Evidence Of Iron Deficiency Research Articles

PWE-050 An Evaluation of Patients Referred to Gastroenterology Anaemia Clinic

IntroductionIron-deficiency anaemia in adults is a common cause of referral to gastroenterologists (4–13% of referrals). NICE guidelines, UK provides clear recommendations regarding upper and lower gastrointestinal investigations for such patients...

Iron deficiency and its management in patients undergoing lipoprotein apheresis. Comparison of two parenteral iron formulations

ObjectivesThere is evidence of iron deficiency (ID) in patients treated with lipoprotein apheresis. Aim of this study was to assess ID in apheresis patients and to study its management comparing safety and efficacy of two approved intravenous (i.v.) iron formulations. MethodsInclusion criteria were defined as a) serum ferritin < 300 μg/l and transferrin saturation < 20%, b) ferritin < 100 μg/l. Both iron deficient alone and ID anemic (IDA) patients were included. Other causes for anemia were ruled out by thorough history-taking and examination/blood tests. Patients were treated with six different lipoprotein apheresis methods: DALI, Liposorber D, TheraSorb LDL, HELP, MONET and Lipidfiltration. 50 patients were randomized to either ferric carboxymaltose (FCM, 500–1000 mg as single shot infusion over 20 min) or ferric gluconate (FG, 62.5 mg once weekly). Results50 of 67 patients of our Lipoprotein Apheresis Center showed iron deficiency. Both i.v. iron formulations studied were equally safe (no serious adverse events (SAEs), 6 patients/group showed adverse events (AEs)) and both effective (clinically and with respect to laboratory data) in lipoprotein apheresis patients, however FCM led to a more rapid and steeper rise of iron parameters. ConclusionsID and IDA are common findings in lipoprotein apheresis patients. The pathogenesis remains yet poorly understood and is probably multifactorial. Differential diagnosis of ID/IDA is as essential as differential therapy. Handled with care, older i.v. iron preparations like FG appear to be safe and effective in lipoprotein apheresis patients. However, novel formulations like FCM can be administered rapidly at higher doses due to high complex stability, allowing faster filling of iron stores.Newer laboratory parameters (Reticulocyte-He, low/medium/high fluorescence reticulocytes (LFR/MFR/HFR)) assessing iron status may be helpful in early detection of ID and in monitoring iron replacement therapy.

79-Year-Old Woman With Forgetfulness

79-Year-Old Woman With Forgetfulness

Helicobacter pylori and Effects on Iron Status in Children: Delineating Causality

<i>Helicobacter pylori</i> and Effects on Iron Status in Children: Delineating Causality

Is there an association between diarrhoea predominant irritable bowel syndrome and small bowel injury on capsule endoscopy?

IntroductionDiarrhoea predominant irritable bowel syndrome (D-IBS) represents a large outpatient gastroenterology workload. There are a subset of patients where their symptoms of D- IBS may overlap with suspected Crohn's disease....

Nutritional Assessment of Bariatric Surgery Patients Presenting for Plastic Surgery: A Prospective Analysis

Assessment of nutritional status in the growing postbariatric patient population remains controversial. Previous literature suggests that these patients have poor nutrition that may have adverse effects on surgical outcomes. The authors sought to determine the optimal method of nutritional assessment in postbariatric patients. One hundred patients presenting for body contouring after bariatric surgery were consecutively enrolled in an institutional review board-approved prospective study. A trained nutritionist assessed protein and calorie intake. All patients underwent baseline laboratory assessment. Eighteen percent of subjects had less than the recommended daily protein intake. Hypoalbuminemia was observed in 13.8 percent of subjects, with hypoprealbuminemia in 6.5 percent. Nearly forty percent of all patients had evidence of iron deficiency, with vitamin B12 deficiency present in 14.5 percent. Ten percent of subjects (all women) were confirmed to have iron deficiency anemia. Impaired fasting glucose was seen in 6.2 percent of subjects, whereas 3.6 percent had hemoglobin A1c levels greater than 6.5. Increasing age (odds ratio, 1.07) and greater change in body mass index (odds ratio, 1.11) were predictors of low protein intake. Dumping syndrome led to 13.3 times increased odds of low albumin levels. The results suggest that inadequate nutrition is common among postbariatric patients presenting for body contouring. The lack of correlation between methods of nutritional assessment supports the combination of multiple methods in determining overall nutritional status. The presence of dumping syndrome, a large change in body mass index, and advanced age may help to identify patients with an increased risk of nutritional deficiency.

