scholarly journals The Value of Duodenal Biopsies in the Evaluation of Megaloblastic Anemia

Author(s):  
Nasrin Nisha N. ◽  
Sakthisankari Shanmugasundaram ◽  
Kartikayan R. K.

Abstract Introduction Megaloblastic anemia is one of the common causes of anemia in India. Duodenal biopsies are routinely performed in the investigation of megaloblastic anemia. The present study was undertaken to analyze the value of duodenal biopsy in megaloblastic anemia and to correlate endoscopic findings with biopsy. As a secondary aim, the study has also analyzed the hematological profile and vitamin B12 and folate status of these patients. Materials and methods All the cases of megaloblastic anemia with bone marrow studies diagnosed at PSG Institute of Medical Sciences and Research during the two year period from January 2016 to December 2017 were retrieved. Clinical and laboratory findings (serum vitamin B12 and folate levels) and endoscopic findings were retrieved from hospital records of the patients. Duodenal biopsies of these patients reported in the histopathology department were retrieved and reviewed. Statistical analysis was done using SPSS software 20.0. Results There were 93 cases of megaloblastic anemia diagnosed on bone marrow biopsies. Tropical sprue was diagnosed in 49.5% of cases, followed by intraepithelial lymphocytosis (17.2%), peptic duodenitis (17.2%), and no significant pathology in 16% of cases. Pancytopenia was present in 54.8% of cases. Isolated vitamin B12 deficiency including low levels was present in 48.38% and folate deficiency was seen in 4.3% cases; 34.48% cases had both vitamin B12 and folate deficiency. Conclusion The incidence of tropical sprue in megaloblastic anemia is 49.5% in the study. Duodenal biopsy is valuable in the work up of megaloblastic anemia, irrespective of the endoscopic changes in identifying the etiology.

Author(s):  
Yoganathan Chidambaram ◽  
Anith Kumar Mambatta ◽  
Sujith K. Sivaraj

Background: The causes of megaloblastic anemia may vary in different geographical regions. The aim of the present study is to evaluate the utilization of bone marrow examination and upper gastrointestinal endoscopy (UGIE) in megaloblastic anemia.Methods: This was a cross-sectional descriptive study done on 50 patients (age ≥15years) of macrocytic anemia after applying inclusion and exclusion criteria. A bone marrow aspiration with biopsy and an UGIE with duodenal biopsy were performed in consented patients with evidence of megaloblastic anemia in the peripheral smear or Vitamin B12 deficiency or folate deficiency or both.Results: Out of 50 cases, 38 patients had pure Vitamin B12 deficiency, 2 patients had pure folate deficiency and 5 patients had combined deficiency. Among 43 patients with vitamin B12 deficiency, only four (9.3%) were vegetarians and remaining 39 (90.7%) were having non-vegetarian diet. Bone marrow study was done in 29 patients (out of 50) and all of them were found to have megaloblastic erythropoiesis in the bone marrow. Thirty three out of 50 consented for UGIE and duodenal biopsy. Out of 33, 17 patients (51.5%) had features of tropical sprue in biopsy.Conclusions: We found a high prevalence of tropical sprue in megaloblastic anemia due to Vitamin B12 and/or folate deficiency. We recommend that UGIE with deep duodenal biopsy should be considered in all patients with megaloblastic anemia to rule out tropical sprue in India.


Blood ◽  
1994 ◽  
Vol 83 (6) ◽  
pp. 1656-1661 ◽  
Author(s):  
SN Wickramasinghe ◽  
S Fida

Bone marrow cells from 15 patients with normal deoxyuridine (dU) suppression test results, 3 healthy subjects, and 11 patients with megaloblastic anemia caused by vitamin B12 or folate deficiency were examined for misincorporation of uracil into DNA. Cells were incubated with [5–3H] uridine for 2 hours and their DNA extracted. The DNA was hydrolyzed to deoxyribonucleosides with DNase 1, phosphodiesterase and alkaline phosphatase, and any dU present was separated from other deoxyribonucleosides by Aminex A6 chromatography. The quantity of dU/mg DNA and the radioactivity in the dU peak/mg DNA were then calculated. The results clearly showed that there was markedly increased uracil misincorporation into the DNA of vitamin B12- or folate-deficient marrow cells. Misincorporation of uracil into DNA may be an important biochemical lesion underlying both the megaloblastic change and the ineffectiveness of hematopoiesis in vitamin B12 and folate deficiency.


