scholarly journals Thrombotic microangiopathy-like hemolysis in vitamin B12 deficiency-related megaloblastic macrocytic anemia

2018 ◽  
Vol 4 (3) ◽  
pp. 145-148
Author(s):  
Damla Çağla Patır
Keyword(s):  
Vitamin B12 ◽  
Thrombotic Microangiopathy ◽  
Macrocytic Anemia ◽  
Vitamin B12 Deficiency ◽  
B12 Deficiency

Thrombotic Microangiopathy-Like Hemolysis in Vitamin B12 Deficiency-Related Macrocytic Anemia

2018 ◽  
Vol 64 (04/2018) ◽  
Author(s):  
Masayoshi Yamanishi ◽  
Shigeru Koba ◽  
Takaaki Jo ◽  
Tohru Kotera ◽  
Shinsaku Imashuku
Keyword(s):  
Vitamin B12 ◽  
Thrombotic Microangiopathy ◽  
Macrocytic Anemia ◽  
Vitamin B12 Deficiency ◽  
B12 Deficiency

scholarly journals Hematologic Manifestations of Vitamin B12 Deficiency in Swine

Blood ◽  
1951 ◽  
Vol 6 (10) ◽  
pp. 867-891 ◽  
Author(s):  
G. E. CARTWRIGHT ◽  
BETTY TATTING ◽  
JEAN ROBINSON ◽  
N. M. FELLOWS ◽  
F. D. GUNN ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Vitamin B12 ◽  
Liver Damage ◽  
Megaloblastic Anemia ◽  
Macrocytic Anemia ◽  
Vitamin B12 Deficiency ◽  
Deficiency Anemia ◽  
Severe Neutropenia ◽  
Pteroylglutamic Acid ◽  
B12 Deficiency

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.

scholarly journals Severe Vitamin B12 Deficiency in Pregnancy Mimicking HELLP Syndrome

2019 ◽  
Vol 2019 ◽  
pp. 1-4
Author(s):  
Shravya Govindappagari ◽  
Michelle Nguyen ◽  
Megha Gupta ◽  
Ramy M. Hanna ◽  
Richard M. Burwick
Keyword(s):  
Vitamin B12 ◽  
Pernicious Anemia ◽  
Thrombotic Microangiopathy ◽  
Hellp Syndrome ◽  
Atypical Hemolytic Uremic Syndrome ◽  
Vitamin B12 Deficiency ◽  
Severe Vitamin ◽  
Elevated Liver Enzymes ◽  
B12 Deficiency ◽  
In Pregnancy

Severe vitamin B12 deficiency may present with hematologic abnormalities that mimic thrombotic microangiopathy disorders such as hemolysis, elevated liver enzymes, and low platelet count (HELLP) syndrome. We report a patient diagnosed with severe vitamin B12 deficiency, following termination of pregnancy for suspected preeclampsia and HELLP syndrome at 21 weeks’ gestation. When hemolysis and thrombocytopenia persisted after delivery, testing was performed to rule out other etiologies of thrombotic microangiopathy, including atypical hemolytic uremic syndrome, thrombotic thrombocytopenic purpura, and vitamin B12 deficiency. This work-up revealed undetectable vitamin B12 levels and presence of intrinsic factor antibodies, consistent with pernicious anemia. Parenteral B12 supplementation was initiated, with subsequent improvement in hematologic parameters. Our case emphasizes the importance of screening for B12 deficiency in pregnancy, especially in at-risk women with unexplained anemia or thrombocytopenia. Moreover, providers should consider B12 deficiency and pernicious anemia in the differential diagnosis of pregnancy-associated thrombotic microangiopathy.

scholarly journals Development delay in children with severe acute malnutrition and its association with Vitamin B12 deficiency

