Journal articles: 'Iron deficiency diseases'

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Bermejo, Fernando, and Santiago García-López. "A guide to diagnosis of iron deficiency and iron deficiency anemia in digestive diseases." World Journal of Gastroenterology 15, no. 37 (2009): 4638. http://dx.doi.org/10.3748/wjg.15.4638.

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Mayer-Pröschel, Margot, Dan Morath, and Mark Noble. "Are Hypothyroidism and Iron Deficiency Precursor Cell Diseases?" Developmental Neuroscience 23, no. 4-5 (2001): 277–86. http://dx.doi.org/10.1159/000048711.

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Boyko, T. "Iron metabolism and diagnostic of iron deficiency in inflammatory bowel diseases." Medicni perspektivi (Medical perspectives) 18, no. 3 (October 2, 2013): 70–77. http://dx.doi.org/10.26641/2307-0404.2013.3.18995.

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Mansoor, Malahat, and Hammad Raza. "IRON DEFICIENCY ANEMIA." Professional Medical Journal 23, no. 06 (June 10, 2016): 673–79. http://dx.doi.org/10.29309/tpmj/2016.23.06.1606.

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Around 65% of pregnant women in South Asia suffer from IDA & in Indiansub-continent alone, the rate of developing IDA during pregnancy is 88%. Moreover anemicpregnant patients are more likely to give birth to low birth weight babies which itself is anotherfactor adding to socio-economic burden on the whole family. The food has not been fortified forIron, Zinc & Vitamin D & hence the prevention of anemia has not yet been achieved Objectives:To study Awareness of women about food fortification & prevention of IDA Vs cost for treatinganemia. Period: August 2015-Dec 2015. Study Design: Observational Study. Settings: At BhattiInternational Hospital, Kasur Results: Among the selected anemic women, almost half (55%)had mild anemia, while rest had moderate to severe anemia indicting that the prevalence is verycommon. The treatment offered was oral &/or IV Iron with blood transfusions. The cost of iv Irontherapy & blood transfusions estimates in thousands with added risks of Transfusion Reactions,allergic reactions& transmission of blood-borne diseases like HCV,HBV,HIV(AIDS)&others. Theawareness level was found to be poor among these women .Only 8/60 i.e 13% had someidea about iron deficiency anemia & almost none knew about food fortifications. The insightabout their own disease of IDA was also 35% (21/60) indicating that most of the women incommunity live with IDA without any understanding of a preventable condition. Conclusion:The cost & time spend to treat IDA can be minimizes creating awareness about food fortification& supplementation.

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Bi, Yaguang, Amir Ajoolabady, Laurie J. Demillard, Wenjun Yu, Michelle L. Hilaire, Yingmei Zhang, and Jun Ren. "Dysregulation of iron metabolism in cardiovascular diseases: From iron deficiency to iron overload." Biochemical Pharmacology 190 (August 2021): 114661. http://dx.doi.org/10.1016/j.bcp.2021.114661.

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Smirnova, N. N., N. B. Kuprienko, V. P. Novikova, and A. I. Khavkin. "Iron metabolism and chronic kidney disease." Voprosy detskoj dietologii 18, no. 6 (2020): 27–34. http://dx.doi.org/10.20953/1727-5784-2020-6-27-34.

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Iron is involved in all kinds of metabolism. Iron deficiency, even in the absence of anaemia, promotes the development of many diseases. But in inflammation-associated diseases iron accumulates in the liver, kidneys and macrophages; resulting in impairment of effective erythropoiesis. The review presents modern evidence of the molecular mechanisms of iron metabolism and metabolic changes in most common diseases of the organs of the urinary system – pyelonephritis, glomerulonephritis, acute kidney injury. In most cases, anaemia has a dual nature – true iron deficiency anaemia and anaemia of chronic disease. Key words: iron, erythropoiesis, anaemia, renal pathology

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Tatarova, Nina A., and Margarita S. Airapetian. "Vitamin D deficiency and iron deficiency anemia in women in menopausal transition period. Clinical case." Gynecology 22, no. 5 (November 23, 2020): 87–90. http://dx.doi.org/10.26442/20795696.2020.5.200446.

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Vitamin D is a regulator of immune response, and plays a role in the development of cardiovascular diseases, insulin resistance and diabetes mellitus, obesity, autoimmune disorders, iron binding, anemia, respiratory viral and other diseases. In addition, vitamin D deficiency contributes to the chronicity of infections and an increased risk for number of oncological pathology. The developing immunosuppression in women with iron deficiency anemia in the menopausal transition period does not allow to fully compensate for iron deficiency with monotherapy if vitamin D deficiency is present. The drug of choice in this situation is micellized (water-soluble) vitamin D3(Aquadetrim).

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de Vizia, Basilio, Vincenzo Poggi, Rodolfo Conenna, Amedeo Fiorillo, and Luigi Scippa. "Iron Absorption and Iron Deficiency in Infants and Children with Gastrointestinal Diseases." Journal of Pediatric Gastroenterology and Nutrition 14, no. 1 (January 1992): 21–26. http://dx.doi.org/10.1097/00005176-199201000-00005.

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Shaw, Julia G., and Jennifer F. Friedman. "Iron Deficiency Anemia: Focus on Infectious Diseases in Lesser Developed Countries." Anemia 2011 (2011): 1–10. http://dx.doi.org/10.1155/2011/260380.

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Iron deficiency anemia is thought to affect the health of more than one billion people worldwide, with the greatest burden of disease experienced in lesser developed countries, particularly women of reproductive age and children. This greater disease burden is due to both nutritional and infectious etiologies. Individuals in lesser developed countries have diets that are much lower in iron, less access to multivitamins for young children and pregnant women, and increased rates of fertility which increase demands for iron through the life course. Infectious diseases, particularly parasitic diseases, also lead to both extracorporeal iron loss and anemia of inflammation, which decreases bioavailability of iron to host tissues. This paper will address the unique etiologies and consequences of both iron deficiency anemia and the alterations in iron absorption and distribution seen in the context of anemia of inflammation. Implications for diagnosis and treatment in this unique context will also be discussed.

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Baizhanova, K. T., and G. Zh Sadirkhanova. "Iron deficiency status associated with diseases of gastrointestinal tract." International Professional Journal "Medicine" 196, no. 10 (October 2018): 29–32. http://dx.doi.org/10.31082/1728-452x-2018-196-10-29-32.