2017 ◽  
Vol 20 (2) ◽  
pp. 172-175
Author(s):  
Lisa Sutton ◽  
Nkechi Mba

Vitamin B12 deficiency is a known cause of megaloblastic anemia and bone marrow failure. Bone marrow biopsies are not frequently performed as part of the diagnostic workup and can demonstrate morphologic features that overlap with myelodysplastic syndrome (MDS) and acute leukemia. We describe a case of a dysplastic bone marrow with increased bone marrow hematogones detected by flow cytometry in a child with vitamin B12 deficiency. Hematogones are normal B cell precursors, and hyperplasia has been described in a variety of often reactive conditions and also disease. Hematogones are not typically seen in MDS. The presence of hematogones may help differentiate the dysplastic changes seen in vitamin B12 deficiency from MDS.


Blood ◽  
1994 ◽  
Vol 83 (6) ◽  
pp. 1656-1661 ◽  
Author(s):  
SN Wickramasinghe ◽  
S Fida

Abstract Bone marrow cells from 15 patients with normal deoxyuridine (dU) suppression test results, 3 healthy subjects, and 11 patients with megaloblastic anemia caused by vitamin B12 or folate deficiency were examined for misincorporation of uracil into DNA. Cells were incubated with [5–3H] uridine for 2 hours and their DNA extracted. The DNA was hydrolyzed to deoxyribonucleosides with DNase 1, phosphodiesterase and alkaline phosphatase, and any dU present was separated from other deoxyribonucleosides by Aminex A6 chromatography. The quantity of dU/mg DNA and the radioactivity in the dU peak/mg DNA were then calculated. The results clearly showed that there was markedly increased uracil misincorporation into the DNA of vitamin B12- or folate-deficient marrow cells. Misincorporation of uracil into DNA may be an important biochemical lesion underlying both the megaloblastic change and the ineffectiveness of hematopoiesis in vitamin B12 and folate deficiency.


2019 ◽  
Vol 6 (2) ◽  
pp. 489
Author(s):  
Nalina Thimmappa ◽  
Vijeth S. B. ◽  
Prashanth G. ◽  
Sreedevi B. K.

Background: Macrocytosis can be seen in many hematological and non-hematological disorders and more than one cause may co-exist in an individual. Serum vitamin B12 and folic acid tests are routinely ordered but they are limited by their low sensitivity and specificity. This study is done to analyze the clinical, hematological and biochemical parameters in macrocytic anemia and to study the difference between megaloblastic and non-megaloblastic anemia in these parameters.Methods: There were 100 patients presenting with macrocytosis were taken in to study. A detailed clinical history and physical examination was done in all cases. CBC, biochemical investigations, peripheral blood examination, Vitamin B12, folate levels, bone marrow aspiration and reticulocyte count was done in all cases.Results: Primary bone marrow disorders were the most common cause of macrocytosis (45%). The other causes in decreasing order of frequency were megaloblastic anemia (36%), alcoholism and liver disease (15%), drug induced (2%) and idiopathic thrombocytopenic purpura (1%). There was a significant difference in the mean values of MCV and serum LDH between megaloblastic and non-megaloblastic macrocytosis. When serum LDH >1124.5IU/L or MCV>120.5fl (criterion values of ROC curve) with reticulocyte count <2% was taken as criteria, the sensitivity was 94.4% and specificity was 93% for diagnosing megaloblastic anemia.Conclusions: Systematic evaluation of macrocytosis will help us to distinguish megaloblastic and non-megaloblastic macrocytosis. The blood and biochemical parameters especially CBC, RC, and serum LDH along with supporting clinical features help us in diagnosing megaloblastic anemia in a setup where vitamin and metabolite levels are difficult to obtain.


