scholarly journals Curcumin induces mild anemia in a DSS-induced colitis mouse model maintained on an iron-sufficient diet

2018 ◽  
Author(s):  
Macha Samba-Mondonga ◽  
Marco Constante ◽  
Gabriela Fragoso ◽  
Annie Calvé ◽  
Manuela M. Santos
Keyword(s):  
Iron Deficiency ◽  
Mouse Strain ◽  
Inflammatory Diseases ◽  
Iron Chelator ◽  
Deficiency Anemia ◽  
Mouse Strains ◽  
Liver Iron ◽  
Iron Stores ◽  
Mild Anemia ◽  
Anti Inflammatory

AbstractAnemia is frequently encountered in patients with inflammatory bowel disease (IBD), decreasing the quality of life and significantly worsening the prognosis of the disease. The pathogenesis of anemia in IBD is multifactorial and results mainly from intestinal blood loss in inflamed mucosa and impaired dietary iron absorption. Multiple studies have proposed the use of the polyphenolic compound curcumin to counteract IBD pathogenesis since it has significant preventive and therapeutic properties as an anti-inflammatory agent and very low toxicity, even at high dosages. However, curcumin has been shown to possess properties consistent with those of an iron-chelator, such as the ability to modulate proteins of iron metabolism and decrease spleen and liver iron content. Thus, this property may further contribute to the development and severity of anemia of inflammation and iron deficiency in IBD. Herein, we evaluate the effects of curcumin on systemic iron balance in the dextran sodium sulfate (DSS) model of colitis in C57Bl/6 and BALB/c mouse strains that were fed an iron-sufficient diet. In these conditions, curcumin supplementation caused mild anemia, lowered iron stores, worsened colitis and significantly decreased overall survival, independent of the mouse strain. These findings suggest that curcumin usage as an anti-inflammatory supplement should be accompanied by monitoring of erythroid parameters to avoid exacerbation of iron deficiency anemia in IBD.Core tipOur study shows that curcumin supplementation of an iron-sufficient diet causes mild anemia, depletes iron stores, worsens colitis and decreases survival, independent of the mouse strain. These findings demonstrate that curcumin may have a potential adverse activity in chronic inflammatory diseases, such as IBD, since the iron chelating properties of curcumin may play a role in iron deficiency and the severity of colitis.

scholarly journals Liver iron sensing and body iron homeostasis

Blood ◽  
2019 ◽  
Vol 133 (1) ◽  
pp. 18-29 ◽  
Author(s):  
Chia-Yu Wang ◽  
Jodie L. Babitt
Keyword(s):  
Iron Deficiency ◽  
Iron Homeostasis ◽  
Inflammatory Diseases ◽  
Genetic Disorders ◽  
Hereditary Hemochromatosis ◽  
Deficiency Anemia ◽  
Iron Loading ◽  
Liver Iron ◽  
Body Iron ◽  
Iron Supply

Abstract The liver orchestrates systemic iron balance by producing and secreting hepcidin. Known as the iron hormone, hepcidin induces degradation of the iron exporter ferroportin to control iron entry into the bloodstream from dietary sources, iron recycling macrophages, and body stores. Under physiologic conditions, hepcidin production is reduced by iron deficiency and erythropoietic drive to increase the iron supply when needed to support red blood cell production and other essential functions. Conversely, hepcidin production is induced by iron loading and inflammation to prevent the toxicity of iron excess and limit its availability to pathogens. The inability to appropriately regulate hepcidin production in response to these physiologic cues underlies genetic disorders of iron overload and deficiency, including hereditary hemochromatosis and iron-refractory iron deficiency anemia. Moreover, excess hepcidin suppression in the setting of ineffective erythropoiesis contributes to iron-loading anemias such as β-thalassemia, whereas excess hepcidin induction contributes to iron-restricted erythropoiesis and anemia in chronic inflammatory diseases. These diseases have provided key insights into understanding the mechanisms by which the liver senses plasma and tissue iron levels, the iron demand of erythrocyte precursors, and the presence of potential pathogens and, importantly, how these various signals are integrated to appropriately regulate hepcidin production. This review will focus on recent insights into how the liver senses body iron levels and coordinates this with other signals to regulate hepcidin production and systemic iron homeostasis.

scholarly journals Socio-economic status, iron deficiency anemia and COVID-19 disease burden – an appraisal

