scholarly journals Abnormal megakaryocytopoiesis in the Belgrade laboratory rat

Blood ◽  
1985 ◽  
Vol 65 (1) ◽  
pp. 60-64 ◽  
Author(s):  
Z Rolovic ◽  
T Jovanovic ◽  
Z Stankovic ◽  
N Marinkovic
Keyword(s):  
Genetic Defect ◽  
Cell Lineage ◽  
Microcytic Anemia ◽  
Severe Anemia ◽  
Red Cell ◽  
Present Evidence ◽  
Hypochromic Microcytic Anemia ◽  
Laboratory Rat ◽  
Maturation Rate ◽  
Normal Rat

Abstract The Belgrade laboratory rat (b/b rat) has hereditary, hypochromic, microcytic anemia with a variety of red cell abnormalities. Although this anemic syndrome has been recently ascribed to the defective delivery of iron to the developing red cell, the basic hematopoietic defect is still unknown. In this article we present evidence that the b/b rat has an additional hematologic defect. We have found that the megakaryocyte number in the marrow of the b/b rat is decreased to one half that of the normal rat, but the maturation rate of recognizable megakaryocytes is accelerated and the size is increased. The platelet count is moderately reduced. These findings indicate that megakaryocytopoiesis in the anemic b/b rat is abnormal and suggest that the genetic defect may involve the progenitors of the megakaryocyte cell lineage. Alternatively, the megakaryocytic abnormalities may be secondary to the severe anemia.

scholarly journals Abnormal megakaryocytopoiesis in the Belgrade laboratory rat

Blood ◽  
1985 ◽  
Vol 65 (1) ◽  
pp. 60-64 ◽  
Author(s):  
Z Rolovic ◽  
T Jovanovic ◽  
Z Stankovic ◽  
N Marinkovic
Keyword(s):  
Genetic Defect ◽  
Cell Lineage ◽  
Microcytic Anemia ◽  
Severe Anemia ◽  
Red Cell ◽  
Present Evidence ◽  
Hypochromic Microcytic Anemia ◽  
Laboratory Rat ◽  
Maturation Rate ◽  
Normal Rat

The Belgrade laboratory rat (b/b rat) has hereditary, hypochromic, microcytic anemia with a variety of red cell abnormalities. Although this anemic syndrome has been recently ascribed to the defective delivery of iron to the developing red cell, the basic hematopoietic defect is still unknown. In this article we present evidence that the b/b rat has an additional hematologic defect. We have found that the megakaryocyte number in the marrow of the b/b rat is decreased to one half that of the normal rat, but the maturation rate of recognizable megakaryocytes is accelerated and the size is increased. The platelet count is moderately reduced. These findings indicate that megakaryocytopoiesis in the anemic b/b rat is abnormal and suggest that the genetic defect may involve the progenitors of the megakaryocyte cell lineage. Alternatively, the megakaryocytic abnormalities may be secondary to the severe anemia.

HYPOCHROMIC MICROCYTIC ANEMIA OF INFANCY: IRON DEPLETION AS A FACTOR

PEDIATRICS ◽  
1956 ◽  
Vol 18 (6) ◽  
pp. 959-978
Author(s):  
Hugh W. Josephs
Keyword(s):  
Iron Deficiency ◽  
Severe Infection ◽  
Microcytic Anemia ◽  
Severe Anemia ◽  
Iron Depletion ◽  
Hypochromic Microcytic Anemia ◽  
Premature Babies ◽  
Number Of Factors ◽  
The Difference ◽  
Insight Into

