Application of HbA 2 levels and red cell indices‐based new model in the differentiation of thalassemia traits from iron deficiency in hypochromic microcytic anemia Cases

2020 ◽  
Vol 42 (5) ◽  
pp. 526-532
Author(s):  
Yuan Zhou ◽  
Jibo Zhang ◽  
Chao Wang ◽  
Lihua Zhou ◽  
Lu Zhou ◽  
...  
2021 ◽  
Vol 25 (3) ◽  
pp. 625-632
Author(s):  
Shno Hussein ◽  
Abbas Rabaty

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.


PEDIATRICS ◽  
1956 ◽  
Vol 18 (6) ◽  
pp. 959-978
Author(s):  
Hugh W. Josephs

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.


Blood ◽  
1985 ◽  
Vol 65 (1) ◽  
pp. 60-64 ◽  
Author(s):  
Z Rolovic ◽  
T Jovanovic ◽  
Z Stankovic ◽  
N Marinkovic

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.


Blood ◽  
2011 ◽  
Vol 118 (24) ◽  
pp. 6418-6425 ◽  
Author(s):  
Lara Krieg ◽  
Oren Milstein ◽  
Philippe Krebs ◽  
Yu Xia ◽  
Bruce Beutler ◽  
...  

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.


Pathology ◽  
1974 ◽  
Vol 6 (2) ◽  
pp. 107-117 ◽  
Author(s):  
R.F. Croft ◽  
A.M. Streeter ◽  
B.J. O'Neill

2020 ◽  
Vol 10 (3) ◽  
pp. 182-186
Author(s):  
Md Abdul Baki ◽  
Shahida Akhter ◽  
Jebun Nahar ◽  
Fauzia Mohsin ◽  
Shareen Khan

Background: Fetal iron stores are affected by maternal diabetes and it is lower at birth in infants of diabetic mothers (IDMs). Risks for developing iron deficiency and neurocognitive impairment are reported in IDMs. This study was done to assess serum ferritin and red cell indices in IDMs and to compare the values with infants born to mothers without diabetes mellitus. Methods: This cross-sectional study was carried out at BIRDEM General Hospital from March to October, 2018. Total 102 full term neonates were included in this study. Among them 70 neonates were IDMs and 32 were infants born to mother without diabetes mellitus. Serum ferritin and red cell indices like hemoglobin (Hb), packed cell volume (PCV), mean corpuscular volume (MCV), mean corpuscular hemoglobin (MCH), mean corpuscular hemoglobin concentration (MCHC), red cell distribution width (RDW) were measured within 48 hours of birth. Comparison of red cell indices and serum ferritin level were done between IDMs and infants of non-diabetes mothers. Statistical analysis was performed by using Epi info, and p value of <0.05 was considered statistically significant. Results: IDMs had significantly higher value of Hb% (19.00 vs 17.47 g/dl), PCV (57.60 vs 52.67 %) and RDW (20.09 vs17.77 %) than infant of non-diabetic mother (p <0.05). But there was no significant difference regarding the values of MCV, MCH and MCHC between IDMs and infants of non-diabetic mothers (p >0.05). Serum ferritin level was found significantly low in IDMs (94.51 vs 307.50 ng/ml, p <0.001). Conclusion: Iron stores of IDMs were found significantly lower at birth despite higher hemoglobin content, as indicated by lower serum ferritin level. Further studies and long-term follow up are needed to determine whether these infants are at risk for developing iron deficiency anemia or iron-deficient neurocognitive disorder Birdem Med J 2020; 10(3): 182-186


Blood ◽  
2008 ◽  
Vol 112 (5) ◽  
pp. 2089-2091 ◽  
Author(s):  
Flavia Guillem ◽  
Sarah Lawson ◽  
Caroline Kannengiesser ◽  
Mark Westerman ◽  
Carole Beaumont ◽  
...  

Abstract Genetic causes of hypochromic microcytic anemia include thalassemias and some rare inherited diseases such as DMT1 deficiency. Here, we show that iron deficiency anemia with poor intestinal absorption and defective iron utilization of IV iron is caused by inherited mutations in TMPRSS6, a liver-expressed gene that encodes a membrane-bound serine protease of previously unknown role that was recently reported to be a regulator of hepcidin expression.


Blood ◽  
2005 ◽  
Vol 106 (10) ◽  
pp. 3625-3631 ◽  
Author(s):  
Robert S. Ohgami ◽  
Dean R. Campagna ◽  
Brendan Antiochos ◽  
Emily B. Wood ◽  
John J. Sharp ◽  
...  

AbstractHypochromic, microcytic anemias are typically the result of inadequate hemoglobin production because of globin defects or iron deficiency. Here, we describe the phenotypic characteristics and pathogenesis of a new recessive, hypochromic, microcytic anemia mouse mutant, nm1054. Although the mutation nm1054 is pleiotropic, also resulting in sparse hair, male infertility, failure to thrive, and hydrocephaly, the anemia is the focus of this study. Hematologic analysis reveals a moderately severe, congenital, hypochromic, microcytic anemia, with an elevated red cell zinc protoporphyrin, consistent with functional erythroid iron deficiency. However, serum and tissue iron analyses show that nm1054 animals are not systemically iron deficient. From hematopoietic stem cell transplantation and iron uptake studies in nm1054 reticulocytes, we provide evidence that the nm1054 anemia is due to an intrinsic hematopoietic defect resulting in inefficient transferrin-dependent iron uptake by erythroid precursors. Linkage studies demonstrate that nm1054 maps to a genetic locus not previously implicated in microcytic anemia or iron phenotypes.


1980 ◽  
Vol 1 (7) ◽  
pp. 196-222

The only hypochromic microcytic anemias in young children are iron deficiency, lead poisoning, and thalassemia. Clinical features helpful in the diagnosis include the following. Iron deficiency: peak incidence from 1 to 2 years of age, diet deficient in iron, or ingestion of more than one quart of milk per day. Alpha-thalassemia trait: occurs in any age group and predominantly in Oriental, black, and Mediterranean races. Beta-thalassemia trait occurs in children more than 6 months of age and predominately in black and Mediterranean races. Lead poisoning: peak incidence from 6 months to 4 years of age and a history of pica. It occurs largely in urban children.


Sign in / Sign up

Export Citation Format

Share Document