scholarly journals Massive Splenomegaly: A Rare Presentation of Megaloblastic Anemia

2021 ◽  
Author(s):  
Tahereh Gholipur-Shahraki ◽  
Alireza Sadeghi ◽  
Padideh Oghab ◽  
Pegah Farrokhi ◽  
Azadeh Moghaddas
Keyword(s):  
Vitamin B12 ◽  
Early Treatment ◽  
Blood Count ◽  
Megaloblastic Anemia ◽  
Folate Deficiency ◽  
Massive Splenomegaly ◽  
Rare Presentation ◽  
Common Disorder ◽  
The Many

Megaloblastic anemia is a common disorder with various manifestations. Of the many causes, cobalamin or folate deficiency can eventuate into megaloblastic anemia. It can lead to pancytopenia and mild to moderate splenomegaly, but massive splenomegaly rarely seen in this situation. We describe a 39-yearold woman with marked enlargement of the spleen and pancytopenia that was found to have megaloblastic anemia. The splenomegaly and blood count resolved 4 months after initiation of vitamin B12 therapy. It is important to know massive splenomegaly may occur in megaloblastic anemia, and although it is rare, bur can reversible with early treatment.

scholarly journals Bone marrow cells from vitamin B12- and folate-deficient patients misincorporate uracil into DNA

Blood ◽  
1994 ◽  
Vol 83 (6) ◽  
pp. 1656-1661 ◽  
Author(s):  
SN Wickramasinghe ◽  
S Fida
Keyword(s):  
Bone Marrow ◽  
Vitamin B12 ◽  
Bone Marrow Cells ◽  
Megaloblastic Anemia ◽  
Folate Deficiency ◽  
Test Results ◽  
Dnase 1 ◽  
Biochemical Lesion ◽  
Suppression Test ◽  
Marrow Cells

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.

scholarly journals The effect of folate analogues and vitamin B12 on provision of thymine nucleotides for DNA synthesis in megaloblastic anemia

Blood ◽  
1982 ◽  
Vol 59 (3) ◽  
pp. 634-640
Author(s):  
MR Taheri ◽  
RG Wickremasinghe ◽  
BF Jackson ◽  
AV Hoffbrand
Keyword(s):  
Vitamin B12 ◽  
De Novo ◽  
Megaloblastic Anemia ◽  
Vitamin B12 Deficiency ◽  
Folate Deficiency ◽  
Minor Role ◽  
B12 Deficiency ◽  
Thymidylate Synthesis ◽  
Marrow Cells

The role of vitamin B12 in the folate dependent biosynthesis of thymidine nucleotides is controversial. In an attempt to clarify this, three methods have been used to assess the relative efficacy of vitamin B12 (hydroxocobalamin) and various folate analogues in titrated concentrations at correcting ‘de novo’ thymidylate synthesis by megaloblastic human marrow cells: (1) The deoxyuridine (dU) suppression test which analyses the reduction in (3H)-thymidine labeling of DNA by unlabeled dU. Marrow cells were also labeled with (6–3H)-dU with assessment of (2) its incorporation into DNA and (3) the accumulation of (6–3H)-deoxyuridine monophosphate (3H-dUMP). The three methods gave similar results. In both, N6-formyl tetrahydrofolate (formyl-FH4) was the most effective agent at correcting thymidylate synthesis in megaloblastic anemia due to vitamin B12 or folate deficiency. Vitamin B12 corrected the lesion in vitamin B12 deficiency but not in folate deficiency. Tetrahydrofolate (FH4) and folic acid were effective in deficiency of vitamin B12 or folate, although in both deficiencies they were less effective than formyl-FH4. Methyl-FH4 was effective in folate deficiency but not in vitamin B12 deficiency. These results confirm the failure of methyl-FH4 utilisation in vitamin B12 deficiency. They suggest that if vitamin B12 is needed in the formylation of FH4, this is a minor role in provision of the correct coenzyme for thymidylate synthesis compared with its major role of provision of FH4 from methyl- FH4.