2021 ◽  
Vol 19 (1) ◽  
pp. 52-58
Author(s):  
Kusum Ghosh ◽  
◽  
Diptendu Chatterjee ◽  
Abhisikta Ghosh Roy ◽  
Arup Ratan Bandyopadhyay ◽  
...  
Keyword(s):  
Iron Deficiency ◽  
Infectious Diseases ◽  
Iron Deficiency Anemia ◽  
Economic Status ◽  
Case Fatality ◽  
Therapeutic Interventions ◽  
Deficiency Anemia ◽  
Iron Stores ◽  
Socio Economic Status ◽  
Mild Anemia

Introduction. Severe Acute Respiratory Syndrome-2, possesses varying degrees of susceptibility and lethality worldwide and WHO declared this as a pandemic of this century. Aim. In this background, the aim of this present narrative is to provide a complementary overview of how low iron stores and mild anemia offers protection from infectious diseases like COVID-19 by restricting the viral replication and also to suggest some potential adjuvant therapeutic interventions. Material and methods. Therefore, we performed a literature search reviewing pertinent articles and documents. PubMed, Google Scholar, Chemrxiv, MedRxiv, BioRxiv, Preprints and ResearchGate were investigated. Analysis of the literature. Recent studies reported drastic systemic events taking place that contribute to the severe clinical outcomes such as decreased hemoglobin indicating anemia, hypoxia, altered iron metabolism, hypercoagulability, oxidative stress, cytokine storm, hyper-ferritinemia and thus Multi Organ Failure, reportedly hailed as the hallmark of the COVID-19 hyper- inflammatory state. Interestingly it is globally observed that, countries with higher Socio-economic status (SES) have considerably lower prevalence of Iron Deficiency Anemia (IDA) but higher Case Fatality Rate (CFR) rate due to COVID-19 while, low SES countries characterized by the higher prevalence of IDA, are less affected to COVID-19 infection and found to have less CFR, which is almost half to that of the higher SES counterpart. Conclusion. Present review presumed that,low iron stores and mild anemia may play a beneficial role in some cases by offering protection from infectious diseases as low iron restricts the viral replication.Thus, suggested iron chelation or iron sequestration as an alternative beneficial adjuvant in treating COVID-19 infection.

scholarly journals Anemia and Pregnancy

2021 ◽  
Vol 9 (3) ◽  
pp. 127-130
Author(s):  
Swapana John ◽  
Keyword(s):  
Iron Deficiency ◽  
Iron Deficiency Anemia ◽  
World Health ◽  
Health Concern ◽  
Deficiency Anemia ◽  
Balanced Diet ◽  
Mild Anemia ◽  
The Future ◽  
The Government ◽  
Adverse Pregnancy

Anemia during pregnancy is a major world health concern especially in developing countries affecting the life of the women and the future of the child thereby influencing the present as well the future of the nation and the world at large. Nutritional deficiency still emerges out the main cause of iron deficiency anemia affecting the life of the pregnant women. The iron deficiency anemia has a major say in adverse pregnancy outcomes like pre term delivery, IUGR, morbidity even leading to mortality, however it is noted that severe anemia has a significant effect than moderate and mild anemia. A well balanced diet can avert this condition, nonetheless iron supplementations as per the government guidelines and various treatment available also help to tackle the situation. Education of the women and more awareness programmes on health, pregnancy and nutrition by the stakeholders can further reduce the incidence of anemia in pregnancy.

scholarly journals Maternal Hepcidin Suppression Is Essential for Healthy Pregnancy

Blood ◽  
2020 ◽  
Vol 136 (Supplement 1) ◽  
pp. 43-44
Author(s):  
Veena Sangkhae ◽  
Tomas Ganz ◽  
Elizabeta Nemeth
Keyword(s):  
Iron Deficiency ◽  
Molecular Mechanisms ◽  
Hematological Parameters ◽  
Critical Role ◽  
Physiological Mechanism ◽  
Deficiency Anemia ◽  
Private Company ◽  
Iron Stores ◽  
Primary Mouse