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König, Peter, Kristine Jimenez, Gerda Saletu-Zyhlarz, Martina Mittlböck, and Christoph Gasche. "Iron deficiency, depression, and fatigue in inflammatory bowel diseases." Zeitschrift für Gastroenterologie 58, no. 12 (December 2020): 1191–200. http://dx.doi.org/10.1055/a-1283-6832.

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Abstract Background Iron deficiency and anemia are common findings in IBD. Treatment of anemia improves quality of life. Neurological symptoms like depression or anxiety are also common in IBD; however, their relationship with ID has not been studied in detail. Methods Prospective, single center, non-interventional trial in an IBD cohort (n = 98), which is generally at risk for ID. Quality of sleep (using the Pittsburgh Sleep Quality Index, Epworth Sleepiness Scale, and Insomnia Severity Index) and the presence of fatigue (Piper fatigue scale), depression (Self-rating Depression Scale [SDS]) or anxiety (Self-rating Anxiety Scale [SAS]) were related to ID (ferritin, transferrin saturation), anemia (hemoglobin), and inflammatory disease activity (CRP). Results ID was present in 35 %, anemia in 16 %, and inflammation in 30 %. The overall quality of sleep in this cohort was similar to that reported for the general population. ID, anemia, or inflammation had no influence on the PSQI (median 4.0 [CI 3.0–5.0]), the ESS 5.5 (5.0–7.0), and the ISI 4.00 (2.5–5.5). Fatigue (PFS; present in 30 %), anxiety (SAS; present in 24 %), and depression (SDS; present in 33 %) were more common than in the general population. Iron deficient and anemic patients were more likely to be depressed (p = 0.02 and p < 0.01) and showed a trend towards presence of fatigue (p = 0.06 and 0.07). Systemic inflammation as measured by CRP had no effect on any of these conditions. Conclusion In this IBD cohort, ID and anemia affect depression and possibly fatigue independent of the presence of inflammation.

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Gargallo-Puyuelo, Carla, Erika Alfambra, Jose García-Erce, and Fernando Gomollon. "Iron Treatment May Be Difficult in Inflammatory Diseases: Inflammatory Bowel Disease as a Paradigm." Nutrients 10, no. 12 (December 11, 2018): 1959. http://dx.doi.org/10.3390/nu10121959.

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Iron plays a key role in many physiological processes; cells need a very exact quantity of iron. In patients with inflammatory bowel disease, anaemia is a unique example of multifactorial origins, frequently being the result of a combination of iron deficiency and anaemia of chronic disease. The main cause of iron deficiency is the activity of the disease. Therefore, the first aim should be to reach complete clinical remission. The iron supplementation route should be determined according to symptoms, severity of anaemia and taking into account comorbidities and individual risks. Oral iron can only be used in patients with mild anaemia, whose disease is inactive and who have not been previously intolerant to oral iron. Intravenous iron should be the first line treatment in patients with moderate-severe anaemia, in patients with active disease, in patients with poor tolerance to oral iron and when erythropoietin agents or a fast response is needed. Erythropoietin is used in a few patients with anaemia to overcome functional iron deficiency, and blood transfusion is being restricted to refractory cases or acute life-threatening situations.

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Kabakus, N. "Reversal of Iron Deficiency Anemia-induced Peripheral Neuropathy by Iron Treatment in Children with Iron Deficiency Anemia." Journal of Tropical Pediatrics 48, no. 4 (August 1, 2002): 204–9. http://dx.doi.org/10.1093/tropej/48.4.204.

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Tański, Wojciech, Mariusz Chabowski, Beata Jankowska-Polańska, and Ewa Anita Jankowska. "Anaemia and iron deficiency in patients with rheumatoid arthritis and other chronic diseases." Postępy Higieny i Medycyny Doświadczalnej 75 (March 2, 2021): 143–51. http://dx.doi.org/10.5604/01.3001.0014.7838.

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Anaemia is one of the most common symptoms accompanying many chronic diseases, e.g. collagenases, neoplasms, and chronic inflammations (inflammatory bowel disease, chronic kidney disease and heart failure). Iron deficiency anaemia is the most common type of anaemia (80%). It affects 1% to 2% of the population. Iron deficiency (ID) – absolute or functional – is characterised by reduced ferritin levels and transferrin saturation (TSAT) of less than 20%. Iron deficiency is the most common dietary deficiency. However, iron deficiency might be one of the common causes of anaemia of chronic disease (ACD). Anaemia affects 33% to 60% of patients with RA. Rheumatoid arthritis (RA) is a chronic immune-mediated systemic connective tissue disease, in which chronic inflammation of the synovial tissue of the joints damages articular cartilages, bones and other joint structures. The prevalence of RA is approximately 0.3% to 2%. Low haemoglobin levels in RA patients are significantly correlated with disability, activity and duration of the disease as well as damage to joints and joint pain. Treatment of anaemia in RA patients includes iron supplementation, blood transfusions, the use of erythropoiesis-stimulating agents, and treatment of the underlying condition. Biological treatments used in RA patients, such as e.g. infliximab, tocilizumab and anakinra, not only slow the progression of joint involvement but also prevent anaemia.

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Henrika, Fify, T. Silangit, and Riadi Wirawan. "ANEMIA DAN DEFISIENSI BESI PADA SISWA SLTP NEGERI I CURUG, TANGERANG." INDONESIAN JOURNAL OF CLINICAL PATHOLOGY AND MEDICAL LABORATORY 15, no. 1 (August 23, 2018): 5. http://dx.doi.org/10.24293/ijcpml.v15i1.943.

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A research was conducted to 69 female students from a junior high school (SLtP) Negeri I Curug, tangerang aged 12–14 yearsto obtain percentages of anemia and iron deficiency in female adolescents. Anemia was found on 10.2% of the students, with 4.3%of normocytic normochromic anemia and 5.8% of microcytic hypochromic anemia. Microcytic hypochromic erythrocytes was foundon 21.7% of the subjects which consist of 2.9% iron deficiency anemia, 1.4% phase 2 iron deficiency (latent) with possibility ofhemoglobinopathy, and 2.9% phase 1 iron deficiency (pre-latent) with possibility of hemoglobinopathy. Anemia without iron deficiencywith possibility of chronic diseases and/or hemoglobinopathy was 2.9%, and without anemia nor iron deficiency but with possibility ofhemoglobinopathy was 11.6%. Iron deficiency was found among 26.1% of subjects which consist of 11.6% pre-latent iron deficiency,8.7% latent iron deficiency, and 5.8% iron deficiency anemia with 2.9% and 2.9% were normocytic normochromic anemia andmicrocytic hypochromic anemia, respectively.