scholarly journals A Clockface Chromatin Pattern in the Intermediate Megaloblast of Vitamin B12 or Folate Deficiency

Blood ◽  
1968 ◽  
Vol 32 (5) ◽  
pp. 711-716 ◽  
Author(s):  
LAWRENCE KASS
Keyword(s):  
Vitamin B12 ◽  
Nuclear Membrane ◽  
Chromosomal Abnormalities ◽  
Megaloblastic Anemia ◽  
Folate Deficiency ◽  
Chromatin Pattern

Abstract In the fully-developed megaloblast of vitamin B12 or folate deficiency, unique alterations occur in the chromatin adherent to the nuclear membrane. This chromatin is often tenuously connected to or separated from other chromatin, and gives the nucleus a clockface appearance. A clockface chromatin pattern appears only rarely in "megaloblastoid" erythroblasts from cases of refractory megaloblastic anemia. Normal erythroblasts and developing erythroblasts from a variety of anemias do not exhibit this chromatin pattern. Although the pathogenesis of the "clockface sign" is unknown, alterations in megaloblast histone might cause both the clockface chromatin pattern and subsequent chromosomal abnormalities. When the "clockface sign" appears in an intermediate megaloblast, it may provide a morphological clue to a deficiency of vitamin B12 or folate.

scholarly journals Bone marrow cells from vitamin B12- and folate-deficient patients misincorporate uracil into DNA

Blood ◽  
1994 ◽  
Vol 83 (6) ◽  
pp. 1656-1661 ◽  
Author(s):  
SN Wickramasinghe ◽  
S Fida
Keyword(s):  
Bone Marrow ◽  
Vitamin B12 ◽  
Bone Marrow Cells ◽  
Megaloblastic Anemia ◽  
Folate Deficiency ◽  
Test Results ◽  
Dnase 1 ◽  
Biochemical Lesion ◽  
Suppression Test ◽  
Marrow Cells

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.

scholarly journals Severe Haemolytic Anaemia, a Rare Presentation of Nutritional Vitamin B12 Deficiency: A Case Report

2019 ◽  
Vol 2 (1) ◽  
pp. 188-190
Author(s):  
Aamir Siddiqui
Keyword(s):  
Case Report ◽  
Vitamin B12 ◽  
Hemolytic Anemia ◽  
Megaloblastic Anemia ◽  
Vitamin B12 Deficiency ◽  
Pernicious Anaemia ◽  
Rare Form ◽  
Rare Presentation ◽  
B12 Deficiency ◽  
Nutritional Vitamin

Vitamin B12 deficiency usually presents with megaloblastic anemia, pancytopenia, and neurological symptoms. The cause is usually, nutritional deficiency, increase demand, decrease absorption. This report describes a case with symptoms of apathy and findings suggestive of severe hemolytic anemia, diagnosed with vitamin B12 deficiency. Haemolysis is a rare hematological finding in cases of B12 deficiency, and descriptions of a nutritional vitamin B12 deficiency, without evidence of pernicious anaemia, causing haemolysis, are even scarcer, and this paper was intended to draw physicians’ attention to this rare form of presentation.

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

2021 ◽  
Author(s):  
Nasrin Nisha N. ◽  
Sakthisankari Shanmugasundaram ◽  
Kartikayan R. K.
Keyword(s):  
Bone Marrow ◽  
Vitamin B12 ◽  
Megaloblastic Anemia ◽  
Serum Vitamin ◽  
Folate Deficiency ◽  
Duodenal Biopsy ◽  
Tropical Sprue ◽  
Bone Marrow Biopsies ◽  
Endoscopic Findings ◽  
Duodenal Biopsies

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.

