Přehledový článek, věnující se diferenciální diagnostice anémií, jako jednomu z nejčastějších klinických symptomů napříč všemi obory medicíny. Jedná se o stav definovaný nižší hodnotou koncentrace hemoglobinu v erytrocytech, než je stanovená fyziologická dolní hranice. Z mnoha kritérií, podle kterých lze anémie rozdělovat, je v tomto článku použité morfologické dělení na základě velikosti erytrocytů na makrocytární, mikrocytární a normocytární a speciální skupinu věnující se anémiím s retikulocytózou v periferní krvi. Vzhledem k primárnímu zaměření na diagnostiku, je u každé definované skupiny věnován prostor patofyziologii, diagnostickým postupům a klinickému stavu, vzhledem k rozsahu je terapie zmiňována pouze v zásadních bodech. Vzhledem k multioborovému přesahu anémie a nutnosti správného stanovení její příčiny pro nastavení terapie, se tato problematika týká valné většiny oborů současné medicíny.

This work presents an overwiev od the differential diagnosis of anaemia - one of the most frequent clinical symptom in all fields of medicine. Anaemia is defined as an hemoglobin concentration in erythrocytes lower than normal range. There are various criteria for categorising anaemia and we have selected the morfological classification based on erythorocyte size, i.e. macrocytic, microcytic, normocytic. We have also included a special group of anaemia associated with peripheral reticulocytosis. This article thus mainly focuses pathophysiology and diagnostic tools, while treatment is discussed only at key points. Given the multi - disciplinary implications ans the necessity of correct diagnosis for subsequent appropriate treatment, this issue touches most fields of modern medicine.

• MeSH
• Anemia * diagnosis   classification   therapy   MeSH
• Diagnosis, Differential MeSH
• Enzymes MeSH
• Hemoglobinopathies diagnosis   classification   MeSH
• Humans MeSH
• Iron Metabolism Disorders MeSH
• Reticulocytes MeSH
• Congenital Abnormalities MeSH
• Check Tag
• Humans MeSH
• Publication type
• Review MeSH

• MeSH
• Precursor Cell Lymphoblastic Leukemia-Lymphoma blood   MeSH
• Anemia diagnosis   etiology   drug therapy   classification   therapy   MeSH
• Child MeSH
• Erythrocytes MeSH
• Hematologic Tests MeSH
• Anemia, Hypochromic diagnosis   etiology   drug therapy   therapy   MeSH
• Purpura, Thrombocytopenic, Idiopathic MeSH
• Blood Coagulation Disorders diagnosis   classification   MeSH
• Hematologic Diseases * classification   MeSH
• Leukemia diagnosis   blood   MeSH
• Leukocytes MeSH
• Humans MeSH
• Adolescent MeSH
• Neutropenia diagnosis   classification   therapy   MeSH
• Reticulocytes MeSH
• Age Factors MeSH
• Iron administration & dosage   MeSH
• Check Tag
• Child MeSH
• Humans MeSH
• Adolescent MeSH
• Publication type
• Review MeSH

• MeSH
• Hematologic Tests * methods   instrumentation   MeSH
• Hemoglobinometry methods   instrumentation   MeSH
• Humans MeSH
• Reticulocytes cytology   MeSH
• Thrombocytopenia blood   MeSH
• Check Tag
• Humans MeSH
• Publication type
• Newspaper Article MeSH

• MeSH
• Anemia, Iron-Deficiency diagnosis   MeSH
• Anemia * diagnosis   MeSH
• Kidney Failure, Chronic complications   MeSH
• Spherocytosis, Hereditary MeSH
• Diagnosis, Differential MeSH
• Erythropoietin therapeutic use   MeSH
• Erythrocytes * MeSH
• Humans MeSH
• Reticulocytes * MeSH
• Check Tag
• Humans MeSH

• MeSH
• Chemotherapy, Adjuvant adverse effects   MeSH
• Anemia chemically induced   MeSH
• Erythropoietin analogs & derivatives   administration & dosage   therapeutic use   MeSH
• Erythropoiesis MeSH
• Hemoglobins MeSH
• Reticulocytes MeSH

• Conspectus
• Patologie. Klinická medicína
• NML Fields
• onkologie
• farmakoterapie
• farmacie a farmakologie
• NML Publication type
• studie

