scholarly journals VITAMIN B12 AND FOLIC ACID LEVELS AFTER IRON THERAPY IN IRON-DEFICIENCY ANEMIA

2020 ◽  
Vol 3 (3) ◽  
pp. 261-267
Author(s):  
Didar Yanardağ Açık ◽  
Bilal Aygun
PEDIATRICS ◽  
1964 ◽  
Vol 34 (3) ◽  
pp. 315-323
Author(s):  
Samuel Gross ◽  
Vicki Keefer ◽  
Arthur J. Newman

In summary, it appears that thrombocytosis frequently accompanies the less severe anemia of iron deficiency and may be related to platelet stimulation in a manner analogous to the erythropoietin increase seen in many of the anemic states. In some of the severely anemic individuals, thrombopenia has been observed related suggestively to several factors, including severe depletion of iron as iron enzymes, a folate deficiency or a transient thrombopoietin deficit. In order to determine with any degree of certainty the etiology of the thrombocytopenia, one would have to evaluate the platelet response in a similarly afflicted group of infants treated with folic acid or simply thrombopoietin rich plasma prior to iron therapy. In regard to the intriguing difference in the platelet response to oral and parenteral iron, subsequent studies, using either extremely small amounts of parenteral iron or large amounts of oral iron, regardless of the initial platelet and hemoglobin values, might cast light on the etiology of this occurrence.


2013 ◽  
Author(s):  
Ashraf Soliman ◽  
Mohamed Yassin ◽  
Osman Abdelrahmanm ◽  
Vincenzo Desanctis ◽  
Ahmed Elawwa

1993 ◽  
Vol 33 (6) ◽  
pp. 661-661
Author(s):  
Helena U Suzuki ◽  
Mauro B Morais ◽  
Jose N Corral ◽  
Ulisses Fagundes-Neto ◽  
Nelson L Machado

Author(s):  
Manal Mahmoud Atia ◽  
Rasha Mohamed Gama ◽  
Mohamed Attia Saad ◽  
Mohammed Amr Hamam

Greater prevalence of iron deficiency (ID) has been observed in overweight and obese children and adolescents. Hepcidin acts as a key regulator of iron metabolism. Hepcidin synthesis increases in response inflammatory cytokines especially Interleukin-6 (IL-6). Considering that obesity represents a low grade chronic inflammatory state, a high concentration of hepcidin has been found in obese children. Elevated hepcidin level in obese children is associated with diminished response to oral iron therapy. Lactoferrin is an iron-binding multifunctional glycoprotein and has strong capacity to modulate the inflammatory response by its capacity to reduce pro-inflammatory cytokine expression in vivo, including IL-6 and hepcidin. Aim of the Work: To compare the efficacy of lactoferrin versus oral iron therapy in treatment of obese children and adolescents with iron deficiency anemia and the effect of therapy on serum hepcidin and interleukin 6 levels. Methodology: This prospective randomized clinical trial was conducted on 40 obese children and adolescents aged between 6 –18 years suffering from iron deficiency anemia (IDA). They were equally randomized into one of 2 groups. Group A received regular oral lactoferrin in a dose of 100 mg/day. Group B received regular oral iron supplementation (Ferric hydroxide polymaltose) in a dose of 6 mg elemental iron/kg /day.Baseline investigations included complete blood count (CBC), iron profile (Serum ferritin, serum iron, total iron binding capacity (TIBC), transferrin saturation), serum Interleukin 6, and serum hepcidin. Reevaluation of CBC was done monthly while iron status parameters, serum IL-6 and serum hepcidin were reevaluated after 3 months of receiving regular therapy. Results: Significant elevations in hemoglobin, MCV, MCH, Serum ferritin, serum iron and transferrin saturation with lactoferrin therapy compared to oral iron therapy. Significantly Lower TIBC after 3 months of lactoferrin therapy while the decrease in TIBC was insignificant in the iron therapy group.Lower serum hepcidin and IL6 after 3 months of lactoferrin therapy with no significant change in serum hepcidin and IL6 after iron therapy. Conclusion: This study clearly demonstrated the superiority of lactoferrin over iron use as oral in the treatment of iron deficiency anemia in obese children not only for the better response of hematological and iron status parameters and less gastrointestinal side effects but also for its effect on decreasing inflammatory biomarkers as hepcidin and IL6.