Influence of infection on iron profile in severely malnourished children

To study the iron profile and find out an accurate diagnostic tool which reflects iron status in different types of infection in severely malnourished children aged 12 months to 71 months. Hundred and Eight (108) children of whom 72 children were infected and 36 non infected severely malnourished children according to WHO criteria in the age group of 12-71 months were interrogated. 36 healthy control in the same age group were also interrogated. Mean serum iron, total iron binding capacity (TIBC), ferritin concentration in normal children were significantly higher (P<0.001) than non-infected severely malnourished children. On the other hand mean serum ferritin concentration was significantly higher (P<0.001) in infected group than non-infected group but still lower than normal. Mean serum TIBC concentration significantly reduced in severely malnourished children than normal children but no significant difference was observed between non-infected and infected group. Mean serum iron, and transferrin saturation were significantly reduced (P<0.05) in parasitic infestation. Severely malnourished children had reduced mean serum iron profile. Parasitic infestation influenced the marked reduction of mean serum iron concentration and transferrin saturation level. Mean serum iron concentration was reduced in acute respiratory infection(ARI) and parasitic infestation than other infections. Serum ferritin concentration was elevated in all types of infection as acute phase protein but still lower than normal. So Iron, TIBC and Transferin saturation <16% constitute good evidence for iron deficiency in both infected and non-infected severely malnourished children.

Gastrointestinal evaluation of anaemic patients without evidence of iron deficiency

Bleeding lesions are commonly identified in the gastrointestinal (GI) tract of patients with iron deficiency anaemia (IDA). Gastroenterologists, however, are frequently referred patients with anaemia without supporting evidence of iron deficiency, where the merit of GI investigation is unknown. We conducted a retrospective, case-control study to determine the prevalence of bleeding GI lesions in 100 anaemic patients without evidence of iron deficiency [noniron deficiency anemia (NIDA) group] and 271 patients with confirmed IDA (IDA group). The prevalence of bleeding lesions in the upper GI tract was significantly lower in NIDA patients (8%) compared with IDA patients (22.9%) (odds ratio 0.29, 95% confidence interval 0.15-0.55, P<0.0009). The prevalence of lower GI bleeding lesions was also significantly lower in NIDA patients (6.9%) compared with IDA patients (20.2%) (odds ratio 0.26, 95% confidence interval 0.12-0.57, P<0.025). No cases of GI malignancy were identified in the NIDA group, but in the IDA group 5.5% had an upper GI cancer and 10.7% colorectal cancer (P<0.002 and P<0.0002, respectively). Subgroup analysis of patients aged more than or equal to 70 years stratified according to serum ferritin concentration (low, intermediate and high), revealed that the prevalence of bleeding lesions in both the upper (26.4% vs. 23.5% vs. 2.9%) and lower (26.8% vs. 16.7% vs. 0%) GI tract did not differ significantly between patients with a low serum ferritin and intermediate serum ferritin concentrations, but was significantly lower in the low ferritin group compared with high ferritin group (P<0.003 and P<0.0001, respectively). NIDA patients were also significantly more likely to have chronic kidney disease (33%), compared with IDA patients (12%), P<0.0001, and to subsequently undergo bone marrow sampling (P<0.02) with a potential cause for their anaemia being found. GI bleeding lesions are infrequently found in anaemic patients without evidence of iron deficiency and alternative causes should first be sought. Elderly patients, however, with an intermediate ferritin concentration (30-100 microg/l) also had a high yield of bleeding lesions and should be considered for GI evaluation.

