scholarly journals Stroke in a Young Adult Secondary to Vitamin B12 Deficiency induced Hyperhomocysteinemia

2015 ◽  
Vol 1 (1) ◽  
pp. 10-13
Author(s):  
LS Yashaswini ◽  
Mamatha B Patil

ABSTRACT Stroke in young adults is less frequent than in older population but has major impact on individual and society. Stroke in young justifies an extensive etiologic work up—both common and uncommon. Pernicious anemia is characterized by lack of intrinsic factor in gastric mucosa which is essential for absorption of vitamin B12. Deficiency of vitamin B12 contributes to hyperhomocysteinemia which promotes both arterial and venous thrombosis. We present a rare case of stroke in young adult caused by hyperhomocysteinemia secondary to vitamin B12 deficiency. How to cite this article Yashaswini LS, Patil MB. Stroke in a Young Adult Secondary to Vitamin B12 Deficiency induced Hyperhomocysteinemia. J Med Sci 2015;1(1):10-13.

Author(s):  
Joao Galaz Tavares ◽  
Bernardo Baptista ◽  
Bebiana Gonçalves ◽  
Alexandra Bayão Horta

A 49-year-old female patient presented to our hospital with asthenia, odynophagia, low grade fever, worsening symptoms of chronic depression, and symmetric leg paresthesias. Investigations showed macrocytic anaemia, leucopenia, thrombocytopenia, high lactate dehydrogenase levels and a normal Coombs test. Trilineage dysplasia was detected in the bone marrow biopsy specimen. The diagnostic work-up led us to the diagnosis of pernicious anaemia with a spuriously normal value of vitamin B12 and high titres of anti-intrinsic factor autoantibodies. This case highlights the importance of considering vitamin B12 deficiency in the differential diagnosis of myelodysplasia, even when vitamin B12 levels seem to be normal.


2020 ◽  
Vol 2 (8) ◽  
pp. 01-03
Author(s):  
Rateesh Sareen

Vitamin B12 assay is one of the most frequently ordered tests particularly as a part of regular medical checkups. The deficiency is rampant in vegetarian population. It is of immense importance that laboratories establish their own reference interval (RI) of analyte specially Vitamin B12 as a diagnosis of Vitamin B12 deficiency based on RI of kit insert inadvertently leads to unnecessary treatment or work up. A blind reliance on RI of kit insert should be discouraged as they do not take into account population characteristics and do not truly reflect RI specific to the population under study.


PLoS ONE ◽  
2021 ◽  
Vol 16 (3) ◽  
pp. e0249325
Author(s):  
Samuel Asamoah Sakyi ◽  
Edwin Ferguson Laing ◽  
Richard Mantey ◽  
Alexander Kwarteng ◽  
Eddie-Williams Owiredu ◽  
...  

Background The association between prolong metformin usage and B12 deficiency has been documented. However, the prevalence estimates of metformin-induced vitamin B12 deficiency showed substantial disparity among studies due to varied study definitions of vitamin B12 deficiency. Metformin blocks the calcium dependent absorption of the vitamin B12-Intrinsic Factor complex at the terminal ileum. Lack of intrinsic factor due to the presence of auto-antibodies to parietal cells (IFA) could lead to vitamin B12 deficiency and subsequently cause peripheral neuropathy. We investigated the prevalence of vitamin B12 deficiency using more sensitive, combined markers of vitamin B12 status (4cB12) and the immuno-biochemical mediators of vitamin B12 deficiency. Methods In this observational study, 200 consecutive consenting metformin-treated T2DM patients, aged 35 and above, attending the diabetic clinic at KATH were recruited. Vitamin B12 deficiency was classified based on the Fedosov age-normalized wellness quotient. Anthropometric measurement was taken as well as blood samples for immunological and biochemical mediators. Peripheral neuropathy was assessed using the Michigan Neuropathy Screening Instrument (MNSI). Statistical analysis was performed using the R Language for Statistical Computing. Results Using the combined indicator (4cB12), the prevalence of metformin induced vitamin B12 deficiency was 40.5% whilst the prevalence of MNSI-Q and MNSI-PE diabetic neuropathy was 32.5% and 6.5% respectively. Participants with vitamin B12 deficiency had significantly higher levels of IFA, GPA, TNF-α, TC, LDL and albumin compared to those with normal vitamin B12 levels (p < 0.05). Correlation analysis revealed a statistically significant negative association between 4cB12 and the immunological markers [IFA (rs = -0.301, p<0.0001), GPA (rs = -0.244, p = 0.001), TNF-α (rs = -0.242, p = 0.001) and IL-6 (rs = -0.145, p = 0.041)]. Likewise, 4cB12 was negatively associated with TC (rs = -0.203, p = 0.004) and LDL (rs = -0.222, p = 0.002) but positively correlated with HDL (rs = 0.196, p = 0.005). Conclusion Vitamin B12 deficiency and diabetic neuropathy are very high among metformin-treated T2DM patients and it is associated with increased GPA, IFA, TNF-α and cardiometabolic risk factors (higher LDL and TC and lower HDL). Upon verification of these findings in a prospective case-control study, it may be beneficial to include periodic measurement of Vitamin B12 using the more sensitive combined indicators (4cB 12) in the management of patients with T2DM treated with metformin in Ghana.


