intermediate in group B (87.5±62.5), and lowest in group C (69.8±43.3). The initial P/H ratio was significantly higher in group A than in group C (p<0.05). This probably affected the efficacy of iron therapy in the three groups. The P/H ratio decreased significantly in each of the three groups after iron therapy (A and B : p<0.001; C p<0.01). Mean Hb concentration and serum ferritin increased in all three groups post therapy; however, the magnitude of change in P/H ratio in all three groups was much greater. This indicated that the predominant contributory factor for anemia was iron deficiency in this group of pregnant women. Serum iron and percent transferrin saturation are difficult to interpret in our population, as iron is freely available over the counter and is prescribed as soon as anemia is detected in patients; therefore, the reduction in P/H ratio may be used to monitor response to iron therapy in population groups. Received: October 17, 1998 / Accepted: January 28, 1999     

Serum transferrin receptor: a quantitative measure of tissue iron deficiency

This study was undertaken to evaluate the role of serum transferrin receptor measurements in the assessment of iron status. Repeated phlebotomies were performed in 14 normal volunteer subjects to obtain varying degrees of iron deficiency. Serial measurements of serum iron, total iron-binding capacity, mean cell volume (MCV), free erythrocyte protoporphyrin (FEP), red cell mean index, serum ferritin, and serum transferrin receptor were performed throughout the phlebotomy program. There was no change in receptor levels during the phase of storage iron depletion. When the serum ferritin level reached subnormal values there was an increase in serum receptor levels, which continued throughout the phlebotomy program. Functional iron deficiency was defined as a reduction in body iron beyond the point of depleted iron stores. The serum receptor level was a more sensitive and reliable guide to the degree of functional iron deficiency than either the FEP or MCV. Our studies indicate that the serum receptor measurement is of particular value in identifying mild iron deficiency of recent onset. The iron status of a population can be fully assessed by using serum ferritin as a measure of iron stores, serum receptor as a measure of mild tissue iron deficiency, and hemoglobin concentration as a measure of advanced iron deficiency.     

Serum soluble transferrin receptor in the diagnosis of iron deficiency in chronic liver disease

Fifty-one consecutive patients with chronic liver disease (CLD) underwent investigations of their iron status (full blood count, serum iron [Fe], total iron binding capacity [TIBC], transferrin saturation [TS], serum ferritin and serum soluble transferrin receptor [sTfR] level). Twenty-six patients were anaemic; 12 patients had iron deficiency, and 10 had iron deficiency anaemia (IDA). The median (range) sTfR in the IDA patients was 16.6 (11.2–24.8) mg/l, compared with 6.6 mg/l (11.2–24.8) in the 16 patients with anaemia due to other causes (P = 0.01). The sensitivity of sTfR for diagnosing iron deficiency in CLD was 91.6% (100% if only anaemic patients are included) and the specificity was 84.6%. Patients with haemolysis and recent blood loss may have falsely elevated sTfR levels. The results suggest that the sTfR is as useful as serum ferritin in identifying a potentially treatable cause of anaemia in CLD.     

Iron deficiency in inflammatory bowel disease

The prevalence of iron-deficiency anemia was defined in 105 patients with inflammatory bowel disease and an appraisal made of the diagnostic value of serum ferritin for the assessment of iron stores. Iron deficiency, defined by the absence of bone-marrow hemosiderin was found with anemia in 36% of 41 patients with ulcerative colitis (UC) and 22% of 64 patients with Crohn's disease (CD). Iron deficiency without impaired erythropoiesis was detected in an additional 32% of patients with UC and 2% with CD. Anemia with plentiful bone-marrow iron was present in 33 (51%) of patients with CD, only one of whom had vitamin B₁₂ deficiency. Red blood cell morphology, RBC indices, serum iron, and percent transferrin saturation correlated poorly with stainable marrow iron. Serum ferritin, assayed in samples from 45 patients, was <18 ng/ml in 4/12 with iron-deficiency anemia and 0/5 with absent marrow iron and a normal hemoglobin level; values >55 ng/ml were invariably associated with the presence of marrow hemosiderin. Based on a lower normal limit of 18 ng/ml, the serum ferritin had an excellent predictive value (100%) but a high predictive error (32%) in the diagnosis of iron deficiency in inflammatory bowel disease. Serum ferritin >55 ng/ml ruled out iron deficiency as the basis for anemia.