scholarly journals Microcytic Anemia Hiding Vitamin B12 Deficiency Anemia

Cureus ◽  
2021 ◽  
Author(s):  
Fadi Busaleh ◽  
Omkolthoom A Alasmakh ◽  
Fatimah Almohammedsaleh ◽  
Maram F Almutairi ◽  
Juwdaa S Al Najjar ◽  
...  
Author(s):  
Shyama . ◽  
P. Kumar ◽  
Surabhi .

Introduction: An unusual case of a 19 year old female, presenting with fever, pallor and hepatosplenomegaly for one month. She had microcytic anemia on peripheral smear examination but her bone marrow aspiration & biopsy revealed a hypercelluar marrow with megaloblastic erythroid hyperplasia. Resolution of fever within 48 hours of Vitamin B12 supplementation, initiated in view of the megaloblastic bone marrow picture & low serumVitamin B12 level, suggests a causal association. Conclusion: Vitamin B12 deficiency seems to be an unusual cause of PUO (Pyrexia of unkown origin) which should be ruled out in every case of PUO.


2021 ◽  
Vol 12 (2) ◽  
pp. 54-58
Author(s):  
Vinay Krishnamurthy ◽  
Akhila Rao Kerekoppa

Background: Diabetes is one of the largest global health emergencies of the 21st century. Prevalence of anemia in diabetic patients is two to three times higher than for patients with comparable renal impairment and iron stores in the general population. Aims and Objective: This study was done to analyse the prevalence of anemia and its profile in patients with preserved renal function. Materials and Methods: One-hundred diabetic patients with anemia with normal renal functions were selected. Complete blood count, peripheral blood smear, iron studies, vitamin B12 levels were assessed. Diabetic control was monitored by HbA1c. Patients were identified to have specific type of anemia, based on iron profile and vitamin B12 levels. Severity of anemia was also assessed. Appropriate statistical tests were applied to analyse the results. Results: Mean age of subjects in the study group was 53.4±13.6 years. The mean haemoglobin level was 9.41±2.18 g/dl. Out of the 100 cases, 43 patients had iron deficiency anemia, 40 patients had anemia of inflammation, and 8 patients had vitamin B12 deficiency, 8 patients had combined iron and vitamin B12 deficiency, and 1 patient had pancytopenia. Mean HbA1c was higher in iron deficient individuals with a significant p value and mean HbA1c was lower in Vitamin B12 deficient individuals. Among the cases, 16% had mild anemia, 61% had moderate anemia, and 23% had severe anemia. Severe anemia had a significantly lower HbA1c, which was statistically significant. Conclusion: According to our study, iron deficiency anemia was the commonest, followed by anemia of inflammation in diabetic patients with preserved renal function. Diabetes being a pro-inflammatory state had a higher incidence of anemia of inflammation compared to general population. We have to identify and acknowledge the higher prevalence of Anemia of Inflammation in diabetic patients in the absence of renal dysfunction.


Blood ◽  
1951 ◽  
Vol 6 (10) ◽  
pp. 867-891 ◽  
Author(s):  
G. E. CARTWRIGHT ◽  
BETTY TATTING ◽  
JEAN ROBINSON ◽  
N. M. FELLOWS ◽  
F. D. GUNN ◽  
...  

Abstract In an effort to produce a deficiency of vitamin B12 a total of 70 pigs were fed a purified diet containing soybean alpha protein in place of casein. One group of animals was started on the diet at 2 to 7 days of age. A second group began at 21 to 28 days of age. Methionine, iodinate casein, desiccated thyroid and pteroylglutamic acid were added to the diet of certain animals and! omitted from the diet of other pigs. In addition, 9 pigs were gastrectomized. Forty-three of the animals survived for a sufficiently long period of time for adequate evaluation of the results of the experiment. Severe liver damage was observed in 24 of the 25 animals autopsied. The only animal not showing liver damage received vitamin B12 from the beginning of the experiment. Necrosis of the liver cells, fatty infiltration, or both, occurred in the presence of a high fat diet containing apparently adequate amounts of protein, choline, vitamin E and methionine. These pathologic changes were apparently prevented but not reversed by the administration of vitamin B12. Growth of the animals on the above diets without added vitamin B12 was retarded as compared with the growth of animals on the same diet supplemented with this vitamin. The administration of vitamin B12 to the deficient animals resulted in rapid growth. Of the 39 animals not receiving vitamin B12 13 failed to develop anemia, 16 developed a mild anemia and in 10 a moderately severe anemia was present. When present the anemia was normocytic and in 24 pigs was accompanied by a moderately severe neutropenia. Differential cell counts on the sternal marrow were normal except for a slight increase in the proportion of normoblasts. These hematologic alterations were neither consistently or completely corrected by the administration of vitamin B12 in spite of the fact that definite and sometimes marked reticulocyte increases followed. When methionine deficiency was associated with vitamin B12 deficiency, anemia appeared to be more severe. The administration of aureomycin, an "animal protein factor," did not stimulate growth and failed to induce a hemopoietic response. There was no macrocytic anemia, the bone marrow was not megaloblastic, and neurologic disturbances or morphologic alterations in the neutrophils were not observed. These results are in contrast to those obtained in pigs with an experimentally produced deficiency of pteroylglutamic acid. Such animals develop macrocytic anemia, leukopenia and a macronormoblastic type of bone marrow. It is not possible to give with any assurance the reason why megaloblastic anemia was not produced in the "B12-deficient" animals. This may have been due to the fact that (1) the deficiency was not sufficiently severe to result in such a change in the hemopoietic system; or (2) because pteroylglutamic acid prevents the development of megaloblastic anemia even in the absence of vitamin B12.