Cervical esophageal web and celiac disease

There is paucity of prospective data on association between cervical esophageal webs and celiac disease. It is not clear whether all patients with cervical esophageal web need screening for celiac disease. Hence, the present study was carried out to determine the association of cervical esophageal web with celiac disease. This prospective study included consecutive patients with symptomatic cervical esophageal web diagnosed over a period of 4.5 years. Tissue transglutaminase antibody was measured in serum of each patient. Patients with elevated tissue transglutaminase antibody titer were subjected to esophagogastroduodenoscopy and biopsies were obtained from the descending duodenum to look for histological changes of celiac disease. Esophageal web was treated with bougie dilatation. Celiac disease was diagnosed on the basis of elevated tissue transglutaminase antibody and suggestive duodenal histology. Twenty one patients were diagnosed to have cervical esophageal web. Eighteen (85.7%) had evidence of iron deficiency. Five (23.8%) patients with cervical esophageal web fulfilled criteria for diagnosis of celiac disease. All five had evidence of iron deficiency. None of these patients gave a history of chronic diarrhea. All patients were treated with bougie dilatation. Patients with celiac disease were advised of a gluten-free diet. All five celiac disease patients are free of dysphagia without recurrence after a mean follow up of 10 months (range: 3 to 16 months). There is association between cervical esophageal web and celiac disease. All adult patients with cervical esophageal web and iron deficiency need screening for celiac disease even in the absence of chronic diarrhea.

Hypoferraemia and serum ferritin (author's transl)

The wide use of serum iron determination by automatic analysers may lead to low values being taken as evidence of iron deficiency. Determining serum ferritin concentration in such cases provides rapid and reliable information to distinguish between reactive hypoferraemia and iron deficiency hypoferraemia, as demonstrated in tests on 71 patients with reproducible hypoferraemia. In 31 patients there was reactive hypoferraemia, in 40 iron deficiency hypoferraemia.

Effect of Intravenous Iron Sucrose in Peritoneal Dialysis Patients Who Receive Erythropoiesis-Stimulating Agents for Anemia

Although iron therapy is essential to optimize use of erythropoiesis-stimulating agents (ESA), randomized, controlled trials have heretofore been unavailable to evaluate reliably the efficacy of intravenous iron as an adjuvant to ESA treatment in peritoneal dialysis (PD) patients. In a multicenter trial, patients who had anemia, PD-dependent chronic kidney disease, stable ESA therapy, and a broad range of iron status (ferritin < or = 500 ng/ml, transferrin saturation < or = 25%) were randomly assigned to receive either 1 g of iron sucrose intravenously in three divided doses (300 mg over 1.5 h on days 1 and 15, 400 mg over 2.5 h on day 29) or no supplemental iron. No serious adverse drug events occurred after intravenous iron administration. The primary end point, peak hemoglobin increase, was higher (1.3 +/- 1.1 versus 0.7 +/- 1.1, mean +/- SD; P = 0.0028), and anemia intervention (transfusion, increase in ESA dose, or intravenous iron therapy not called for in protocol) occurred later (P = 0.0137) and less often in intravenous iron-treated patients compared with untreated control subjects (one of 66 [1.3%] versus five of 30 [16.7%]). Among patients who did not require intervention, iron-treated patients showed a calculated net ESA dose decrease compared with untreated control subjects. Baseline iron status did not predict responsiveness to intravenous iron therapy. Intravenous iron sucrose is an effective adjunct to ESA therapy in anemic patients with PD-dependent chronic kidney disease and is administered safely as 300 mg over 1.5 h or 400 mg over 2.5 h. Evidence of iron deficiency at baseline is not required to demonstrate intravenous iron efficacy.

Molecular Analysis of β-Thalassemia Cases in Poland.