OBJECTIVES: MicroRNAs (miRNAs) play key roles in a wide variety of normal and pathological cellular processes. A number of studies identified hematopoietic-specific miRNAs that are necessary for correct function of blood cells. Out of our microarray data, we chose 13 miRNAs that showed differential expression in peripheral blood cells (miR-15b, miR-16, miR-24, miR-30c, miR-106b, miR-142-3p, miR-142-5p, miR-150, miR-155, miR-181, miR-223, miR-342, and miR-451) and examined their expression in separated hematopoietic cell lineages. METHODS: Using quantitative real-time polymerase chain reaction, we measured relative expression of the miRNAs in fractions of reticulocytes, platelets, granulocytes, monocytes, B- and T-lymphocytes as well as in several hematopoietic cell lines. RESULTS: We observed that miR-16 and miR-142-3p were highly expressed in all native cell lineages, miR-451 reached the maximal expression in reticulocytes, miR-223 in platelets, granulocytes and monocytes, and miR-150 in B- and T-lymphocytes. Hierarchical clustering analysis grouped the lineage samples according to their origin based on the expression of these miRNAs. To validate discrimination power of the miRNAs, we quantified expression of the 13 miRNAs in several immortalized cell lines. Although the cell lines showed miRNA expression patterns considerably different from those of native cell lineages, clustering analysis distinguished between myeloid, lymphoid and non-hematopoietic cells. CONCLUSIONS: In conclusion, the study reports the expression levels of 13 miRNAs in particular blood cell lineages as well as immortalized cell lines. We demonstrate that the expression profiles of these miRNAs may be used for discrimination of the hematopoietic cell lineages.

• MeSH
• Cell Differentiation physiology   MeSH
• K562 Cells MeSH
• Financing, Organized MeSH
• HeLa Cells MeSH
• Leukocytes cytology   metabolism   MeSH
• Humans MeSH
• Lymphoid Progenitor Cells cytology   metabolism   MeSH
• MicroRNAs biosynthesis   MeSH
• Granulocyte Precursor Cells cytology   metabolism   MeSH
• Gene Expression Regulation physiology   MeSH
• Reticulocytes cytology   metabolism   MeSH
• Oligonucleotide Array Sequence Analysis methods   MeSH
• Gene Expression Profiling methods   MeSH
• Blood Platelets cytology   metabolism   MeSH
• Check Tag
• Humans MeSH

Cellular prion protein (PrPc) participates in the pathogenesis of prion diseases but its normal function remains unclear. PrPc is expressed on hematopoietic cells, including erythroid precursors. We investigated the role of PrPc in erythropoiesis in vivo with phenylhydrazine-induced acute anemia. Induction of equivalent anemia in wild-type (WT) and Prnp-/- mice resulted in a higher number of circulating reticulocytes, hematocrits and spleen weights in WT mice than in Prnp-/- mice on Days 5 and 7. Examination of bone marrow erythroid precursor cells (Ter119+) on Day 5 revealed no significant differences in the number of these cells between the two types of animals. However, a higher percentage of Ter119+ cells were going through apoptosis in Prnp-/- mice than in WT mice. Plasma erythropoietin (Epo) levels and Epo mRNA in kidneys peaked on Day 3 in response to anemia for both types of animals but rose less in Prnp-/- (5500 pg/ml ) than in WT (18,000 pg/ml) animals. Administration of recombinant human Epo to mice produced an equivalent reticulocyte response in both types of animals suggesting that the potential for erythroid generation is intact in Prnp-/- animals. These observations indicate that PrPc may modulate tissue hypoxia-sensing mechanisms or effect hypoxia target gene expression.