2020 ◽  
Vol 59 (6) ◽  
pp. 859-861
Author(s):  
Hiroyuki Fukuda ◽  
Munetaka Takekuma ◽  
Yasuyuki Hirashima

2019 ◽  
Vol 60 (5) ◽  
pp. 579-580 ◽  
Author(s):  
Akihiro Tamura ◽  
Nanako Nino ◽  
Nobuyuki Yamamoto ◽  
Akiyoshi Naito ◽  
Kousaku Matsubara ◽  
...  

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 ◽  
1976 ◽  
Vol 48 (5) ◽  
pp. 669-677 ◽  
Author(s):  
DR Clarkson ◽  
EM Moore

Abstract Alterations in reticulocyte size occur 2–3 days after the onset of iron deficient or megaloblastic erythropoiesis and precede, by several weeks, changes in mean corpuscular volume (MCV). Iron-deficiency anemia induced in a normal subject by repeated phlebotomies was characterized by the initial development of larger than normal reticulocytes followed by an abrupt decrease in reticulocyte size. Microreticulocytes appeared 3 days after the fall in per cent iron saturation and antedated the decrease in MCV to below normal by 6 wk. Mean reticulocyte size was disproportionately smaller than normal in patients presenting with iron deficiency. In contrast, reticulocyte size increased abruptly in a patient (and rats) 2–3 days after administration of methotrexate. Mean reticulocyte size was disproportionately larger than normal in patients presenting with folate or vitamin B12 deficiency. Specific replacement therapy with iron, folate, or vitamin B12 was quickly followed by normalization of reticulocyte size.


Nutrients ◽  
2019 ◽  
Vol 11 (11) ◽  
pp. 2557 ◽  
Author(s):  
Martín-Masot ◽  
Nestares ◽  
Diaz-Castro ◽  
López-Aliaga ◽  
Alférez ◽  
...  

Celiac disease (CD) is a multisystemic disorder with different clinical expressions, from malabsorption with diarrhea, anemia, and nutritional compromise to extraintestinal manifestations. Anemia might be the only clinical expression of the disease, and iron deficiency anemia is considered one of the most frequent extraintestinal clinical manifestations of CD. Therefore, CD should be suspected in the presence of anemia without a known etiology. Assessment of tissue anti-transglutaminase and anti-endomysial antibodies are indicated in these cases and, if positive, digestive endoscopy and intestinal biopsy should be performed. Anemia in CD has a multifactorial pathogenesis and, although it is frequently a consequence of iron deficiency, it can be caused by deficiencies of folate or vitamin B12, or by blood loss or by its association with inflammatory bowel disease (IBD) or other associated diseases. The association between CD and IBD should be considered during anemia treatment in patients with IBD, because the similarity of symptoms could delay the diagnosis. Vitamin B12 deficiency is common in CD and may be responsible for anemia and peripheral myeloneuropathy. Folate deficiency is a well-known cause of anemia in adults, but there is little information in children with CD; it is still unknown if anemia is a symptom of the most typical CD in adult patients either by predisposition due to the fact of age or because biochemical and clinical manifestations take longer to appear.


2013 ◽  
Vol 185 (12) ◽  
pp. E582-E582 ◽  
Author(s):  
E. T. Stoopler ◽  
A. S. Kuperstein

2017 ◽  
Vol 64 (12) ◽  
pp. e26698 ◽  
Author(s):  
Deepti Verma ◽  
Jagdish Chandra ◽  
Praveen Kumar ◽  
Shailaja Shukla ◽  
Shantanu Sengupta

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