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Osipenko, M. F., E. A. Zhuk, N. G. Grishchenko, T. A. Kolpakova, S. D. Nikonov, and L. V. Poddubnaya. "Iron deficiency anemia in the practice of a gastroenterologist (according to AGA recommendations)." Experimental and Clinical Gastroenterology, no. 7 (September 27, 2021): 56–61. http://dx.doi.org/10.31146/1682-8658-ecg-191-7-56-61.

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Iron deficiency anemia (IDA) is the most common type of anemic disorder, accounting for 41.5% of cases. According to the WHO, the clear lack of iron is fixed at 30% of the world’s population, but 2 times more likely to observe a latent iron deficiency. The article discusses the diagnosis of iron deficiency anemia in the practice of a gastroenterologist. A list of diseases of the gastrointestinal tract and algorithms for detecting iron deficiency anemia in them are presented.

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Andreichev, Nail’ A., and E. N. Andreicheva. "The differential diagnostic of anemias associated with iron metabolism." Medical Journal of the Russian Federation 22, no. 4 (August 15, 2016): 213–21. http://dx.doi.org/10.18821/0869-2106-2016-22-4-213-221.

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The iron-deficiency conditions continue to be an actual problem all over the world being present in half of population of the terrestrial globe. The development of iron deficiency often depends on gender and age. In females specific role is played by hypermenorrhea and repeated pregnancies (iron deficiency and iron-deficiency anemia are found 6 times more often in females than in males). The anemia of chronic diseases by it prevalence takes second place after iron-deficiency anemia. The prevalence of anemia of chronic diseases in elder and senile age varies within range 2,9-61% in males and 3,3-41% in females. In young and mature age anemia of chronic diseases more often occurs in females. There are anemias when content of iron in organism and its resources are within limits of norm or higher - sideroahrestical anemias. The percentage of them in structure of hypochromic anemias is smallish. The diagnostic and differential diagnostic of anemias related to iron metabolism. The anemias are diverse according to clinical hematological characteristics. At selection of diagnostic schemes, treatment of anemias differs on leading pathogenic mechanism. However, to facilitate diagnostic and differential diagnostic the color indicator and morphological classifications are considered. The differentiated diagnostic of anemias is based on data of clinical, laboratory and instrumental analysis. The blood analysis under anemia is to take into account indices of Hb, size of erythrocytes, their saturation with Hb, average volume of erythrocytes, and average content of hemoglobin in erythrocytes, amount of reticulocytes and other cells permitting judging about character and activity of erythropoiesis. The article presents algorithm of examination of patient under hypochromic and microcytic anemia, diagnostic and differentiated diagnostic of acute post-hemorrhagic anemia, anemia of chronic course, iron-deficiency anemia, anemia of chronic diseases, sideroahrestical anemia, iron-saturated anemia due to leaden intoxication, inherent iron-saturated anemia of pharmaceutical genesis, thyroprival anemia and thalassemia.

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Lelliott, Patrick M., Brendan J. McMorran, Simon J. Foote, and Gaetan Burgio. "Erythrocytic Iron Deficiency Enhances Susceptibility to Plasmodium chabaudi Infection in Mice Carrying a Missense Mutation in Transferrin Receptor 1." Infection and Immunity 83, no. 11 (August 24, 2015): 4322–34. http://dx.doi.org/10.1128/iai.00926-15.

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ABSTRACTThe treatment of iron deficiency in areas of high malaria transmission is complicated by evidence which suggests that iron deficiency anemia protects against malaria, while iron supplementation increases malaria risk. Iron deficiency anemia results in an array of pathologies, including reduced systemic iron bioavailability and abnormal erythrocyte physiology; however, the mechanisms by which these pathologies influence malaria infection are not well defined. In the present study, the response to malaria infection was examined in a mutant mouse line,TfrcMRI24910, identified during anN-ethyl-N-nitrosourea (ENU) screen. This line carries a missense mutation in the gene for transferrin receptor 1 (TFR1). Heterozygous mice exhibited reduced erythrocyte volume and density, a phenotype consistent with dietary iron deficiency anemia. However, unlike the case in dietary deficiency, the erythrocyte half-life, mean corpuscular hemoglobin concentration, and intraerythrocytic ferritin content were unchanged. Systemic iron bioavailability was also unchanged, indicating that this mutation results in erythrocytic iron deficiency without significantly altering overall iron homeostasis. When infected with the rodent malaria parasitePlasmodium chabaudi adami, mice displayed increased parasitemia and succumbed to infection more quickly than their wild-type littermates. Transfusion of fluorescently labeled erythrocytes into malaria parasite-infected mice demonstrated an erythrocyte-autonomous enhanced survival of parasites within mutant erythrocytes. Together, these results indicate that TFR1 deficiency alters erythrocyte physiology in a way that is similar to dietary iron deficiency anemia, albeit to a lesser degree, and that this promotes intraerythrocytic parasite survival and an increased susceptibility to malaria in mice. These findings may have implications for the management of iron deficiency in the context of malaria.

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Wang, Chia-Yu, and Jodie L. Babitt. "Liver iron sensing and body iron homeostasis." Blood 133, no. 1 (January 3, 2019): 18–29. http://dx.doi.org/10.1182/blood-2018-06-815894.

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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.

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Elstrott, Benjamin, Lubna Khan, Sven Olson, Vikram Raghunathan, Thomas DeLoughery, and Joseph J. Shatzel. "The role of iron repletion in adult iron deficiency anemia and other diseases." European Journal of Haematology 104, no. 3 (December 26, 2019): 153–61. http://dx.doi.org/10.1111/ejh.13345.

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Danquah, Ina, George Bedu‐Addo, and Frank P. Mockenhaupt. "Iron Deficiency andPlasmodium falciparumInfection During Pregnancy." Journal of Infectious Diseases 198, no. 10 (November 15, 2008): 1573–74. http://dx.doi.org/10.1086/592449.

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Lakhal-Littleton, Samira. "Iron Deficiency as a Therapeutic Target in Cardiovascular Disease." Pharmaceuticals 12, no. 3 (August 28, 2019): 125. http://dx.doi.org/10.3390/ph12030125.