β-thalassemia is a heterogenous, inherited disease resulting from reduced or absent synthesis of β-globin chain of haemoglobin. This disorder is very common in the Mediterranean, Middle Eastern, African and South-East Asian populations. The aim of the present investigation was to verify a common view that thalassemia in Poland is a very rare disease. 600 patients (270 men and 330 women), aged 2–85 years, with microcytosis and no evidence of iron deficiency, were examined for β-thalassemia. Hemoglobin A2 was increased in 106 patients. In 48 patients there was also an elevation of hemoglobulin F and in 42 patients of serum bilirubin.All 106 patients were examined for 8 common Mediterranean mutations. 7 different mutations were detected in 46 heterozygous patients (number of patients wit a particular mutations are in square brackets): IVS1-6(T>C) [15]; IVS2-745(C>G)[14]; IVS2-1(G>A) [10]; IVS1-1(G>A) [2]; CD6-A [2]; CD39(C>T) [2]; IVS1-110(G>A) [1].We also discuss the effect of these mutations on the expression level of the β-globin gene. Frequencies of individual mutations in Poland were different from those encountered in Mediterranean and some Centrak European countries. We also detect two novel mutations:IVS-1-1(G>A) G^GTTGGT>AGATTGGT and 5′UTR; +33(C>T). The first novel mutation significantly decreased the mRNA level of the β-globin gene. The second mutation seems to be silent and does not affect β-globin synthesis. In this case, this particular mutation occurs with IVS-1-6(G>C) mutation in compound the heterozygotes stage.

The prevalence of iron deficiency among patients presenting with colorectal cancer

To examine prospectively the prevalence of iron deficiency among new patients presenting with colorectal cancer and to compare transferrin saturation and serum ferritin as markers of iron deficiency in this group of patients. Data were gathered on all patients presenting with a new diagnosis of colorectal cancer over a 12-month period. Iron status was estimated and, when possible, confirmed by measurement of serum ferritin concentration and transferrin saturation. Iron status was further examined in relation to tumour site and Dukes' stage. During the study 157 patients presented with a new colorectal cancer. Of these, 130 could be evaluated and 78[60%] had evidence of iron deficiency. Transferrin saturation was below the reference range in 55 patients, but serum ferritin was below in only 18 patients. Among the 49 patients with right-sided cancers, 39[80%] were iron deficient. Iron deficiency was significantly more likely in patients with right sided cancers compared with those with cancers at or distal to the splenic flexure (chi2 = 13, P < 0.001). The majority of patients with a new diagnosis of colorectal cancer are iron deficient at presentation. In such patients transferrin saturation measurement is a more sensitive marker of iron deficiency than serum ferritin. The potential role of measuring serum transferrin saturation as an adjunct to faecal occult blood screening should be explored further.

To have and have not: Health and health care disparities in chronic kidney disease

A 50-year-old African American man came to the emergency room complaining of substernal chest discomfort over the past 2 months, as well as anorexia, general malaise, and decreased urinary frequency over the past 2 weeks. The patient stated that his chest pain lasted 2 to 3 minutes; did not radiate to the neck, jaw, or shoulder; was precipitated by lifting heavy objects; and did not occur at rest. He admitted to mild shortness of breath when walking up the stairs at home. He noted that for 2 weeks, he had been feeling exhausted and had had poor appetite, weight loss, and less frequent urination than usual. The patient had last seen a physician 4 years ago at an urgent care facility for a pilonidal cyst abscess. Five years prior to that, he had been told by a primary care physician that he had hypertension. He was treated with an unknown medication and, after a follow-up visit, was told that his blood pressure was normal. He has no other known history of cardiovascular or renal disease. He takes no medications. He lost his job as a cook and the health insurance that the job provided; he now says that he is unable to continue seeing the physician. He completed high school, is married, and works as a taxi driver as well as at a local farmers market on weekends. His father had hypertension and died suddenly at age 55. His mother is 71 and has diabetes. He has one older brother who

An Ethiopian pattern of human adaptation to high-altitude hypoxia.