Iron is essential for maternal and fetal health during pregnancy, and iron requirements increase substantially in the second half of gestation1. However, the molecular mechanisms ensuring increased iron availability during pregnancy are not well understood. Hepcidin is the key iron-regulatory hormone and functions by occluding and degrading the iron exporter ferroportin (FPN) to inhibit dietary iron absorption and mobilization of iron from stores. In healthy human and rodent pregnancies, maternal hepcidin decreases starting in the second trimester and is nearly undetectable by late pregnancy2,3 (Figure A). We explored the role of maternal and embryo hepcidin in regulating embryo iron endowment using mouse models. By generating combinations of dams and embryos lacking hepcidin or not, we showed that in normal mouse pregnancy, only maternal but not embryo or placental hepcidin determines embryo iron endowment4. Maternal hepcidin was inversely related to embryo iron stores, and embryos from hepcidin-deficient dams had significantly higher hepatic iron stores regardless of their own hepcidin genotype. When maternal hepcidin was elevated during the second half of pregnancy in mice by administering a hepcidin mimetic, this led to dose-dependent embryo iron deficiency, anemia, and in severe cases, embryo death4. Embryos were particularly sensitive to maternal iron restriction as they developed iron deficiency in the liver and the brain even when maternal hematological parameters were unaffected. These data highlight the critical role of maternal hepcidin suppression for heathy pregnancy. Yet, the physiological mechanism of maternal hepcidin suppression remains unknown. We showed in mice that maternal hepcidin decreases prior to a significant decrease in liver iron and without any changes in serum iron, suggesting that maternal hepcidin suppression is not driven solely by iron deficiency. Using an in vitro model, we determined that the placenta secretes a hepcidin-suppressing factor. Exposure of primary mouse hepatocytes to supernatants from cultured human placenta cells, but not control media, suppressed hepcidin mRNA more than 10-fold (Figure B) and for up to 48hrs. The suppressive factor in the supernatant was >100kDa in size and not associated with exosomes. Studies to identify the placenta-derived hepcidin suppressor are ongoing. In summary, suppression of maternal hepcidin is essential to ensure adequate iron supply for transfer to the fetus and for the increase in maternal red blood cell mass2, and a placenta-derived hepcidin suppressor likely plays an important role in this adaptation. 1Fisher AL and Nemeth E, Am J Clin Nutr, 2017 2Sangkhae V et al, JCI, 2020 3van Santen S et al, Clin Chem Lab Med, 2013 4Sangkhae V et al, Blood, 2020 Figure 1 Disclosures Ganz: Global Blood Therapeutics: Consultancy; Ionis Pharmaceuticals: Consultancy; American Regent: Consultancy; Rockwell: Consultancy; Vifor: Consultancy; Astellas: Consultancy; Akebia: Consultancy; Gossamer Bio: Consultancy; Silarus Therapeutics: Current equity holder in private company; Sierra Oncology: Consultancy; Ambys: Consultancy; Disc Medicine: Consultancy; Intrinsic LifeSciences: Current equity holder in private company. Nemeth:Intrinsic LifeSciences: Current equity holder in private company; Silarus Therapeutics: Current equity holder in private company; Ionis Pharmaceuticals: Consultancy; Protagonist: Consultancy; Vifor: Consultancy.

PITFALLS IN THE DIAGNOSIS AND TREATMENT OF IRON DEFICIENCY ANEMIA IN PEDIATRICS

PEDIATRICS ◽  
1964 ◽  
Vol 34 (1) ◽  
pp. 117-121
Author(s):  
David H. Clement
Keyword(s):  
Iron Deficiency ◽  
Physical Examination ◽  
Iron Deficiency Anemia ◽  
Ferrous Iron ◽  
Reticulocyte Count ◽  
Diagnosis And Treatment ◽  
Deficiency Anemia ◽  
Iron Stores ◽  
Mother Loss ◽  
Oral Preparation

Errors in the diagnosis and treatment of iron-deficiency anemia involve several areas. In the history one may overlook anemia in the mother, loss of infant blood from the placental circuit or later as melena, as well as a diet high in milk and low in iron-rich foods. In the physical examination pallor should not be estimated from facial color alone. In the laboratory a reticulocyte count should be determined before as well as during treatment. Regarding treatment it is important to give enough iron (6 mg/kg/day) for long enough to replenish iron stores. An effective, oral preparation of ferrous iron alone in gradually increasing doses is preferred. Failure to respond suggests several possibilities discussed above.

scholarly journals The Effect of Iron Deficiency Anemia Early in the Third Trimester on Small for Gestational Age and Birth Weight: A Retrospective Cohort Study on Iron Deficiency Anemia and Fetal Weight

2019 ◽  
Vol 2019 ◽  
pp. 1-4 ◽  
Author(s):  
Ilknur Col Madendag ◽  
Mefkure Eraslan Sahin ◽  
Yusuf Madendag ◽  
Erdem Sahin ◽  
Mustafa Bertan Demir ◽  
...  
Keyword(s):  
Iron Deficiency ◽  
Pregnant Women ◽  
Iron Deficiency Anemia ◽  
Fetal Weight ◽  
Deficiency Anemia ◽  
Control Group ◽  
Third Trimester ◽  
Mild Anemia ◽  
Moderate Anemia ◽  
Anemia Group