• MeSH
• Acute Disease MeSH
• Erythropoietin blood   administration & dosage   pharmacology   MeSH
• Erythroid Precursor Cells physiology   MeSH
• Erythropoiesis MeSH
• Phenylhydrazines MeSH
• Financing, Organized MeSH
• Anemia, Hemolytic chemically induced   blood   metabolism   MeSH
• Hypoxia metabolism   MeSH
• Mice, Mutant Strains MeSH
• Mice, Knockout MeSH
• Mice MeSH
• Oxidants pharmacology   MeSH
• PrPC Proteins physiology   blood   MeSH
• Reticulocytes physiology   drug effects   MeSH
• Animals MeSH
• Check Tag
• Mice MeSH
• Animals MeSH

Mitochondrial uncoupling protein 2 (UCP2) is abundant in developing monocyte/macrophage cells and may affect hematopoiesis by reducing formation of reactive oxygen species. The aims of this study were to further characterize the involvement of UCP2 in hematopoiesis. In situ hybridization in mouse embryos identified UCP2-positive cells in liver and inside primitive blood vessels from 10.5 days of prenatal development. High UCP2 transcript levels were detected in reticulocytes and other maturating erythroid cells in peripheral blood of mice exposed to hypoxia, and in umbilical cord blood of human neonates and peripheral blood of adults. Our results suggest involvement of UCP2 in erythropoiesis.

• MeSH
• Embryo, Mammalian MeSH
• Erythroid Cells cytology   chemistry   MeSH
• Erythropoiesis genetics   MeSH
• Fetal Blood MeSH
• Liver cytology   MeSH
• Humans MeSH
• RNA, Messenger analysis   MeSH
• Mice MeSH
• Proteins analysis   physiology   genetics   MeSH
• Reticulocytes chemistry   MeSH
• Cellular Senescence genetics   MeSH
• Animals MeSH
• Check Tag
• Humans MeSH
• Mice MeSH
• Animals MeSH
• Publication type
• Research Support, Non-U.S. Gov't MeSH

The effects of nitroglycerine (NTG) are mediated by liberated nitric oxide (NO) after NTG enzymatic bio-transformation in cells. The aim of this study was to evaluate some products of NTG bio-transformation and their consequences on the redox status of rat erythrocytes and reticulocytes, considering the absence and presence of functional mitochondria in these cells, respectively. Rat erythrocyte and reticulocyte-rich red blood cell (RBC) suspensions were aerobically incubated (2 h, 37 0C) without (control) or in the presence of different concentrations of NTG (0.1, 0.25, 0.5, 1.0 and 1.5 mM). In rat erythrocytes, NTG did not elevate the concentrations of any reactive nitrogen species (RNS). However, NTG robustly increased concentration of methemoglobin (MetHb), suggesting that NTG bio-transformation was primarily connected with hemoglobin (Hb). NTG-induced MetHb formation was followed by the induction of lipid peroxidation. In rat reticulocytes, NTG caused an increase in the levels of nitrite, peroxinitrite, hydrogen peroxide, MetHb and lipid peroxide levels, but it decreased the level of the superoxide anion radical. Millimolar concentrations of NTG caused oxidative damage of both erythrocytes and reticulocytes. These data indicate that two pathways of NTG bio-transformation exist in reticulocytes: one generating RNS and the other connected with Hb (as in erythrocytes). In conclusion, NTG bio-transformation is different in erythrocytes and reticulocytes due to the presence of mitochondria in the latter. .

• MeSH
• Erythrocytes cytology   physiology   drug effects   MeSH
• Financing, Government MeSH
• Data Interpretation, Statistical MeSH
• Nitroglycerin analogs & derivatives   pharmacokinetics   MeSH
• Nitric Oxide physiology   chemistry   MeSH
• Oxidation-Reduction drug effects   MeSH
• Oxidative Stress radiation effects   MeSH
• Rats, Wistar blood   MeSH
• Reticulocytes cytology   physiology   drug effects   MeSH
• Animals MeSH
• Check Tag
• Animals MeSH
• Publication type
• Comparative Study MeSH

• MeSH
• Erythrocytes cytology   physiology   pathology   MeSH
• Hematologic Tests * methods   instrumentation   utilization   MeSH
• Hematopoietic Stem Cells * cytology   MeSH
• Hemoglobins physiology   isolation & purification   MeSH
• Clinical Laboratory Techniques instrumentation   trends   utilization   MeSH
• Leukocytes cytology   physiology   pathology   MeSH
• Humans MeSH
• Flow Cytometry * methods   utilization   MeSH
• Reticulocytes cytology   physiology   pathology   MeSH
• Blood Platelets cytology   physiology   pathology   MeSH
• Check Tag
• Humans MeSH
• Publication type
• Research Support, Non-U.S. Gov't MeSH