We describe, in Ethiopia, a third successful pattern of human adaptation to high-altitude hypoxia that contrasts with both the Andean "classic" (erythrocytosis with arterial hypoxemia) and the more recently identified Tibetan (normal venous hemoglobin concentration with arterial hypoxemia) patterns. A field survey of 236 Ethiopian native residents at 3,530 m (11,650 feet), 14-86 years of age, without evidence of iron deficiency, hemoglobinopathy, or chronic inflammation, found an average hemoglobin concentration of 15.9 and 15.0 gdl for males and females, respectively, and an average oxygen saturation of hemoglobin of 95.3%. Thus, Ethiopian highlanders maintain venous hemoglobin concentrations and arterial oxygen saturation within the ranges of sea level populations, despite the unavoidable, universal decrease in the ambient oxygen tension at high altitude.

Iron and Protein Sufficiency and Red Cell Indices in Phenylketonuria

Objective and Methods: We reviewed records of 41 children with treated phenylketonuria (PKU) in order to evaluate hematopoiesis and the effect of iron and protein sufficiency.Results: Six children (15%) were found to have anemia. Combined depletion of iron and protein stores was most likely to result in anemia, and two of the three children with this finding were anemic. Four children (10%) had evidence of iron deficiency without anemia (a precursor stage of iron deficiency anemia). Clinically significant iron depletion was found in older as well as younger children (well beyond the traditional infant/toddler deficient years). Plasma albumin was normal in all children and was not adequately sensitive to detect protein depletion sufficient to cause anemia or decreased growth. However, low plasma prealbumin (a more sensitive marker of protein sufficiency) correlated significantly with altered hematopoiesis or poor growth.Conclusion: Compared to non-affected individuals, children with treated PKU make fewer red cells that have normal volume but increased hemoglobin per cell, resulting in a lower calculated hematocrit when measured by electronic cell counting. In the presence of iron or protein depletion, anemia may result. Routine monitoring of ferritin, complete blood counts and prealbumin are recommended for children with PKU at all ages.

Intravenous iron dextran treatment in predialysis patients with chronic renal failure

Iron deficiency anemia is common in patients with chronic renal failure not undergoing hemodialysis. Current therapy consists of oral or intravenous (IV) iron dextran (IVID). The standard IV regimen is 100 to 200 mg/dose for a 1-g total dose. We hypothesized that 500 mg/wk of IVID for two doses would be less costly and equally effective as 200 mg/wk for five doses. We prospectively studied 22 patients with creatinine clearances less than 50 mL/min who were not undergoing dialysis and had anemia and evidence of iron deficiency (ferritin level <100 ng/mL or transferrin saturation [TSAT] <20%). Patients were randomized into two groups: group I (n = 8), 200 mg/wk of IVID for 5 weeks, and group II (n = 14), 500 mg/wk of IVID for 2 weeks. All patients tolerated IVID infusions without serious adverse reactions. Over the 6-month follow-up, both groups experienced an increase in hemoglobin levels from baseline. Ferritin levels in both groups increased (P < 0.005), peaked at 2 weeks, then declined thereafter. Over the 6-month follow-up, both groups experienced significant improvement, although the beneficial effects of group II declined at a significantly faster rate than group I (P = 0.003). There was no significant difference in change in ferritin levels between groups. TSAT peaked at 2 weeks in both groups (P < 0.001). Group I experienced a significant increase in TSAT throughout the 6-month follow-up (P < 0.03), and group II achieved a significant increase in TSAT at 2 weeks, but not at 3 and 6 months. There was no significant difference in pretreatment to posttreatment change in TSAT. Treatment in group II was 35.2% more cost-effective than in group I ($965 versus $1,490, respectively). We conclude that IVID, 500 mg/wk, for 2 weeks is as effective and safe as 200 mg/wk for 5 weeks, but much less costly.

Evaluation of Anemia in Angiotensin Converting Enzyme (ACE) Knockout Mice.