2019 ◽  
Vol 6 (6) ◽  
pp. 2484
Author(s):  
Aishvarya Adhualia ◽  
Manisha Maurya ◽  
A. D. Tewari
Keyword(s):  
Vitamin B12 ◽  
Developmental Delay ◽  
Complete Blood Count ◽  
Severe Acute Malnutrition ◽  
Megaloblastic Anemia ◽  
Macrocytic Anemia ◽  
Vitamin B12 Deficiency ◽  
Acute Malnutrition ◽  
Rehabilitation Centre ◽  
B12 Deficiency

Background: About half of the under five children are malnourished in India and so is morbidity associated with it. Malnutrition is also associated with multiple vitamin deficiency one of which is vitamin B12. Vitamin B12 is essential for DNA, RNA and protein synthesis; and for myelination of brain during the early childhood period. Deficiency of vitamin B12 can lead to megaloblastic anemia and neurological problems. So, authors aimed to look prevalence of vitamin B12 deficiency and; its hematological and neurological effects in severe acute malnourished children.Methods: it was an observational case control study, in which severe acute malnourished (SAM) children aged 0- 59 months who were admitted in Nutritional Rehabilitation Centre (NRC) were enrolled. Vitamin B12 levels were estimated and levels <200 pg/ml, 200-350 pg/ml, and >350 pg/ml were considered deficient, insufficiency and sufficient. Complete blood count was done for hematological effects and; developmental assessment was done to look for neurological effects.Results: Vitamin B12 was deficient, insufficient, normal in 15(16.3%), 25 (27.5%) and 52 (56.5%) children respectively. Vitamin B12 deficiency was significantly associated with hyperpigmentation and glossitis. Infant and young child feeding practices were not associated vitamin B12 deficiency. Macrocytic anemia was found in 23.4% SAM children and macrocytosis was not significantly associated with vitamin B12 deficiency.  Developmental delay was found in 55.3 % children and was not significantly associated with severe acute malnutrition. Conclusions: There is high prevalence of Vitamin B12 deficiency and insufficiency in children with severe acute malnourished children. Macrocytic anemia and developmental delay are not significantly associated with vitamin B12 deficiency.

scholarly journals Life-threatening Pseudo-thrombotic Microangiopathy Caused by Severe Vitamin B12 Deficiency

2021 ◽  
Vol 9 (11) ◽  
pp. 532-534
Author(s):  
Ziad Abuhelwa ◽  
Talal Khan ◽  
Rana Daas ◽  
Sami Ghazaleh ◽  
Ragheb Assaly
Keyword(s):  
Vitamin B12 ◽  
Thrombotic Microangiopathy ◽  
Vitamin B12 Deficiency ◽  
Severe Vitamin ◽  
Life Threatening ◽  
B12 Deficiency

Vitamin B12 Deficiency in Patients with Chronic Myeloid Leukemia

Blood ◽  
2008 ◽  
Vol 112 (11) ◽  
pp. 4278-4278
Author(s):  
Muhammad K Siddique ◽  
Hafiz M. Y. Sarwar
Keyword(s):  
Chronic Myeloid Leukemia ◽  
Vitamin B12 ◽  
Patient Population ◽  
Myeloid Leukemia ◽  
Macrocytic Anemia ◽  
Serum Vitamin ◽  
Vitamin B12 Deficiency ◽  
Normal Range ◽  
B12 Deficiency ◽  
Work Up