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Iron deficiency is the most common nutritional disorder in the world. It is prevalent amongst patients with cardiovascular disease, in whom it is associated with worse clinical outcomes. The benefits of iron supplementation have been established in chronic heart failure, but data on their effectiveness in other cardiovascular diseases are lacking or conflicting. Realising the potential of iron therapies in cardiovascular disease requires understanding of the mechanisms through which iron deficiency affects cardiovascular function, and the cell types in which such mechanisms operate. That understanding has been enhanced by recent insights into the roles of hepcidin and iron regulatory proteins (IRPs) in cellular iron homeostasis within cardiovascular cells. These studies identify intracellular iron deficiency within the cardiovascular tissue as an important contributor to the disease process, and present novel therapeutic strategies based on targeting the machinery of cellular iron homeostasis rather than direct iron supplementation. This review discusses these new insights and their wider implications for the treatment of cardiovascular diseases, focusing on two disease conditions: chronic heart failure and pulmonary arterial hypertension.

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Ebner, Nicole, and Stephan von Haehling. "Why is Iron Deficiency Recognised as an Important Comorbidity in Heart Failure?" Cardiac Failure Review 5, no. 3 (November 4, 2019): 173–75. http://dx.doi.org/10.15420/cfr.2019.9.2.

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There is an increasing awareness of the prevalence of iron deficiency in patients with heart failure (HF), and its contributory role in the morbidity and mortality of HF. Iron is a trace element necessary for cells due to its capacity to transport oxygen and electrons. The prevalence of iron deficiency increases with the severity of HF. For a long time the influence of iron deficiency was underestimated, especially in terms of worsening of cardiovascular diseases and developing anaemia. In recent years, studies with intravenous iron agents in patients with iron deficiency and HF showed new insights into the improvement of iron therapy. Additionally, experimental studies supporting the understanding of iron metabolism and the resulting pathophysiological pathways of iron have been carried out. The aim of this mini review is to highlight why iron deficiency is recognised as an important comorbidity in HF.

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Fedorovа, T. A., O. M. Borzykina, E. M. Bakuridze, T. Yu Ivanets, E. V. Strelnikova, and S. G. Tsakhilova. "Коррекция железодефицитной анемии у пациенток с гинекологическими заболеваниями с использованием липосомального железа." Gynecology 19, no. 1 (2017): 68–72. http://dx.doi.org/10.26442/2079-5696_19.1.68-72.

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Stelle, Isabella, Anastasia Z. Kalea, and Dora I. A. Pereira. "Iron deficiency anaemia: experiences and challenges." Proceedings of the Nutrition Society 78, no. 1 (July 10, 2018): 19–26. http://dx.doi.org/10.1017/s0029665118000460.

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Iron deficiency remains the largest nutritional deficiency worldwide and the main cause of anaemia. Severe iron deficiency leads to anaemia known as iron deficiency anaemia (IDA), which affects a total of 1·24 billion people, the majority of whom are children and women from resource-poor countries. In sub-Saharan Africa, iron deficiency is frequently exacerbated by concomitant parasitic and bacterial infections and contributes to over 120 000 maternal deaths a year, while it irreparably limits the cognitive development of children and leads to poor outcomes in pregnancy.Currently available iron compounds are cheap and readily available, but constitute a non-physiological approach to providing iron that leads to significant side effects. Consequently, iron deficiency and IDA remain without an effective treatment, particularly in populations with high burden of infectious diseases. So far, despite considerable investment in the past 25 years in nutrition interventions with iron supplementation and fortification, we have been unable to significantly decrease the burden of this disease in resource-poor countries.If we are to eliminate this condition in the future, it is imperative to look beyond the strategies used until now and we should make an effort to combine community engagement and social science approaches to optimise supplementation and fortification programmes.

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Peng, Ying Y., and James Uprichard. "Ferritin and iron studies in anaemia and chronic disease." Annals of Clinical Biochemistry: International Journal of Laboratory Medicine 54, no. 1 (November 7, 2016): 43–48. http://dx.doi.org/10.1177/0004563216675185.

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Anaemia is a condition in which the number of red cells necessary to meet the body's physiological requirements is insufficient. Iron deficiency anaemia and the anaemia of chronic disease are the two most common causes of anaemia worldwide;1 iron homeostasis plays a pivotal role in the pathogenesis of both diseases. An understanding of how iron studies can be used to distinguish between these diseases is therefore essential not only for diagnosis but also in guiding management. This review will primarily focus on iron deficiency anaemia and anaemia of chronic disease; however, iron overload in anaemia will also be briefly discussed.

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Li, Yikun, Xiali Huang, Jingjing Wang, Ruiling Huang, and Dan Wan. "Regulation of Iron Homeostasis and Related Diseases." Mediators of Inflammation 2020 (May 2, 2020): 1–11. http://dx.doi.org/10.1155/2020/6062094.

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The liver is the organ for iron storage and regulation; it senses circulating iron concentrations in the body through the BMP-SMAD pathway and regulates the iron intake from food and erythrocyte recovery into the bloodstream by secreting hepcidin. Under iron deficiency, hypoxia, and hemorrhage, the liver reduces the expression of hepcidin to ensure the erythropoiesis but increases the excretion of hepcidin during infection and inflammation to reduce the usage of iron by pathogens. Excessive iron causes system iron overload; it accumulates in never system and damages neurocyte leading to neurodegenerative diseases such as Parkinson’s syndrome. When some gene mutations affect the perception of iron and iron regulation ability in the liver, then they decrease the expression of hepcidin, causing hereditary diseases such as hereditary hemochromatosis. This review summarizes the source and utilization of iron in the body, the liver regulates systemic iron homeostasis by sensing the circulating iron concentration, and the expression of hepcidin regulated by various signaling pathways, thereby understanding the pathogenesis of iron-related diseases.

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Dobrokhotova, Yu E., and E. A. Markova. "Peroral retard iron preparation for iron-deficiency anemia: case study and pharmacoeconomic analysis." Russian Journal of Woman and Child Health 3, no. 2 (2020): 88–94. http://dx.doi.org/10.32364/2618-8430-2020-3-2-88-94.