2000 ◽  
Vol 97 (5) ◽  
pp. 281-285 ◽  
Author(s):  
Ahmet Emin Kürekçi ◽  
A.Avni Atay ◽  
S.Ümit Sarı́cı́ ◽  
Cengiz Zeybek ◽  
Vedat Köseoğlu ◽  
...  

2017 ◽  
Vol 55 (1) ◽  
pp. 3-7 ◽  
Author(s):  
Mahmoud Arshad ◽  
Sara Jaberian ◽  
Abdolreza Pazouki ◽  
Sajedeh Riazi ◽  
Maryam Aghababa Rangraz ◽  
...  

Abstract Background. The association between obesity and different types of anemia remained uncertain. The present study aimed to assess the relation between obesity parameters and the occurrence of iron deficiency anemia and also megaloblastic anemia among Iranian population. Methods and Materials. This cross-sectional study was performed on 1252 patients with morbid obesity that randomly selected from all patients referred to Clinic of obesity at Rasoul-e-Akram Hospital in 2014. The morbid obesity was defined according to the guideline as body mass index (BMI) equal to or higher than 40 kg/m2. Various laboratory parameters including serum levels of hemoglobin, iron, ferritin, folic acid, and vitamin B12 were assessed using the standard laboratory techniques. Results. BMI was adversely associated with serum vitamin B12, but not associated with other hematologic parameters. The overall prevalence of iron deficiency anemia was 9.8%. The prevalence of iron deficiency anemia was independent to patients’ age and also to body mass index. The prevalence of vitamin B12 deficiency was totally 20.9%. According to the multivariable logistic regression model, no association was revealed between BMI and the occurrence of iron deficiency anemia adjusting gender and age. A similar regression model showed that higher BMI could predict occurrence of vitamin B12 deficiency in morbid obese patients. Conclusion. Although iron deficiency is a common finding among obese patients, vitamin B12 deficiency is more frequent so about one-fifth of these patients suffer vitamin B12 deficiency. In fact, the exacerbation of obesity can result in exacerbation of vitamin B12 deficiency.


Blood ◽  
1959 ◽  
Vol 14 (12) ◽  
pp. 1269-1279 ◽  
Author(s):  
MIGUEL LAYRISSE ◽  
NORMA BLUMENFELD ◽  
IRIS DUGARTE ◽  
MARCEL ROCHE

Abstract Studies on the metabolism of B12 and folic acid were performed in patients with heavy hookworm infection and severe iron deficiency anemia, and in patients with light infection, noninfected patients and normal subjects. Patients with heavy hookworm infection showed a marked decrease of the serum B12 as compared with normal subjects. Eight of 21 cases studied showed values of serum B12 below 100 µµg./ml. Twelve of 13 patients with severe hookworm infection showed impairment of the pteroylglutamic acid intestinal absorption; however, none of them exhibited megaloblastic proliferation in the bone marrow. They all recovered with iron therapy alone. The patients with light infection and the noninfected patients with iron deficiency anemia did not demonstrate significant differences from the normal subjects studied.


PEDIATRICS ◽  
2013 ◽  
Vol 131 (2) ◽  
pp. e620-e625 ◽  
Author(s):  
D.-A. Khuong-Quang ◽  
J. Schwartzentruber ◽  
M. Westerman ◽  
P. Lepage ◽  
K. E. Finberg ◽  
...  

1992 ◽  
Vol 29 (5) ◽  
pp. 400-404 ◽  
Author(s):  
D. E. Morin ◽  
F. B. Garry ◽  
M. G. Weiser ◽  
M. J. Fettman ◽  
L. W. Johnson

Iron deficiency anemia was identified and characterized in three 14 to 29-month-old male llamas (llama Nos. 1–3) from separate herds in Colorado. The identification of iron deficiency anemia was based on hypoferremia (serum iron = 20–60 μg/dl), erythrocytic features, and hematologic response to iron therapy. The anemia was moderate and nonregenerative and characterized by erythrocyte hypochromia, microcytosis (mean cell volume = 15–18 fl), and decreased mean corpuscular hemoglobin concentration (36.0–41.0 g/dl). Morphologic features unique to llamas with iron deficiency anemia included irregular distribution of hypochromia within erythrocytes and increased folded cells and dacryocytes. The cause of iron deficiency was not determined. The llamas were treated with various doses and schedules of parenteral iron dextran. Two of the llamas were monitored for up to 14 months after the start of iron therapy and experienced increases in hematocrit and mean cell volume values. In one llama, progressive replacement of microcytic cells with normal cells was visualized on sequential erythrocyte volume distribution histograms following iron therapy.


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