In this work the author has attempted to gain insight into the significance of iron depletion by the use of 4 simple calculations, justification for which is found in recent articles. These are: (a) iron with which the infant is born; (b) iron retained from the food; (c) iron being used by the tissues and therefore unavailable for hemoglobin, and (d) iron combined with the total mass of hemoglobin. With these 4 figures it is possible to estimate the iron still potentially available for use (the "reserves" or "stones"). When the difference between a + b and c + d has reached about zero, depletion is considered to exist. The following characteristics of depletion may be emphasized: Depletion is the result of gain in weight and maximum possible usage of iron. It is therefore a normal result of growth and need not be associated with anemia. As soon as depletion has occurred, the organism is thereafter dependent on current absorption of iron. This is ordinarily sufficient, even with a diet of milk alone, to maintain an adequate concentration of hemoglobin after about 8 to 10 months of age. Severe anemia due to depletion alone is practically confined to premature babies whose relative gain in weight is rapid. Severe anemia in other than premature babies is the result of a number of factors by which iron becomes unavailable or is actually diverted from hemoglobin to storage. Response to iron medication is considerably better in infants with depletion than in those in whom some factor is present that interferes with iron utilization, and which is not connected by the mere giving of iron. The dependence on current absorption, whether the result of depletion or non-availability, introduces a certain precariousness which is apparently characteristic of this time of life. The organism gets along from day to day if nothing happens, but may not be able to meet an emergency, whether this appears as a rapid gain in weight, or a necessity to repair damage done by severe infection. If we consider iron deficiency as the cause of anemia, we can think of deficiency as due to a number of factors of which depletion is only one. The development and characteristics of depletion have been considered in this paper; other factors in iron deficiency will be considered in subsequent papers.

scholarly journals Abnormal megakaryocytopoiesis in the Belgrade laboratory rat

Blood ◽  
1991 ◽  
Vol 77 (3) ◽  
pp. 456-460 ◽  
Author(s):  
Z Rolovic ◽  
N Basara ◽  
N Stojanovic ◽  
N Suvajdzic ◽  
V Pavlovic-Kentera
Keyword(s):  
Iron Transport ◽  
Basic Mechanism ◽  
Microcytic Anemia ◽  
Severe Anemia ◽  
Erythroid Progenitors ◽  
Hypochromic Microcytic Anemia ◽  
Iron Treatment ◽  
Full Correction ◽  
Partial Correction ◽  
Cell Disorder

Abstract The Belgrade laboratory (b/b) rat has a hereditary hypochromic microcytic anemia because of defective transmembrane iron transport into erythroblasts. The present study was prompted by our previous work in which we showed that the b/b rat has hypomegakaryocytic thrombocytopenia associated with increased megakaryocyte size. To define the basic mechanism underlying this abnormality in the b/b rat we have studied both megakaryocytopoiesis and granulopoiesis in anemic b/b rats, chronically transfused b/b rats, iron-treated b/b rats, and controls. We have found decreased concentrations of megakaryocyte and granulocyte progenitors in the marrow of b/b rats. Full correction of the severe anemia by chronic transfusion resulted in normalization of megakaryocyte progenitors, small acetylcholinesterase positive cells, megakaryocyte size, and platelet counts, along with granulocyte progenitors. In contrast, the partial correction of anemia obtained by iron treatment resulted in improvement, but not normalization, of these parameters. These findings indicate that abnormal megakaryocytopoiesis in the b/b rat can be best interpreted as a consequence of hypoxia because of the severe anemia. Because we have recently shown that the number of erythroid progenitors in b/b rats is also low, we propose that abnormal megakaryocytopoiesis in this animal is a reflection of an acquired stem cell disorder induced by the prolonged hypoxia resulting from the severe anemia.

scholarly journals HEREDITARY HYPOCHROMIC MICROCYTIC ANEMIA IN THE LABORATORY RAT

Genetics ◽  
1966 ◽  
Vol 53 (6) ◽  
pp. 1079-1089 ◽  
Author(s):  
D Sladic-Simic ◽  
N Zivkovic ◽  
D Pavic ◽  
D Marinkovic ◽  
J Martinovic ◽  
...  
Keyword(s):  
Microcytic Anemia ◽  
Hypochromic Microcytic Anemia ◽  
Laboratory Rat

scholarly journals Brief Report: Microcytic Anemia with Erythroblastosis in Offspring of Magnesium-deprived Rats