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Iron-deficiency anemia (IDA) is an important issue. The prevalence of IDA in women of reproductive age and women in perimenopause is high and has no tendency to reduce. Pharmacoeconomic aspects and recent data on clinical efficacy of iron supplements for obstetrical gy-necological disorders are addressed. The authors review international and domestic published data on iron supplements prescribed in women with obstetrical gynecological diseases. The paper describes the results of cost-effectiveness analysis and clinical trials published earlier that compare the efficacy of the treatment with iron supplements in women who experienced IDA or gynecological disorders complicated by iron deficiency during the pregnancy. One of the bivalent iron retard preparations, Tardyferon®, is discussed. In addition, Tardyferon® is compared with similar iron supplements and Fe(III)-hydroxide-polymaltose complex. Pharmacoeconomic utility of bivalent iron preparation from the viewpoint of the patient and the doctor is validated.Keywords: pharmacoeconomic analysis, iron deficiency, iron-deficiency anemia, pregnancy, iron supplements, bivalent iron.For citation: Dobrokhotova Yu.E., Markova E.A. Peroral retard iron preparation for iron-deficiency anemia: case study and pharmacoecono-mic analysis. Russian Journal of Woman and Child Health. 2020;3(2):88–94. DOI: 10.32364/2618-8430-2020-3-2-88-94.

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Bayraktar, Ulas D. "Treatment of iron deficiency anemia associated with gastrointestinal tract diseases." World Journal of Gastroenterology 16, no. 22 (2010): 2720. http://dx.doi.org/10.3748/wjg.v16.i22.2720.

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Abeuova, B. "PO-0351 Iron-deficiency Anaemia And Dental Diseases Among Children." Archives of Disease in Childhood 99, Suppl 2 (October 2014): A360.2—A360. http://dx.doi.org/10.1136/archdischild-2014-307384.999.

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Talarico, Valentina, Laura Giancotti, Giuseppe Antonio Mazza, Roberto Miniero, and Marco Bertini. "Iron Deficiency Anemia in Celiac Disease." Nutrients 13, no. 5 (May 17, 2021): 1695. http://dx.doi.org/10.3390/nu13051695.

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The iron absorption process developsmainly in the proximal duodenum. This portion of the intestine is typically destroyed in celiac disease (CD), resulting in a reduction in absorption of iron and subsequent iron deficiency anemia (IDA). In fact, the most frequent extra-intestinal manifestation (EIM) of CD is IDA, with a prevalence between 12 and 82% (in relation with the various reports) in patients with new CD diagnosis. The primary treatment of CD is the gluten-free diet (GFD), which is associated with adequate management of IDA, if present. Iron replacement treatment historically has been based on oral products containing ferrous sulphate (FS). However, the absorption of FS is limited in patients with active CD and unpredictable in patients on a GFD. Furthermore, a poor tolerability of this kind of ferrous is particularly frequent in patients with CD or with other inflammatory bowel diseases. Normalization from anemic state typically occurs after at least 6 months of GFD, but the process can take up to 2 years for iron stores to replenish.

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MANTADAKIS, ELPIS. "IRON DEFICIENCY ANEMIA IN CHILDREN RESIDING IN HIGH AND LOW-INCOME COUNTRIES: RISK FACTORS, PREVENTION, DIAGNOSIS AND THERAPY." Mediterranean Journal of Hematology and Infectious Diseases 12, no. 1 (June 28, 2020): e2020041. http://dx.doi.org/10.4084/mjhid.2020.041.

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Iron deficiency and iron deficiency anemia (IDA) affect approximately two billion people worldwide and most of them reside in low- and middle-income countries. In these countries, additional causes of anemia include parasitic infections like malaria, other nutritional deficiencies, chronic diseases, hemoglobinopathies and lead poisoning. Maternal anemia in resource-poor nations is associated with low birth weight, increased perinatal mortality and decreased work productivity. Maintaining a normal iron balance in these settings is challenging, as iron-rich foods with good bioavailability are of animal origin that are expensive and/or available in short supply. Apart from infrequent consumption of meat, inadequate vitamin C intake and diets rich in inhibitors of iron absorption are additional important risk factors for IDA in low-income countries. In-home iron fortification of complementary foods with micronutrient powders has been shown to effectively reduce the risk of iron deficiency and IDA in infants and young children in developing countries but is associated with unfavorable changes in gut flora and induction of intestinal inflammation that may lead to diarrhea and hospitalization. In developed countries, iron deficiency is the only frequent micronutrient deficiency. In the industrialized world, IDA is more common in infants beyond the sixth month of life, in adolescent females with heavy menstrual bleeding, in women of childbearing age and elderly people. Other special at-risk populations for IDA in developed countries are regular blood donors, endurance athletes and vegetarians. Several medicinal ferrous or ferric oral iron products exist, and their use is not apparently associated with harmful effects on the overall incidence of infectious illnesses in sideropenic and/or anemic subjects. Further research is needed to clarify the risks and benefits of supplemental iron for children exposed to parasitic infections in the third world, and for children genetically predisposed to iron overload.

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Fatali, Somaye, Omid Sadeghpour, Amir-Hosein Emami, Jale Aliasl, and Mitra Mehrabani. "Dietary recommendation for Iron Deficiency Anemia in Persian Medicine." International Journal of Ayurvedic Medicine 11, no. 1 (March 24, 2020): 6–9. http://dx.doi.org/10.47552/ijam.v11i1.1334.

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Background: Iron deficiency is the most common nutritional deficiency in the world. Iron deficiency anemia may be associated with various symptoms, and most patients are treated with oral supplements or infusion therapy. In recent years, importance of nutrition in the improvement of Iron deficiency anemia has been highlighted. Based on the Iranian Traditional Medicine, foods have major effects on prevention and treatment of diseases. Method: In this study Traditional Persian Medicine (TPM) books such as Canon of Avicenna, Kamel al -Sina'ah al- Tibbiyah and Makhzan al Advieh were assessed and the information about blood-producing foods and their effect on improving iron deficiency were investigated. Result: There are some foods, which can be effective in iron deficiency anemia. Some of these foods have animal origin such as eggs and meat and some have plant origin such as chickpeas, grapes and figs. Conclusion: According TPM, Nutritious foods and Blood humor-producing foods are the right options for iron supply. Also, these foods can help iron deficiency through various mechanisms alone or with medication.

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Zhorova, V. E. "Therapy of iron-deficiency anemia in gynecological patients." Medical Council, no. 7 (April 5, 2019): 148–52. http://dx.doi.org/10.21518/2079-701x-2019-7-148-152.