Aim. The aim of the present study was to evaluate the relationship between iron deficiency anemia and small for gestational age (SGA) in early third trimester pregnancies. Methods. A total of 4800 pregnant women who met the inclusion criteria were analyzed retrospectively. We included pregnant women who had iron deficiency anemia between 26+0 and 30+0 weeks of gestation and delivered singletons between 37+0 and 41+6 weeks of gestation. Patients were divided into four groups according to anemia level: (1) hemoglobin (Hb) < 7 mg/dl (n = 80), (2) Hb 7–9.9 mg/dl (n = 320), (3) Hb 10–10.9 mg/dl (n = 1300), and (4) Hb > 11 mg/dl (n = 3100, control group). The primary outcome of this study was the presence of SGA. Results. The demographic and obstetric characteristics were similar among all the groups. Maternal age, BMI <30 kg/m2, nulliparity rates, and previous cesarean delivery rates were similar among groups. Ethnicity was significantly different in the severe and moderate anemia groups (<0.001). Mean fetal weight was 2900 ± 80 g in the severe anemia group, 3050 ± 100 g in the moderate anemia group, 3350 ± 310 g in the mild anemia group, and 3400 ± 310 g in the control group. Fetal weight was significantly lower in the severe and moderate anemia groups compared to the mild anemia and control groups (<0.001). The SGA rate was 18.7% in the severe anemia group, 12.1% in the moderate anemia group, 5.3% in the mild anemia group, and 4.9% in the control group. SGA was significantly higher in the severe and moderate anemia groups compared to the mild anemia and control groups (<0.001). Conclusion. The results of this study indicated that early third trimester severe and moderate iron deficiency anemia was associated with SGA. Iron deficiency anemia in pregnant women may lead to low birth weight.

scholarly journals The Treatment of Iron Deficiency Anemia

Blood ◽  
1955 ◽  
Vol 10 (6) ◽  
pp. 567-581 ◽  
Author(s):  
DANIEL H. COLEMAN ◽  
ALEXANDER R. STEVENS ◽  
CLEMENT A. FINCH
Keyword(s):  
Iron Deficiency ◽  
Gastrointestinal Symptoms ◽  
The Body ◽  
Deficiency Anemia ◽  
Deficient Diet ◽  
Significant Group ◽  
Body Iron ◽  
Iron Stores ◽  
Iron Deficient ◽  
Full Complement

Abstract In the normal individual the amount of iron absorbed and lost from the body each day is exceedingly small. There are certain periods during life when body iron requirements are increased; the most important of these is infancy. Here, existing iron stores are rapidly depleted, and a deficient diet can soon produce iron deficiency. Once a full complement of body iron has been accrued, the adult is independent of iron intake and becomes iron deficient only through blood loss. In the production of iron deficiency, iron stores are exhausted before anemia appears. If any question in diagnosis from usual laboratory tests exists, the direct. examination of marrow for hemosiderin will establish the diagnosis. It is of obvious importance to confirm the diagnosis by specific therapy and to determine the cause of the iron depletion. Response to oral iron is highly predictable and failure of response usually in dictates a mistaken diagnosis. In a small but significant group of patients, either unable to take iron because of gastrointestinal symptoms, unable to absorb iron, or in need of iron reserves, parenteral administration of iron has distinct advantages. The saccharated oxide of iron is an effective preparation for this purpose.

scholarly journals Iron Deficiency in Chronic Kidney Disease: Updates on Pathophysiology, Diagnosis, and Treatment

2020 ◽  
Vol 31 (3) ◽  
pp. 456-468 ◽  
Author(s):  
Elizabeth Katherine Batchelor ◽  
Pinelopi Kapitsinou ◽  
Pablo E. Pergola ◽  
Csaba P. Kovesdy ◽  
Diana I. Jalal
Keyword(s):  
Iron Deficiency ◽  
Iron Supplementation ◽  
Deficiency Anemia ◽  
Iron Stores ◽  
Iv Iron ◽  
Potential Risks ◽  
Liberal Approach ◽  
Absolute Iron Deficiency ◽  
Relative Deficiency ◽  
Reduced Kidney Function

Anemia is a complication that affects a majority of individuals with advanced CKD. Although relative deficiency of erythropoietin production is the major driver of anemia in CKD, iron deficiency stands out among the mechanisms contributing to the impaired erythropoiesis in the setting of reduced kidney function. Iron deficiency plays a significant role in anemia in CKD. This may be due to a true paucity of iron stores (absolute iron deficiency) or a relative (functional) deficiency which prevents the use of available iron stores. Several risk factors contribute to absolute and functional iron deficiency in CKD, including blood losses, impaired iron absorption, and chronic inflammation. The traditional biomarkers used for the diagnosis of iron-deficiency anemia (IDA) in patients with CKD have limitations, leading to persistent challenges in the detection and monitoring of IDA in these patients. Here, we review the pathophysiology and available diagnostic tests for IDA in CKD, we discuss the literature that has informed the current practice guidelines for the treatment of IDA in CKD, and we summarize the available oral and intravenous (IV) iron formulations for the treatment of IDA in CKD. Two important issues are addressed, including the potential risks of a more liberal approach to iron supplementation as well as the potential risks and benefits of IV versus oral iron supplementation in patients with CKD.