scholarly journals Hemolytic Anemia Mimicking Megaloblastic Anemia

JMS SKIMS ◽  
2015 ◽  
Vol 18 (2) ◽  
pp. 156-157
Author(s):  
Fayaz Ahmad Sofi ◽  
Mushtaq Ahmad ◽  
Ashiq Ahmad
Keyword(s):  
Folic Acid ◽  
Vitamin B12 ◽  
Hemolytic Anemia ◽  
Autoimmune Hemolytic Anemia ◽  
Megaloblastic Anemia ◽  
Macrocytic Anemia ◽  
Folate Deficiency ◽  
Young Female ◽  
Anemia Patient

Young female diagnosed case of SLE with secondary APLA presented with severe symptomatic anemia, CBC revealed Macrocytic anemia (MCV 129), PBF was suggestive of megaloblastic anemia. Patient was put on treatment parenteral vitamin B12 and folic acid. Anemia worsened; patient was reevaluated and found to have autoimmune hemolytic anemia. Responded to steroids optimally. Macrocytosis in SLE is secondary to folate deficiency and ovalocytosis. JMS 2015; 18(2):156-157

scholarly journals Tropical sprue in megaloblastic anemia

2017 ◽  
Vol 5 (9) ◽  
pp. 4133 ◽  
Author(s):  
Yoganathan Chidambaram ◽  
Anith Kumar Mambatta ◽  
Sujith K. Sivaraj
Keyword(s):  
Bone Marrow ◽  
Vitamin B12 ◽  
Megaloblastic Anemia ◽  
Macrocytic Anemia ◽  
Vitamin B12 Deficiency ◽  
Folate Deficiency ◽  
Duodenal Biopsy ◽  
Tropical Sprue ◽  
Geographical Regions ◽  
B12 Deficiency

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.

scholarly journals The effect of folate analogues and vitamin B12 on provision of thymine nucleotides for DNA synthesis in megaloblastic anemia

Blood ◽  
1982 ◽  
Vol 59 (3) ◽  
pp. 634-640 ◽  
Author(s):  
MR Taheri ◽  
RG Wickremasinghe ◽  
BF Jackson ◽  
AV Hoffbrand
Keyword(s):  
Vitamin B12 ◽  
De Novo ◽  
Megaloblastic Anemia ◽  
Vitamin B12 Deficiency ◽  
Folate Deficiency ◽  
Minor Role ◽  
B12 Deficiency ◽  
Thymidylate Synthesis ◽  
Marrow Cells

Abstract The role of vitamin B12 in the folate dependent biosynthesis of thymidine nucleotides is controversial. In an attempt to clarify this, three methods have been used to assess the relative efficacy of vitamin B12 (hydroxocobalamin) and various folate analogues in titrated concentrations at correcting ‘de novo’ thymidylate synthesis by megaloblastic human marrow cells: (1) The deoxyuridine (dU) suppression test which analyses the reduction in (3H)-thymidine labeling of DNA by unlabeled dU. Marrow cells were also labeled with (6–3H)-dU with assessment of (2) its incorporation into DNA and (3) the accumulation of (6–3H)-deoxyuridine monophosphate (3H-dUMP). The three methods gave similar results. In both, N6-formyl tetrahydrofolate (formyl-FH4) was the most effective agent at correcting thymidylate synthesis in megaloblastic anemia due to vitamin B12 or folate deficiency. Vitamin B12 corrected the lesion in vitamin B12 deficiency but not in folate deficiency. Tetrahydrofolate (FH4) and folic acid were effective in deficiency of vitamin B12 or folate, although in both deficiencies they were less effective than formyl-FH4. Methyl-FH4 was effective in folate deficiency but not in vitamin B12 deficiency. These results confirm the failure of methyl-FH4 utilisation in vitamin B12 deficiency. They suggest that if vitamin B12 is needed in the formylation of FH4, this is a minor role in provision of the correct coenzyme for thymidylate synthesis compared with its major role of provision of FH4 from methyl- FH4.

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