Blood ◽  
1977 ◽  
Vol 49 (6) ◽  
pp. 987-1000 ◽  
Author(s):  
R Carmel ◽  
B Tatsis ◽  
L Baril

A patient with recurrent pulmonary abscess, weight loss, and alcoholism was found to have extremely high serum vitamin B12 and unsaturated vitamin B12-binding capacity (UBBC) levels. While transcobalamin (TC) II was also increased, most of his UBBC was due to an abnormal binding protein which carried greater than 80% of the endogenous vitamin B12 and was not found in his saliva, granulocytes, or urine. This protein was shown to be a complex of TC II and a circulating immunoglobulin (IgGkappa and IgGlambda). Each IgG molecule appeared to bind two TC II molecules. The reacting site did not interfere with the ability of TC II to bind vitamin B12, but did interfere with its ability to transfer the vitamin to cells in vitro. The site was not identical to that reacting with anti-human TC II antibody produced in rabbits. Because of this abnormal complex, 57Co-vitamin B12 injected intravenously was cleared slowly by the patient. However, no metabolic evidence for vitamin B12 deficiency was demonstrable, although the patient initially had megaloblastic anemia apparently due to folate deficiency. The course of the vitamin B12-binding abnormalities was followed over 4 yr and appeared to fluctuate with the status of the patient's illness. The IgG-TC II complex resembled one induced in some patients with pernicious anemia by intensive treatment with long-acting vitamin B12 preparations. The mechanism of induction of the antibody formation in our patient is unknown.


2020 ◽  
Vol 11 (1) ◽  
pp. 114-120
Author(s):  
Susianto Susianto

Introduction: Vegetarians consume plant-based foods with or without eggs and milk. Vegetarians are at risk of vitamin B12 deficiency, as natural sources of vitamin B12 are limited to animal-based foods. Vitamin B12 deficiency can lead to megaloblastic anemia, nerve damage and increase homocysteine level. Higher homocysteine level can increase the risk of coronary heart disease and stroke. The objective of this study was to investigate the effect of vitamin B12 fortification on the level of serum vitamin B12 and homocysteine in vegetarian. Method: The research design was an experimental study, community trial. The samples were 42 vegetarians with vitamin B12 deficiency (< 156 pmol/L) selected from 118 vegetarians as members of Indonesia Vegetarian Society (IVS) Pekanbaru, treated by vitamin B12 fortified oatmeal for three months from March to June 2010.  Serum vitamin B12 and homocysteine were measured by electrochemiluminescent immunoassay and microparticle enzyme immunoassay method respectively. Result: Prevalence of vitamin B12 deficiency in vegetarian was 35.6%. Statistical analysis showed a significant increase of serum vitamin B12 from 124.6 to 284.6 pmol/L (p=0.001) and significant decrease of serum homocysteine from 20.1 to 15.1 µmol/L (p=0.001). Conclusion: Consumption of vitamin B12 fortified oatmeal increases the level of serum vitamin B12 and decreases the level of serum homocysteine significantly in vegetarian with vitamin B12 deficiency.


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.


Blood ◽  
1971 ◽  
Vol 37 (6) ◽  
pp. 615-623 ◽  
Author(s):  
BEATRICE C. LAMPKIN ◽  
ALLAN PYESMANY ◽  
CAROL B. HYMAN ◽  
DENMAN HAMMOND

Abstract Two sisters with a previously unreported megaloblastic anemia unassociated with a deficiency of either folic acid or vitamin B12 are described. Deficiencies of these vitamins were ruled out by standard studies. All other previously reported forms of megaloblastic anemia not secondary to a vitamin deficiency, such as orotic aciduria, were also excluded by appropriate studies. Optimal hemoglobin responses were obtained after the administration of large amounts of both vitamin B12 and folic acid. Because of this hemoglobin response, the conversion of deoxyuridine-5-monophosphate to deoxythymidine-5-monophosphate in vitro was examined in bone marrow samples from both patients using a modification of a method described by Killmann.18 This preliminary step in DNA synthesis was found to be normal. The results of this test and the optimal hemoglobin response after administration of both vitamins suggest that both folic acid and vitamin B12 may be necessary at some other preliminary step in DNA synthesis.


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