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The article considers the indications for the use of iron carboxymaltosate, peculiarities of its structure, efficiency and safety of its use in various gynecological diseases, proved on the basis of meta-analysis of randomized clinical studies

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Zhang, De-Liang, Manik C. Ghosh, Hayden Ollivierre, Yan Li, and Tracey A. Rouault. "Ferroportin deficiency in erythroid cells causes serum iron deficiency and promotes hemolysis due to oxidative stress." Blood 132, no. 19 (November 8, 2018): 2078–87. http://dx.doi.org/10.1182/blood-2018-04-842997.

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Abstract Ferroportin (FPN), the only known vertebrate iron exporter, transports iron from intestinal, splenic, and hepatic cells into the blood to provide iron to other tissues and cells in vivo. Most of the circulating iron is consumed by erythroid cells to synthesize hemoglobin. Here we found that erythroid cells not only consumed large amounts of iron, but also returned significant amounts of iron to the blood. Erythroblast-specific Fpn knockout (Fpn KO) mice developed lower serum iron levels in conjunction with tissue iron overload and increased FPN expression in spleen and liver without changing hepcidin levels. Our results also showed that Fpn KO mice, which suffer from mild hemolytic anemia, were sensitive to phenylhydrazine-induced oxidative stress but were able to tolerate iron deficiency upon exposure to a low-iron diet and phlebotomy, supporting that the anemia of Fpn KO mice resulted from erythrocytic iron overload and resulting oxidative injury rather than a red blood cell (RBC) production defect. Moreover, we found that the mean corpuscular volume (MCV) values of gain-of-function FPN mutation patients were positively associated with serum transferrin saturations, whereas MCVs of loss-of-function FPN mutation patients were not, supporting that erythroblasts donate iron to blood through FPN in response to serum iron levels. Our results indicate that FPN of erythroid cells plays an unexpectedly essential role in maintaining systemic iron homeostasis and protecting RBCs from oxidative stress, providing insight into the pathophysiology of FPN diseases.

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Brugnara, Carlo. "Iron Deficiency and Erythropoiesis: New Diagnostic Approaches." Clinical Chemistry 49, no. 10 (October 1, 2003): 1573–78. http://dx.doi.org/10.1373/49.10.1573.

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Abstract Iron deficiency anemia is one of the most common diseases worldwide. In the majority of cases, the presence of hypochromic microcytic anemia and biochemical evidence for depletion of body iron stores makes the diagnosis relatively straightforward. However, in several clinical conditions, classic biochemical indices such as serum iron, transferrin saturation, and ferritin may not be informative or may not change rapidly enough to reflect transient iron-deficient states (functional iron deficiency), such as the ones that develop during recombinant human erythropoietin (r-HuEPO) therapy. The identification and treatment of iron deficiency in settings such as r-HuEPO therapy, anemia of chronic disease, and iron deficiency of early childhood may be improved by the use of red cell and reticulocyte cellular indices, which reflect in almost real time the development of iron deficiency and the response to iron therapy. In the anemia of chronic disease, measurements of plasma cytokines and iron metabolism regulators such as hepcidin (when available) may be helpful in the characterization of the pathophysiologic basis of this condition. The ratio of serum transferrin receptor (sTfR) to serum ferritin (R/F ratio) has been shown to have excellent performance in estimating body iron stores, but it cannot be used widely because of the lack of standardization for sTfR assays. The combination of hematologic markers such as reticulocyte hemoglobin content, which decreases with iron deficiency, and R/F ratio may allow for a more precise classification of anemias.

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Kontoghiorghes, George, and Christina Kontoghiorghe. "Iron and Chelation in Biochemistry and Medicine: New Approaches to Controlling Iron Metabolism and Treating Related Diseases." Cells 9, no. 6 (June 12, 2020): 1456. http://dx.doi.org/10.3390/cells9061456.

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Iron is essential for all living organisms. Many iron-containing proteins and metabolic pathways play a key role in almost all cellular and physiological functions. The diversity of the activity and function of iron and its associated pathologies is based on bond formation with adjacent ligands and the overall structure of the iron complex in proteins or with other biomolecules. The control of the metabolic pathways of iron absorption, utilization, recycling and excretion by iron-containing proteins ensures normal biologic and physiological activity. Abnormalities in iron-containing proteins, iron metabolic pathways and also other associated processes can lead to an array of diseases. These include iron deficiency, which affects more than a quarter of the world’s population; hemoglobinopathies, which are the most common of the genetic disorders and idiopathic hemochromatosis. Iron is the most common catalyst of free radical production and oxidative stress which are implicated in tissue damage in most pathologic conditions, cancer initiation and progression, neurodegeneration and many other diseases. The interaction of iron and iron-containing proteins with dietary and xenobiotic molecules, including drugs, may affect iron metabolic and disease processes. Deferiprone, deferoxamine, deferasirox and other chelating drugs can offer therapeutic solutions for most diseases associated with iron metabolism including iron overload and deficiency, neurodegeneration and cancer, the detoxification of xenobiotic metals and most diseases associated with free radical pathology.

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Petzer, Verena, Igor Theurl, and Günter Weiss. "Established and Emerging Concepts to Treat Imbalances of Iron Homeostasis in Inflammatory Diseases." Pharmaceuticals 11, no. 4 (December 11, 2018): 135. http://dx.doi.org/10.3390/ph11040135.

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Inflammation, being a hallmark of many chronic diseases, including cancer, inflammatory bowel disease, rheumatoid arthritis, and chronic kidney disease, negatively affects iron homeostasis, leading to iron retention in macrophages of the mononuclear phagocyte system. Functional iron deficiency is the consequence, leading to anemia of inflammation (AI). Iron deficiency, regardless of anemia, has a detrimental impact on quality of life so that treatment is warranted. Therapeutic strategies include (1) resolution of the underlying disease, (2) iron supplementation, and (3) iron redistribution strategies. Deeper insights into the pathophysiology of AI has led to the development of new therapeutics targeting inflammatory cytokines and the introduction of new iron formulations. Moreover, the discovery that the hormone, hepcidin, plays a key regulatory role in AI has stimulated the development of several therapeutic approaches targeting the function of this peptide. Hence, inflammation-driven hepcidin elevation causes iron retention in cells and tissues. Besides pathophysiological concepts and diagnostic approaches for AI, this review discusses current guidelines for iron replacement therapies with special emphasis on benefits, limitations, and unresolved questions concerning oral versus parenteral iron supplementation in chronic inflammatory diseases. Furthermore, the review explores how therapies aiming at curing the disease underlying AI can also affect anemia and discusses emerging hepcidin antagonizing drugs, which are currently under preclinical or clinical investigation.

