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 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.

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 ◽  
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.

Severe hypochromic microcytic anemia caused by a congenital defect of the iron transport pathway in erythroid cells

Blood ◽  
2004 ◽  
Vol 103 (10) ◽  
pp. 3991-3992 ◽  
Author(s):  
Monika Priwitzerova ◽  
Dagmar Pospisilova ◽  
Josef T. Prchal ◽  
Karel Indrak ◽  
Alice Hlobilkova ◽  
...  
Keyword(s):  
Iron Transport ◽  
Microcytic Anemia ◽  
Congenital Defect ◽  
Erythroid Cells ◽  
Transport Pathway ◽  
Hypochromic Microcytic Anemia ◽  
In Erythroid Cells

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.

Defective iron uptake by the duodenum of Belgrade rats fed diets of different iron contents

1996 ◽  
Vol 270 (5) ◽  
pp. G826-G832 ◽  
Author(s):  
P. S. Oates ◽  
E. H. Morgan
Keyword(s):  
Iron Content ◽  
Iron Uptake ◽  
Iron Transport ◽  
Iron Absorption ◽  
Microcytic Anemia ◽  
Deficient Diet ◽  
Hypochromic Microcytic Anemia ◽  
Iron Deficient

Homozygous Belgrade rats have an inherited hypochromic, microcytic anemia that is due to impaired iron transport into immature erythrocytes. There is also evidence for abnormal iron transport in other tissues such as the intestine. This study was aimed at investigating the intestinal defect in rats that had been fed diets for 12 days that are normal, low, or high in iron. The duodenal uptake, transfer, and absorption of Fe(III)-nitrilotriacetate and Fe(II)-ascorbate were studied using in vivo tied-off gut sacs in genetically normal rats and in heterozygous or homozygous Belgrade rats. In normal and heterozygous Belgrade rats, the handling of Fe(III) and Fe(II) was similar; uptake, transfer, and absorption of Fe(III) and Fe(II) changed inversely with the iron content of the diet. In contrast, in homozygous Belgrade rats the uptake of both Fe(III) and Fe(II) was markedly reduced and absorption of Fe(III) did not change when animals were fed an iron-deficient diet. Since absorption of Fe(II) was similar to Fe(III), there is no evidence that the defect in iron absorption is due to failure of a mechanism for reduction of Fe(III). The lowered uptake of Fe(III) and Fe(II) in homozygous Belgrade rats probably involves a defective iron carrier associated with the microvillous membrane of the duodenum.

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 Intravenous iron is non-inferior to oral iron regarding cell growth and iron metabolism in colorectal cancer associated with iron-deficiency anaemia

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Hafid O. Al-Hassi ◽  
Oliver Ng ◽  
Rayko Evstatiev ◽  
Manel Mangalika ◽  
Natalie Worton ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Iron Deficiency ◽  
Iron Metabolism ◽  
Iron Deficiency Anaemia ◽  
Iron Transport ◽  
Intravenous Iron ◽  
Oral Iron ◽  
Iron Loading ◽  
Deficiency Anaemia ◽  
Iron Treatment

AbstractOral iron promotes intestinal tumourigenesis in animal models. In humans, expression of iron transport proteins are altered in colorectal cancer. This study examined whether the route of iron therapy alters iron transport and tumour growth. Colorectal adenocarcinoma patients with pre-operative iron deficiency anaemia received oral ferrous sulphate (n = 15), or intravenous ferric carboxymaltose (n = 15). Paired (normal and tumour tissues) samples were compared for expression of iron loading, iron transporters, proliferation, apoptosis and Wnt signalling using immunohistochemistry and RT-PCR. Iron loading was increased in tumour and distributed to the stroma in intravenous treatment and to the epithelium in oral treatment. Protein and mRNA expression of proliferation and iron transporters were increased in tumours compared to normal tissues but there were no significant differences between the treatment groups. However, intravenous iron treatment reduced ferritin mRNA levels in tumours and replenished body iron stores. Iron distribution to non-epithelial cells in intravenous iron suggests that iron is less bioavailable to tumour cells. Therefore, intravenous iron may be a better option in the treatment of colorectal cancer patients with iron deficiency anaemia due to its efficiency in replenishing iron levels while its effect on proliferation and iron metabolism is similar to that of oral iron treatment.

scholarly journals Giant adrenal hemangioma: Unusual cause of huge abdominal mass

2015 ◽  
Vol 9 (11-12) ◽  
pp. 834 ◽  
Author(s):  
Mohamed Tarchouli ◽  
Adil Boudhas ◽  
Moulay Brahim Ratbi ◽  
Mohamed Essarghini ◽  
Noureddine Njoumi ◽  
...  
Keyword(s):  
Adrenal Gland ◽  
Abdominal Mass ◽  
Abdominal Distension ◽  
Microcytic Anemia ◽  
Hypochromic Microcytic Anemia ◽  
Normal Limits ◽  
Laboratory Examinations ◽  
Right Lobe ◽  
The Right

Adrenal hemangioma is an extremely rare benign and non-functioning neoplasm of the adrenal gland. We report a case of a 71-year-old woman admitted for intermittent abdominal pain and abdominal distension associated with vomiting and chronic constipation for 5 years. Physical examination revealed a large abdominal mass. Both computed tomography scan and magnetic resonance imaging suggested hemangioma in the right lobe of the liver. Laboratory examinations and tumour markers were within normal limits, except for hypochromic microcytic anemia. The mass was removed intact by conventional surgery and histopathology revealed a cavernous hemangioma of the adrenal gland with no signs of malignancy. Surgical resection was curative, with no recurrence at the 2-year follow-up.

scholarly journals Mutation of the gastric hydrogen-potassium ATPase alpha subunit causes iron-deficiency anemia in mice

Blood ◽  
2011 ◽  
Vol 118 (24) ◽  
pp. 6418-6425 ◽  
Author(s):  
Lara Krieg ◽  
Oren Milstein ◽  
Philippe Krebs ◽  
Yu Xia ◽  
Bruce Beutler ◽  
...  
Keyword(s):  
Iron Deficiency ◽  
Iron Deficiency Anemia ◽  
Iron Absorption ◽  
Osmotic Fragility ◽  
Microcytic Anemia ◽  
Deficiency Anemia ◽  
Α Subunit ◽  
Hypochromic Microcytic Anemia ◽  
Gastric Proton Pump ◽  
Potassium Atpase

Abstract Iron is an essential component of heme and hemoglobin, and therefore restriction of iron availability directly limits erythropoiesis. In the present study, we report a defect in iron absorption that results in iron-deficiency anemia, as revealed by an N-ethyl-N-nitrosourea–induced mouse phenotype called sublytic. Homozygous sublytic mice develop hypochromic microcytic anemia with reduced osmotic fragility of RBCs. The sublytic phenotype stems from impaired gastrointestinal iron absorption caused by a point mutation of the gastric hydrogen-potassium ATPase α subunit encoded by Atp4a, which results in achlorhydria. The anemia of sublytic homozygotes can be corrected by feeding with a high-iron diet or by parenteral injection of iron dextran; rescue can also be achieved by providing acidified drinking water to sublytic homozygotes. These findings establish the necessity of the gastric proton pump for iron absorption and effective erythropoiesis.

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