Blood ◽  
1970 ◽  
Vol 36 (4) ◽  
pp. 500-506 ◽  
Author(s):  
SIDNEY Q. COHLAN ◽  
VALERIE JANSEN ◽  
JOSEPH DANCIS ◽  
SERGIO PIOMELLI
Keyword(s):  
Osmotic Fragility ◽  
Microcytic Anemia ◽  
Severe Anemia ◽  
Red Cell ◽  
Pregnant Rats ◽  
Intrauterine Growth

Abstract Magnesium deprivation of pregnant rats produces in their offspring depression of intrauterine growth and severe anemia. The anemia is characterized by microcytosis, red cell fragmentation, increase in number of normoblasts and markedly decreased osmotic fragility.

scholarly journals Abnormal megakaryocytopoiesis in the Belgrade laboratory rat

Blood ◽  
1991 ◽  
Vol 77 (3) ◽  
pp. 456-460
Author(s):  
Z Rolovic ◽  
N Basara ◽  
N Stojanovic ◽  
N Suvajdzic ◽  
V Pavlovic-Kentera
Keyword(s):  
Iron Transport ◽  
Basic Mechanism ◽  
Microcytic Anemia ◽  
Severe Anemia ◽  
Erythroid Progenitors ◽  
Hypochromic Microcytic Anemia ◽  
Iron Treatment ◽  
Full Correction ◽  
Partial Correction ◽  
Cell Disorder

The Belgrade laboratory (b/b) rat has a hereditary hypochromic microcytic anemia because of defective transmembrane iron transport into erythroblasts. The present study was prompted by our previous work in which we showed that the b/b rat has hypomegakaryocytic thrombocytopenia associated with increased megakaryocyte size. To define the basic mechanism underlying this abnormality in the b/b rat we have studied both megakaryocytopoiesis and granulopoiesis in anemic b/b rats, chronically transfused b/b rats, iron-treated b/b rats, and controls. We have found decreased concentrations of megakaryocyte and granulocyte progenitors in the marrow of b/b rats. Full correction of the severe anemia by chronic transfusion resulted in normalization of megakaryocyte progenitors, small acetylcholinesterase positive cells, megakaryocyte size, and platelet counts, along with granulocyte progenitors. In contrast, the partial correction of anemia obtained by iron treatment resulted in improvement, but not normalization, of these parameters. These findings indicate that abnormal megakaryocytopoiesis in the b/b rat can be best interpreted as a consequence of hypoxia because of the severe anemia. Because we have recently shown that the number of erythroid progenitors in b/b rats is also low, we propose that abnormal megakaryocytopoiesis in this animal is a reflection of an acquired stem cell disorder induced by the prolonged hypoxia resulting from the severe anemia.

scholarly journals Congenital erythropoietic porphyria due to a mutation in GATA1: the first trans-acting mutation causative for a human porphyria

Blood ◽  
2006 ◽  
Vol 109 (6) ◽  
pp. 2618-2621 ◽  
Author(s):  
John D. Phillips ◽  
David P. Steensma ◽  
Michael A. Pulsipher ◽  
Gerald J. Spangrude ◽  
James P. Kushner
Keyword(s):  
Bone Marrow ◽  
Molecular Basis ◽  
Autosomal Recessive ◽  
Autosomal Recessive Disorder ◽  
Microcytic Anemia ◽  
Red Cell ◽  
Globin Genes ◽  
Globin Chain ◽  
Hypochromic Microcytic Anemia ◽  
Congenital Erythropoietic Porphyria

AbstractCongenital erythropoietic porphyria (CEP), an autosomal recessive disorder, is due to mutations of uroporphyrinogen III synthase (UROS). Deficiency of UROS results in excess uroporphyrin I, which causes photosensitization. We evaluated a 3-year-old boy with CEP. A hypochromic, microcytic anemia was present from birth, and platelet counts averaged 70 × 109/L (70 000/μL). Erythrocyte UROS activity was 21% of controls. Red cell morphology and globin chain labeling studies were compatible with β-thalassemia. Hb electrophoresis revealed 36.3% A, 2.4% A2, 59.5% F, and 1.8% of an unidentified peak. No UROS or α- and β-globin mutations were found in the child or the parents. The molecular basis of the phenotype proved to be a mutation of GATA1, an X-linked transcription factor common to globin genes and heme biosynthetic enzymes in erythrocytes. A mutation at codon 216 in the child and on one allele of his mother changed arginine to tryptophan (R216W). This is the first report of a human porphyria due to a mutation in a trans-acting factor and the first association of CEP with thalassemia and thrombocytopenia. The Hb F level of 59.5% suggests a role for GATA-1 in globin switching. A bone marrow allograft corrected both the porphyria and the thalassemia.