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Camaschella, Clara, and Laura Silvestri. "Molecular Mechanisms Regulating Hepcidin Revealed by Hepcidin Disorders." Scientific World JOURNAL 11 (2011): 1357–66. http://dx.doi.org/10.1100/tsw.2011.130.

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Iron is essential for human life, but toxic if present in excess. To avoid iron overload and maintain iron homeostasis, all cells are able to regulate their iron content through the post-transcriptional control of iron genes operated by the cytosolic iron regulatory proteins that interact with iron responsive elements on iron gene mRNA. At the systemic level, iron homeostasis is regulated by the liver peptide hepcidin. Disruption of these regulatory loops leads to genetic diseases characterized by iron deficiency (iron-refractory iron-deficiency anemia) or iron overload (hemochromatosis). Alterations of the same systems are also found in acquired disorders, such as iron-loading anemias characterized by ineffective erythropoiesis and anemia of chronic diseases (ACD) associated with common inflammatory conditions. In ACD, iron is present in the body, but maldistributed, being deficient for erythropoiesis, but sequestered in macrophages. Studies of the hepcidin regulation by iron and inflammatory cytokines are revealing new pathways that might become targets of new therapeutic intervention in iron disorders.

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Daily, Johanna P., and Blair J. Wylie. "Iron Deficiency during Pregnancy: Blessing or Curse?" Journal of Infectious Diseases 198, no. 2 (July 15, 2008): 157–58. http://dx.doi.org/10.1086/589513.

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Mohammad, Faisal, M. Sridhar, Madhusudan Samprathi, and Prakash Vemgal. "Thrombocytopenia in severe iron deficiency anaemia: A report of two cases." Tropical Doctor 51, no. 3 (January 10, 2021): 448–50. http://dx.doi.org/10.1177/0049475520983658.

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Iron deficiency, the commonest cause of anaemia in children, is a global public health problem. Worldwide, almost 50% of children <5 years of age are anaemic. Platelet count in iron deficiency anaemia is mostly normal or high; thrombocytopenia is rare. We describe two children with iron deficiency anaemia and severe thrombocytopenia who recovered with iron supplementation alone.

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Cadenas, Beatriz, Josep Fita-Torró, Mar Bermúdez-Cortés, Inés Hernandez-Rodriguez, José Fuster, María Llinares, Ana Galera, et al. "L-Ferritin: One Gene, Five Diseases; from Hereditary Hyperferritinemia to Hypoferritinemia—Report of New Cases." Pharmaceuticals 12, no. 1 (January 23, 2019): 17. http://dx.doi.org/10.3390/ph12010017.

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Ferritin is a multimeric protein composed of light (L-ferritin) and heavy (H-ferritin) subunits that binds and stores iron inside the cell. A variety of mutations have been reported in the L-ferritin subunit gene (FTL gene) that cause the following five diseases: (1) hereditary hyperferritinemia with cataract syndrome (HHCS), (2) neuroferritinopathy, a subtype of neurodegeneration with brain iron accumulation (NBIA), (3) benign hyperferritinemia, (4) L-ferritin deficiency with autosomal dominant inheritance, and (5) L-ferritin deficiency with autosomal recessive inheritance. Defects in the FTL gene lead to abnormally high levels of serum ferritin (hyperferritinemia) in HHCS and benign hyperferritinemia, while low levels (hypoferritinemia) are present in neuroferritinopathy and in autosomal dominant and recessive L-ferritin deficiency. Iron disturbances as well as neuromuscular and cognitive deficits are present in some, but not all, of these diseases. Here, we identified two novel FTL variants that cause dominant L-ferritin deficiency and HHCS (c.375+2T > A and 36_42delCAACAGT, respectively), and one previously reported variant (Met1Val) that causes dominant L-ferritin deficiency. Globally, genetic changes in the FTL gene are responsible for multiple phenotypes and an accurate diagnosis is useful for appropriate treatment. To help in this goal, we included a diagnostic algorithm for the detection of diseases caused by defects in FTL gene.

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Jee, Sam Ryong. "Helicobacter pylori and Hematologic Diseases." Korean Journal of Helicobacter and Upper Gastrointestinal Research 20, no. 1 (March 10, 2020): 11–20. http://dx.doi.org/10.7704/kjhugr.2019.0047.

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Helicobacter pylori (H. pylori) is a Gram-negative spiral bacterium, classified as a group 1 carcinogen by the World Health Organization. H. pylori infection is a major cause of gastritis, gastric and duodenal ulcers, and gastric cancer. It is associated with the pathogenesis of several hematologic diseases. H. pylori eradication has been proven effective in gastric mucosa-associated lymphoid tissue lymphoma and primary immune thrombocytopenia. As H. pylori causes iron deficiency anemia via several mechanisms, some recent guidelines recommended its eradication from patients with iron deficiency anemia. There are discussions of other conditions that are not included in the international consensus and management guides on H. pylori, including monoclonal gammopathy, myelodysplastic syndrome, childhood leukemia, coagulation disorder, megaloblastic anemia, pernicious anemia, plasma cell dyscrasia, and Henoch-Schönlein purpura. Further studies are required to establish new strategies to improve the management of patients with an infection combined with a hematologic disease of controversial or peculiar association.

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Roth-Walter, Franziska. "Compensating functional iron deficiency in patients with allergies with targeted micronutrition." Allergo Journal International 30, no. 4 (April 20, 2021): 130–34. http://dx.doi.org/10.1007/s40629-021-00171-9.