Abstract High vitamin B12 (cobalamin) levels have been documented in patients with untreated chronic myeloid leukemia. However, the literature about vitamin B12 deficiency in patients with chronic myeloid leukemia who are receiving imatinib is scarce. The objective of this study was to investigate the prevalence of vitamin B12 deficiency in patients with chronic myeloid leukemia. We retrospectively reviewed the medical records of 195 patients with chronic myeloid leukemia seen in the outpatient clinic of our institution between 2006 and 2007. The median age of patients was 35 (range 9 – 77); 118 (60%) patients were males and 77 (40%) were females. All patients included in the study were receiving imatinib. Macrocytic anemia at any given time during the course of treatment was documented in 61 (31%) out of 195 patients. Serum vitamin B12 and folate levels were measured in all patients with macrocytic anemia using chemiluminescent enzyme immunoassay. Among these 61 patients, 33 (54%) had low vitamin B12 levels (&lt; 200 pg/ml), 12 (20%) had indeterminate levels (200 – 300 pg/ml) and 16 (26%) patients had levels &gt; 300 pg/ml. Folate levels were within normal range (3 – 17 ng/ml) in all but two patients and both of these patients had folate levels &lt; 3 ng/ml and vitamin B12 levels &gt; 300 pg/ml. Among 195 study patients, 33 (17%) had macrocytic anemia with low vitamin B12 levels and 12 (6%) had macrocytic anemia with indeterminate vitamin B12 levels. We conclude that vitamin B12 deficiency is prevalent in our patients with chronic myeloid leukemia who are taking imatinib. This is of significance because our patient population is non-vegetarian. Serum vitamin B12 should be measured as a part of work up for anemia in patients with chronic myeloid leukemia. Correction of vitamin B12 deficiency in these patients could improve their tolerance to imatinib, which potentially is a myelosuppressive drug. In our study, measurements of serum methylmalonic acid (MMA) and homocysteine levels in patients with indeterminate vitamin B12 levels were not performed; although these measurements could have confirmed the diagnosis of vitamin B12 deficiency in this subgroup. We suggest that a similar study be conducted in a different patient population elsewhere.

Intractable Epilepsy as the Presentation of Vitamin B12 Deficiency in the Absence of Macrocytic Anemia

Epilepsia ◽  
2005 ◽  
Vol 46 (7) ◽  
pp. 1147-1148 ◽  
Author(s):  
Meng Lee ◽  
Hong-Shiu Chang ◽  
Hsiao-Ting Wu ◽  
Hsu-Huei Weng ◽  
Chiung-Mei Chen
Keyword(s):  
Vitamin B12 ◽  
Macrocytic Anemia ◽  
Intractable Epilepsy ◽  
Vitamin B12 Deficiency ◽  
B12 Deficiency

scholarly journals Extremely severe vitamin B12 deficiency

2019 ◽  
Vol 55 (3) ◽  
pp. 301-310
Author(s):  
Ana Pupić-Bakrač ◽  
Antea Pervan ◽  
Jure Pupić-Bakrač ◽  
Jakov Končurat
Keyword(s):  
Vitamin B12 ◽  
Epigastric Pain ◽  
Macrocytic Anemia ◽  
Vitamin B12 Deficiency ◽  
Laboratory Findings ◽  
B12 Deficiency ◽  
Extensive Information ◽  
Vitamin B12 Screening ◽  
Systemic Symptoms ◽  
Old Men

Aim: Vitamin B12 (cobalamin) is nutrient from the vitamin B complex family. It is essential in the human body for deoxyribonucleic acid (DNA) synthesis and for cellular energy production. Vitamine B12 deficiency is decrease in its serum concentration below 220 pmol/L, and it can be present in various range of hematologic and systemic symptoms and signs. The aim of this article is to provide extensive information on extreme forms of deficiency of vitamin B12. Case report: 83-year-old men presented with fatigue, intolerance of physical activity, vertigo, paresthesia in fingers, dispersion, epigastric pain, vomitting and loss of apetite. Vital parameters were within normal range, and physical examination did not reveal any patological findings, except icterus of sclera and subicterus of skin. Urgent laboratory findings showed erythrocytes 1.18 x 1012/L (4.34-5.72 x 1012/L), hemoglobin 50 g/L (138-175 g/L), mean corpuscular volume (MCV) 123.6 fL (83.0-97.2 fL), vitamin B12 &lt; 61 pmol/L (220-665 pmol/L). Patient started parenteral therapy with vitamin B12. After 5 days, rapid increase in reticulocyte count was observed, with haemogram stabilization within 6 weeks. In a follow-up period of two years, the patient had no symptoms. Conclusion: We presented patient with extreme deficiency of vitamin B12. Screening for vitamin B12 deficiency should be established in each patient with macrocytic anemia, even with slightly elevated MCV.

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