2020 ◽  
Vol 91 (9) ◽  
pp. 746-748
Author(s):  
Roger R. Hesselbrock ◽  
Edwin V. Palileo ◽  
Eddie D. Davenport

BACKGROUND: Syncope and near-syncope are commonly encountered symptoms. Many cases are situationally specific or otherwise benign, with no adverse aeromedical implications. Autonomic dysfunction can produce orthostatic intolerance with resultant symptoms and is aeromedically concerning for potential occurrence in flight. Vitamin B12 deficiency is an insidious condition with protean manifestations, which can present with autonomic dysfunction. Neurological abnormalities are often reversible following adequate replacement.CASE REPORT: We describe a case of vitamin B12 deficiency in a pilot with atypical syncope and abnormal tilt-table testing who had progressively abnormal hematologic findings on review. He was also discovered to have intrinsic factor antibodies. After B12 replacement, he had normal cardiovascular response to exercise stress testing and an unremarkable centrifuge assessment.DISCUSSION: This case highlights the importance of recognizing subtle laboratory findings and serial laboratory data review in cases of atypical syncope to identify potential reversible etiologies.Hesselbrock RR, Palileo EV, Davenport ED. Vitamin B12 deficiency related syncope in a young military pilot. Aerosp Med Hum Perform. 2020; 91(9):746748.


Blood ◽  
2008 ◽  
Vol 112 (11) ◽  
pp. 4278-4278
Author(s):  
Muhammad K Siddique ◽  
Hafiz M. Y. Sarwar

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.


Pulse ◽  
2014 ◽  
Vol 5 (1) ◽  
pp. 57-60 ◽  
Author(s):  
AA Bhuiyan ◽  
SK Dash ◽  
SMH Shahriar ◽  
F Nahid ◽  
S Arefin

Aim and Objective Vitamin B12 deficiency disease, specially associated with pernicious anaemia is a relatively rare disease in the developing countries. Patients with B12 deficiency may present with hematological, gastro-intestinal and neuro-psychiatric manifestations. Here we discuss a case of a fifty five-year-old lady presented with sub-acute combined degeneration of the spinal cord. Case presentation A fifty five year old female was admitted in Neurology ward in Apollo Hospitals, Dhaka from OPD for progressive quadriparesis with tingling in the hands and feet. She had no associated visual, bulbar symptoms, sphincter incontinence or memory impairment. Investigation revealed mild anaemia, macrocytosis on peripheral blood picture, low Vitamin B12 level with megaloblastic changes in bone marrow examination. Anti-Intrinsic factor antibody and anti-parietal cell antibody was not done, as it is not available here. MRI of dorsal spine shows T2 hyper-intense lesions in the posterior cord. GI Endoscopic biopsy revealed chronic atrophic gastritis. Conclusion We presented this case because of its relatively uncommon occurrence in our country. Sub-acute combined degeneration of spinal cord associated with dietary deficiency is common in Indian sub-continent. High index of suspicion is needed for its early diagnosis as delay in treatment can lead to poor neurological recovery. DOI: http://dx.doi.org/10.3329/pulse.v5i1.20193 Pulse Vol.5 January 2011 p.57-60


2010 ◽  
Vol 150 (3) ◽  
pp. 369-371 ◽  
Author(s):  
Ulrik M. Overgaard ◽  
Stephan M. Tanner ◽  
Henrik S. Birgens

2014 ◽  
Vol 19 (2) ◽  
pp. 84-86 ◽  
Author(s):  
Kathleen McNeil ◽  
Dhiman Chowdhury ◽  
Lynette Penney ◽  
Mohsin Rashid

2021 ◽  
Vol 2021 ◽  
pp. 1-5
Author(s):  
Amanda M. Woodford ◽  
Rabhea Chaudhry ◽  
Gabriella A. Conte ◽  
Varsha Gupta ◽  
Madhurima Anne

Vitamin B12 is an essential nutrient which plays an important role in neurological function, hematopoiesis, and DNA synthesis. Low levels usually stem from either poor intake or a malabsorptive process. Presently, the most common cause of vitamin B12 deficiency is food-bound cobalamin malabsorption, which occurs when there is impaired release of vitamin B12 from ingested food due to an outstanding factor preventing the release of the nutrient from its transport protein. Such causes include achlorhydria, gastritis, gastrectomy, or the use of PPIs or antacids. A rarer cause is autoimmune chronic atrophic gastritis, resulting in pernicious anemia. In this disease process, there is destruction of parietal cells and thus a reduction in intrinsic factor, which is essential to the absorption of vitamin B12. Deficiency will result in a variety of abnormalities including but not limited to pancytopenia, paresthesias, and neuropsychiatric symptoms. A rare manifestation of vitamin B12 deficiency is hemolytic anemia, which occurs due to intramedullary and extramedullary dysfunction. This case describes a 46-year-old male with no past medical history who presented with chest pain, fatigue, and progressive weakness, found to have hemolytic anemia, ultimately attributed to vitamin B12 deficiency. Antiparietal cell antibodies and intrinsic factor antibodies (IFA) were both negative. Still, the patient underwent an endoscopy with biopsies of the stomach; pathology was consistent with chronic metaplastic atrophic gastritis. The patient improved with intramuscular vitamin B12 supplementation. This case highlights both a rare cause and presentation of vitamin B12 deficiency. Patients with autoimmune chronic atrophic gastritis should have antiparietal cell or intrinsic factor antibodies. Still, seronegative patients have been reported, like this patient. Additionally, hemolytic anemia secondary to vitamin B12 deficiency is uncommon. The presentation will usually mirror that of a thrombotic microangiopathy (TMA), including hemolytic anemia with schistocytes on peripheral blood smear and thrombocytopenia, as it did in this patient. This clinical entity is described as pseudothrombotic microangiopathy and is crucial to identify in order to prevent the initiation of invasive treatment strategies such as plasmapheresis.


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