Copper Deficiency: An Overlooked Cause of Anemia and Leucopenia

2020 ◽  
pp. 1-4
Author(s):  
Avneek Singh Sandhu ◽  
James Kim ◽  
Sivjot Binepal ◽  
Michael Gentry ◽  
Alejandro Calvo
Keyword(s):  
Gastric Resection ◽  
Copper Deficiency ◽  
Serum Copper ◽  
Microcytic Anemia ◽  
Deficiency Anemia ◽  
Severe Anemia ◽  
Short Bowel ◽  
Hypochromic Microcytic Anemia ◽  
Copper Supplementation ◽  
History Of

Copper deficiency (hypocupremia) is an acknowledged but often overlooked cause of anemia and leukopenia (1-4). It is recognized as a frequent cause of hypochromic microcytic anemia, leukopenia, and neuropathy. Copper deficiency anemia has been reported after gastric resection (e.g., Roux-en-Y) (1, 5, 6), excessive zinc consumption (1, 6-9), and in patients with short bowel syndrome receiving total parenteral or enteral nutrition lacking adequate copper supplementation (1, 2). We report a case of vitamin B12, and iron refractory severe anemia and leucopenia with history of Roux-en-Y surgery. Myelodysplastic syndrome was suspected. Bone marrow biopsy was consistent with copper deficiency and serum copper levels were undetectable. The patient experienced complete hematological recovery after copper replacement therapy.

scholarly journals Red cell distribution width’s role in differentiating iron deficiency anemia from other hypochromic microcytic anemias

2021 ◽  
Vol 25 (3) ◽  
pp. 625-632
Author(s):  
Shno Hussein ◽  
Abbas Rabaty
Keyword(s):  
Iron Deficiency ◽  
Iron Deficiency Anemia ◽  
Serum Iron ◽  
Microcytic Anemia ◽  
Red Cell Distribution Width ◽  
Deficiency Anemia ◽  
Red Cell ◽  
Cell Distribution ◽  
Distribution Width ◽  
Hypochromic Microcytic Anemia

Background and objective: The red cell distribution width is suggested to be a more sensitive indicator for microcytic hypochromic anemia. Therefore, this study aimed to determine the role of red cell distribution width in the diagnosis of iron deficiency anemia from other causes of hypochromic microcytic anemia. Methods: This cross-sectional study involved the children patients who attended Rapareen Teaching Hospital in Erbil city in 2019 and were diagnosed with hypochromic microcytic anemia. Results: The red cell distribution width was determined in a group of 70 children with iron deficiency anemia and 30 cases with a non-iron deficiency (other hypochromic microcytic anemias). Patients with a higher socio-demographic status were more likely to have iron deficiency anemia than those with low socio-demographic status; 82.61% vs. 76.60%, respectively. The patients with symptoms were more likely to be diagnosed with iron deficiency anemia (P = 0.024). The mean red cell distribution width value was 14.38%, 15.73%, and18.02% among mild, moderate, and severely anemic children (P <0.001). Increasing red blood cells (r=-0.271), hemoglobin (r=-0.454), serum iron (r=-0.601), and serum ferritin (r=-0.560) lead to decrease red cell distribution width. The sensitivity, specificity, positive predictive value, negative predictive value, and accuracy of red cell distribution width in diagnosing iron deficiency anemia in children patients were 77.14%, 63.33%, 83.08%, 54.29%, and 73.0%, respectively. Conclusions: This study showed that red cell distribution width has good sensitivity and specificity in diagnosing iron deficiency anemia. Keywords: RDW; IDA; RBC indices; Microcytic anemia; Serum iron.

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