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Query: UMLS:C0026986 (myelodysplastic syndrome)
 14,926 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Anemia in IBD is the result of a combination of iron deficiency and anemia of chronic disease. Therapy of IBD is relief of inflammation, but the drugs usage may cause the development hemolytic anemia and myelodysplastic syndrome. We studied the effect of basic therapy on the incidence of anemia and assess the impact of modern biological therapies on the main markers of AHZ. A total of 153 patients with ulcerative colitis (UC) and 53 patients with Crohn's disease (CD), which at the time of the study received basic anti-inflammatory therapy for at least 1 year. All patients underwent blood tests, iron metabolism parameters were determined by the level of erythropoietin and G-gepsidina C reactive protein. Modern biological therapy increases the effectiveness of the treatment of anemia in patients with IBD. The use of Remicade gives a quick positive response, which is due to the decrease of gepsidin negative influence on iron metabolism and unlocking the synthesis of erythropoietin. The use of MSCs does not inhibit the synthesis of erythropoietin, and is likely to stimulate erythropoiesis at the erythroblast precursors.
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PMID:[Risk of development of clinical and pathogenetic features of anemia on the background of basic therapy of inflammatory bowel disease]. 2262 93

Most iron in the body is utilized as a component of hemoglobin that delivers oxygen to the entire body. Under normal conditions, the iron balance is tightly regulated. However, iron dysregulation does occasionally occur; total iron content reductions cause iron deficiency anemia and overexpression of the iron regulatory peptide hepcidin disturbs iron utilization resulting in anemia of chronic disease. Conversely, the presence of anemia may ultimately lead to iron overload; for example, thalassemia, a common hereditary anemia worldwide, often requires transfusion, but long-term transfusions cause iron accumulation that leads to organ damage and other poor outcomes. On the other hand, there is a possibility that iron overload itself can cause anemia; iron chelation therapy for the post-transfusion iron overload observed in myelodysplastic syndrome or aplastic anemia improves dependency on transfusions in some cases. These observations reflect the extremely close relationship between anemias and iron metabolism.
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PMID:[Iron dysregulation and anemias]. 2645 28

The iron regulatory hormone hepcidin limits iron fluxes to the bloodstream by promoting degradation of the iron exporter ferroportin in target cells. Hepcidin insufficiency causes hyperabsorption of dietary iron, hyperferremia and tissue iron overload, which are hallmarks of hereditary hemochromatosis. Similar responses are also observed in iron-loading anemias due to ineffective erythropoiesis (such as thalassemias, dyserythropoietic anemias and myelodysplastic syndromes) and in chronic liver diseases. On the other hand, excessive hepcidin expression inhibits dietary iron absorption and leads to hypoferremia and iron retention within tissue macrophages. This reduces iron availability for erythroblasts and contributes to the development of anemias with iron-restricted erythropoiesis (such as anemia of chronic disease and iron-refractory iron-deficiency anemia). Pharmacological targeting of the hepcidin/ferroportin axis may offer considerable therapeutic benefits by correcting iron traffic. This review summarizes the principles underlying the development of hepcidin-based therapies for the treatment of iron-related disorders, and discusses the emerging strategies for manipulating hepcidin pathways.
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PMID:Pharmacological Targeting of the Hepcidin/Ferroportin Axis. 2744 4

Myelodysplastic syndromes (MDS) are biologically and clinically heterogenous groups of clonal haematopoietic stem cell diseases characterized by ineffective haematopoiesis and peripheral blood cytopenia, with a variable tendency to transform within acute leukaemia (AL). DNA hypermethylation and hypo-methylation are associated with cancer. Thus, the hypermethylation of DNA is essential for the molecular pathophysiology of MDS by inactivating genes involved in cell growth, differentiation and apoptosis. It was documented that the 5-methylcytosine (5mc) immunostaining score of BM haematopoietic mononuclear cells is higher in MDS patients than in a normal control group, and that the prognosis of the disease significantly correlated with global DNA methylation, age and IPSS score. In our study, we analysed the immunocytochemical expression of 5mc in bone marrow (BM) mononuclear cells from 13 MDS patients and a control group consisting of 13 patients with anaemia of chronic disease. The immunopositivity of 5mc BM mononuclear cells was statistically significantly higher in our MDS patients than in patients with anaemia of chronic disease. In most MDS patients (11 out of 13), a higher 5mc immunopositivity of BM mono-nuclear cells (above 10%) was found. Our results are in concordance with data from literature observing that a higher percentage of 5mc immunopositive BM mononuclear cells is documented in MDS patients.
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PMID:Immunoexpression of 5-methylcytosine (5mc) in Bone Marrow Haematopoietic Cells in Patients with Myelodysplastic Syndromes. 3188 33


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