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SummaryIron deficiency is associated with atopy. Iron deficiency during pregnancy increases the risk of atopic diseases in children, while both allergic children and adults are more likely to have iron deficiency anemia. Immunologically, iron deficiency leads to activation of antigen-presenting cells, promotion of Th2 cells and enables antibody class switch in B cells. In addition, iron deficiency primes mast cells for degranulation, while an increase in their iron content inhibits their degranulation. Many allergens, especially those with lipocalin and lipocalin-like protein structures, are able to bind iron and either deprive or supply this trace element to immune cells. Thus, a local induced iron deficiency will result in immune activation and allergic sensitization. However, lipocalin proteins such as the whey protein β‑lactoglobulin (BLG) can also transport micronutrients into the defense cells (holo-BLG: BLG with micronutrients) and hinder their activation, thereby promoting tolerance and protecting against allergy. Since 2019, several clinical trials have also been conducted in allergic subjects using holo-BLG as a supplementary balanced diet, leading to a reduction in symptom burden. Supplementation with holo-BLG specifically supplied defense cells with micronutrients such as iron and therefore represents a new dietary approach to compensate for functional iron deficiency in allergy sufferers.

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DiGirolamo, Ann M., Geraldine S. Perry, Benjamin D. Gold, Alan Parkinson, Ellen M. Provost, Ibrahim Parvanta, and Laurence M. Grummer-Strawn. "Helicobacter pylori, Anemia, and Iron Deficiency." Pediatric Infectious Disease Journal 26, no. 10 (October 2007): 927–34. http://dx.doi.org/10.1097/inf.0b013e31812e52cd.

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Markova, E. A., A. Z. Khashukoeva, S. A. Khlynova, M. V. Burdenko, and A. Kh Karanasheva. "Anemia in elderly women. Rational prevention. Evidence base." Meditsinskiy sovet = Medical Council, no. 3 (April 15, 2021): 128–34. http://dx.doi.org/10.21518/2079-701x-2021-3-128-134.

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Iron deficiency anemia is a frequent companion in postmenopausal women and those who have reached adulthood. Anemia in mild form in elderly women often occurs almost asymptomatically. Over time, iron deficiency progresses: severe complications occur, the quality of life decreases significantly, and the prognosis for life becomes unfavorable. A cross-section of the literature data in recent years shows that iron, folate, vitamin B12 deficiency, gastrointestinal diseases, pathologies in the processes of erythropoiesis and other somatic diseases come to the fore in terms of the etiological factors of anemia in elderly women. An important role in the development of anemia in older women is played by an irrational diet throughout life, which causes a lack of iron and folate in food. That is why therapy with a complex drug, which includes iron (II) fumarate in combination with folic acid is a rational choice in comparison with iron monotherapy for the prevention and treatment of anemia in elderly women. The administration of oral iron preparations for the correction of iron deficiency and for the purpose of selecting an effective pathogenetic therapy for anemia solves the problem of complications and improves the quality of life of older women. Iron (II) fumarate + folic acid - a tablet form of iron preparation in combination with folic acid for oral use, which has good tolerability, quickly replenishes iron reserves in the body of elderly patients, reducing mortality in this age group.

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Marklová, Eliška. "Microelements and Inherited Metabolic Diseases." Acta Medica (Hradec Kralove, Czech Republic) 45, no. 4 (2002): 129–33. http://dx.doi.org/10.14712/18059694.2019.69.

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In addition to the main groups of inherited metabolic diseases, including mitochondrial, peroxisomal and lysosomal defects, organic acidurias, porphyrias, defects of amino acids, saccharides and fatty acids metabolism, disorders of transport and utilisation of microelements have also been recognized. Recent findings concerning hereditary hemochromatosis (iron), Wilson and Menkes diseases (copper), molybdenum cofactor deficiency (molybdenum), defects of cobalamine synthesis (cobalt) and acrodermatitis enteropathica (zinc) are reviewed.

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Dziegala, Magdalena, Krystian Josiak, Monika Kasztura, Kamil Kobak, Stephan von Haehling, Waldemar Banasiak, Stefan D. Anker, Piotr Ponikowski, and Ewa Jankowska. "Iron deficiency as energetic insult to skeletal muscle in chronic diseases." Journal of Cachexia, Sarcopenia and Muscle 9, no. 5 (September 4, 2018): 802–15. http://dx.doi.org/10.1002/jcsm.12314.

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Maltha, J., and J. Jacobs. "Iron Deficiency and Malaria Mortality: Possible Implication of Invasive Bacterial Diseases." Clinical Infectious Diseases 55, no. 5 (June 5, 2012): 748. http://dx.doi.org/10.1093/cid/cis522.

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Davydova, Iu V., A. Y. Lymanskaya, and O. M. Kravets. "The role of vitamin D3 deficiency correction in optimizing the treatment of anemia in women with autoimmune diseases." Ukrainian journal of Perinatology and Pediatrics, no. 1(85) (March 29, 2021): 7–10. http://dx.doi.org/10.15574/pp.2021.85.7.

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The aim is to analyze the effectiveness of correction vitamin D deficiency in the treatment of anemia in women with systemic lupus erythematosus (SLE). Materials and methods. Concomitant documented levels of 25-hydroxyvitamin D, hemoglobin, ferritin, and serum iron in a group of women with SLE who applied for preconception counseling were analyzed. All women were in remission for SLE activity within 5 to 6 months. A total of 54 women were involved in iron metabolism disorders (decreased ferritin, hemoglobin, serum iron). Vitamin D deficiency was detected at <30 ng/ml, and anemia at hemoglobin <120 g/l. Group 1 consisted of 32 women with vitamin D levels <30 ng/ml who received antianemic therapy with ferrous sulfate with ascorbic acid, correction of vitamin D deficiency with Olidetrim 2000 U (Polpharma), and group 2 — women with vitamin D levels <30 ng/ml (n=22) who received antianemic therapy with ferrous sulfate with ascorbic acid and a vitamin complex containing vitamin D 400 U. The groups were comparable by the main demographic indicators (age, education, socio-economic level). In both groups, iron metabolism and 25-hydroxyvitamin D levels were monitored in 4 weeks after treatment. Results and conclusions. Women with SLE have a high risk of chronic inflammatory anemia development, which can be combined with iron deficiency anemia. To improve the results of treatment, it is proposed to introduce supplementation with a high dose of vitamin D (Olidetrim 2000 U), into complex therapy which contributes to the effectiveness of correction of deficiency of this vitamin, as well as the onset of long-term recovery of iron store, hemoglobin concentration. The study was conducted in accordance with the principles of the Declaration of Helsinki. The research protocol was approved by the Local Ethics Committee of the institution mentioned in the work. Informed consent of women was obtained for the research. The authors declare no conflict of interest. Key words: vitamin D deficiency, pregnant women, systemic lupus erythematosus, supplementation.

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Journal articles on the topic 'Iron deficiency diseases'

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