scholarly journals Curcumin, a cancer chemopreventive and chemotherapeutic agent, is a biologically active iron chelator

Blood ◽  
2009 ◽  
Vol 113 (2) ◽  
pp. 462-469 ◽  
Author(s):  
Yan Jiao ◽  
John Wilkinson ◽  
Xiumin Di ◽  
Wei Wang ◽  
Heather Hatcher ◽  
...  
Keyword(s):  
Iron Deficiency ◽  
Cultured Cells ◽  
Transferrin Saturation ◽  
Iron Chelator ◽  
Biologically Active ◽  
Liver Iron ◽  
Liver Iron Content ◽  
Inflammatory Conditions ◽  
Dose Dependent

Abstract Curcumin is a natural product currently in human clinical trials for a variety of neoplastic, preneoplastic, and inflammatory conditions. We previously observed that, in cultured cells, curcumin exhibits properties of an iron chelator. To test whether the chelator activity of curcumin is sufficient to induce iron deficiency in vivo, mice were placed on diets containing graded concentrations of both iron and curcumin for 26 weeks. Mice receiving the lowest level of dietary iron exhibited borderline iron deficiency, with reductions in spleen and liver iron, but little effect on hemoglobin, hematocrit, transferrin saturation, or plasma iron. Against this backdrop of subclinical iron deficiency, curcumin exerted profound 2 effects on systemic iron, inducing a dose-dependent decline in hematocrit, hemoglobin, serum iron, and transferrin saturation, the appearance of microcytic anisocytotic red blood cells, and decreases in spleen and liver iron content. Curcumin repressed synthesis of hepcidin, a peptide that plays a central role in regulation of systemic iron balance. These results demonstrate that curcumin has the potential to affect systemic iron metabolism, particularly in a setting of subclinical iron deficiency. This may affect the use of curcumin in patients with marginal iron stores or those exhibiting the anemia of cancer and chronic disease.

scholarly journals Serum Transferrin Receptor and Its Ratio to Serum Ferritin in the Diagnosis of Iron Deficiency

Blood ◽  
1997 ◽  
Vol 89 (3) ◽  
pp. 1052-1057 ◽  
Author(s):  
Kari Punnonen ◽  
Kerttu Irjala ◽  
Allan Rajamäki
Keyword(s):  
Bone Marrow ◽  
Iron Deficiency ◽  
Transferrin Receptor ◽  
Laboratory Tests ◽  
Bone Marrow Examination ◽  
Deficiency Anemia ◽  
Serum Transferrin ◽  
Iron Stores ◽  
Serum Transferrin Receptor ◽  
Reference Limits

Abstract The objective of the study was to evaluate the diagnostic efficiency of laboratory tests, including serum transferrin receptor (TfR) measurements, in the diagnosis of iron depletion. The patient population consisted of 129 consecutive anemic patients at the University Hospital of Turku who were given a bone marrow examination. Of these patients, 48 had iron deficiency anemia (IDA), 64 anemia of chronic disease (ACD), and 17 patients had depleted iron stores and an infectious or an inflammatory condition (COMBI). Depletion of iron stores was defined as a complete absence of stainable iron in the bone marrow examination. Serum TfR concentrations were elevated in the vast majority of the IDA and COMBI patients, while in the ACD patients, the levels were within the reference limits reported earlier for healthy subjects. TfR measurement thus provided a reliable diagnosis of iron deficiency anemia (AUCROC 0.98). Serum ferritin measurement also distinguished between IDA patients and ACD patients. However, the optimal decision limit for evaluation of ferritin measurements was considerably above the conventional lower reference limits, complicating the interpretation of this parameter. Calculation of the ratio TfR/log ferritin (TfR-F Index) is a way of combining TfR and ferritin results. This ratio provided an outstanding parameter for the identification of patients with depleted iron stores (AUCROC 1.00). In anemic patients, TfR measurement is a valuable noninvasive tool for the diagnosis of iron depletion, and offers an attractive alternative to more conventional laboratory tests in the detection of depleted iron stores.

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