P2 Using targeted homologous recombination, we made two lines of mice that lack ACE. ACE.1 mice are null for all ACE activity while ACE.2 mice lack tissue ACE but retain 1/3 normal plasma ACE activity. Both strains have a marked decrease in blood pressure and are unable to produce a concentrated urine. ACE.1 mice have renal failure, as measured by a reduced creatinine clearance and an elevated serum creatinine, when compared to wild type mice; ACE.2 mice have no evidence of renal failure as indicated by a normal serum creatinine and creatine clearance. Surprisingly, both ACE.1 and ACE.2 mice are anemic with a reduction in hematocrit (38.5 +/- 1.3% and 38.3 +/- 0.8% respectively vs 48.4 +/- 0.9% for wild type) and serum hemoglobin (12.0 +/- 0.3 mg/dl and 11.7 +/- 0.2 mg/dl vs 14.7 +/- 0.3 mg/dl for wild type). In both strains, serum erythropoietin is elevated. Neither strain differs from wild type in regard to MCV, MCH, or MCHC, nor does either strain show chemical evidence of iron deficiency or hemolysis. Both ACE.1 and ACE.2 mice have equally low serum angiotensin II levels with a significant elevation of serum angiotensin I and the stem cell inhibitory peptide AcSDKP. Due to the presence of renal failure in ACE.1 mice, we have characterized in detail the anemia of ACE.2 mice. These animals demonstrate a significant reduction in total circulating red cell mass (24.2 +/- 1.1 μl/g vs 31.7 +/- 1.8 μl/g for wild type mice) without a change in total blood volume (57.8 +/- 1.2 μl/g vs 56.0 +/- 5.0 μl/g for wild type mice) as measured by the infusion of 51 Cr labeled erythrocytes. ACE.2 mice also have an increase in total plasma volume as determined by Evans Blue Dye infusion. The administration of angiotensin II to ACE.2 knockouts significantly increases their hematocrit and serum hemoglobin. Conclusion: The finding of significant anemia in ACE.2 mice, animals without renal failure, suggests a previously unappreciated role of the renin-angiotensin system in regulating erythropoiesis.

Elevated serum transferrin receptor concentration in children with juvenile chronic arthritis as evidence of iron deficiency.

Active juvenile chronic arthritis (JCA) is accompanied by anaemia of chronic disease, which may be indistinguishable from anaemia due to iron deficiency. We speculate that elevation of the serum transferrin receptor (sTfR) concentration, which should not be influenced by inflammation, would be useful for detecting the role of iron status in anaemic children with JCA. sTfR concentrations were measured in 30 children with JCA. The median sTfR was elevated, 6.1 (range 3.4-13.0) mg/l. In 13 patients (43%) the concentrations exceeded the upper limit for healthy subjects. Haemoglobin (r = - 0.48, P = 0.008), mean corpuscular volume (r = - 0.47, P = 0.009) and mean corpuscular haemoglobin (r = - 0.65, P = 0.0001) correlated inversely with sTfR concentration. In 13 of the 30 patients with JCA, the sTfR concentration, which is an indicator of iron status and erythropoiesis, was elevated. The results raise the possibility that sTfR is able to distinguish iron-deficiency anaemia from anaemia of chronic disease. It should be further explored as a candidate.

Increased Serum Transferrin Saturation Is Associated with Lower Serum Transferrin Receptor Concentration

Serum transferrin receptor (sTfR) concentrations are increased in iron deficiency. We wished to examine whether they are decreased in the presence of potential iron-loading conditions, as reflected by increased transferrin saturation (TS) on a single occasion. We compared sTfR concentrations between 570 controls with normal iron status and 189 cases with increased serum TS on a single occasion; these latter individuals may be potential cases of iron overload. Cases and controls were selected from adults who had been examined in the third National Health and Nutrition Examination Survey (1988-1994) and for whom excess sera were available to perform sTfR measurements after the survey's completion. Increased TS was defined as >60% for men and >55% for women; normal iron status was defined as having no evidence of iron deficiency, iron overload, or inflammation indicated by serum ferritin, TS, erythrocyte protoporphyrin, and C-reactive protein. Mean sTfR and mean log sTfR:ferritin were approximately 10% and 24% lower, respectively, in cases than in controls (P <0.002). Cases were significantly more likely to have an sTfR value <2.9 mg/L, the lower limit of the reference interval, than were controls (odds ratio = 1.8; 95% confidence interval, 1.04-2.37). Our results support previous studies that suggested that sTfR may be useful for assessing high iron status in populations.