Vitamin B12 Deficiency Related Syncope in a Young Military Pilot

2020 ◽  
Vol 91 (9) ◽  
pp. 746-748
Author(s):  
Roger R. Hesselbrock ◽  
Edwin V. Palileo ◽  
Eddie D. Davenport
Keyword(s):  
Vitamin B12 ◽  
Autonomic Dysfunction ◽  
Orthostatic Intolerance ◽  
Cardiovascular Response ◽  
Laboratory Data ◽  
Intrinsic Factor ◽  
Vitamin B12 Deficiency ◽  
Exercise Stress ◽  
Laboratory Findings ◽  
B12 Deficiency

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.

Analiza obrazu klinicznego niedokrwistości z niedoboru witaminy B12 u dzieci

2019 ◽  
Vol 23 (1) ◽  
Author(s):  
Aleksandra Pankiewicz ◽  
Anna Adamowicz-Salach ◽  
Marek W. Karwacki ◽  
Katarzyna Pawelec ◽  
Katarzyna Albrecht ◽  
...  
Keyword(s):  
Vitamin B12 ◽  
Metabolic Pathways ◽  
Essential Role ◽  
Vitamin B12 Deficiency ◽  
Neurological Damage ◽  
Laboratory Findings ◽  
Delay In Diagnosis ◽  
B12 Deficiency ◽  
Late Manifestation

Diagnosis of vitamin B12 deficiency could be difficult due to various and rather unspecific symptoms and often late manifestation in hematological findings. B12 has a crucial role as cofactor of many metabolic pathways and has essential role in many processes such as DNA synthesis, neuron myelination and gluconeogenesis. Blood smear has a huge role in early diagnosis and should be performed. B12 deficiency is not very common, however could be underestimated especially in developing countries. In children main cause of deficiency is exclusively breastfeeding by vitamin B12 depleted mothers. Consequences of low intake in children are more severe than in adults, because of lower liver storage. Early detection and treatment is very important, because long term deficiency could result in persistent neurological damage. Coexistence iron or folate deficiencies could result delay in diagnosis. In this article different manifestation and laboratory findings in group of children with B12 deficiency is described.

scholarly journals Profiling immuno-metabolic mediators of vitamin B12 deficiency among metformin-treated type 2 diabetic patients in Ghana

PLoS ONE ◽  
2021 ◽  
Vol 16 (3) ◽  
pp. e0249325
Author(s):  
Samuel Asamoah Sakyi ◽  
Edwin Ferguson Laing ◽  
Richard Mantey ◽  
Alexander Kwarteng ◽  
Eddie-Williams Owiredu ◽  
...  
Keyword(s):  
Peripheral Neuropathy ◽  
Diabetic Neuropathy ◽  
Vitamin B12 ◽  
Intrinsic Factor ◽  
Vitamin B12 Deficiency ◽  
Anthropometric Measurement ◽  
Diabetic Patients ◽  
Vitamin B ◽  
Tnf Α ◽  
B12 Deficiency

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.

scholarly journals A Case of Sub-acute Combined Degeneration of the Spinal Cord with Associated Pernicious Anaemia

Pulse ◽  
2014 ◽  
Vol 5 (1) ◽  
pp. 57-60 ◽  
Author(s):  
AA Bhuiyan ◽  
SK Dash ◽  
SMH Shahriar ◽  
F Nahid ◽  
S Arefin
Keyword(s):  
Spinal Cord ◽  
Vitamin B12 ◽  
Intrinsic Factor ◽  
Vitamin B12 Deficiency ◽  
Pernicious Anaemia ◽  
Bone Marrow Examination ◽  
Chronic Atrophic Gastritis ◽  
Endoscopic Biopsy ◽  
B12 Deficiency ◽  
Hands And Feet

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

scholarly journals Vitamin B12 deficiency in a 15-year old boy due to mutations in the intrinsic factor gene, GIF

2010 ◽  
Vol 150 (3) ◽  
pp. 369-371 ◽  
Author(s):  
Ulrik M. Overgaard ◽  
Stephan M. Tanner ◽  
Henrik S. Birgens
Keyword(s):  
Vitamin B12 ◽  
Intrinsic Factor ◽  
Vitamin B12 Deficiency ◽  
Factor Gene ◽  
B12 Deficiency

scholarly journals Vitamin B12 deficiency with intrinsic factor antibodies in an infant with poor growth and developmental delay

2014 ◽  
Vol 19 (2) ◽  
pp. 84-86 ◽  
Author(s):  
Kathleen McNeil ◽  
Dhiman Chowdhury ◽  
Lynette Penney ◽  
Mohsin Rashid
Keyword(s):  
Vitamin B12 ◽  
Developmental Delay ◽  
Intrinsic Factor ◽  
Vitamin B12 Deficiency ◽  
Poor Growth ◽  
B12 Deficiency

scholarly journals Chronic Atrophic Gastritis Presenting as Hemolytic Anemia due to Severe Vitamin B12 Deficiency

2021 ◽  
Vol 2021 ◽  
pp. 1-5
Author(s):  
Amanda M. Woodford ◽  
Rabhea Chaudhry ◽  
Gabriella A. Conte ◽  
Varsha Gupta ◽  
Madhurima Anne
Keyword(s):  
Vitamin B12 ◽  
Atrophic Gastritis ◽  
Hemolytic Anemia ◽  
Neuropsychiatric Symptoms ◽  
Intrinsic Factor ◽  
Vitamin B12 Deficiency ◽  
Disease Process ◽  
Chronic Atrophic Gastritis ◽  
Invasive Treatment ◽  
B12 Deficiency

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.

scholarly journals Profiling Immuno-Metabolic Mediators of Vitamin B12 Deficiency Among Metformin-Treated Type II Diabetes Patients in Ghana

2020 ◽  
Author(s):  
Samuel Sakyi ◽  
Edwin F. Laing ◽  
Richard Mantey ◽  
Alexander Kwarteng ◽  
Eddie-Williams Owiredu ◽  
...  
Keyword(s):  
Peripheral Neuropathy ◽  
Diabetic Neuropathy ◽  
Vitamin B12 ◽  
Intrinsic Factor ◽  
Vitamin B12 Deficiency ◽  
Anthropometric Measurement ◽  
Vitamin B ◽  
Calcium Dependent ◽  
Tnf Α ◽  
B12 Deficiency

Abstract 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 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 version 3.6.0. 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 67.5% and 93.5% 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 [AIF (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). It is imperative Ghana include routine measurement of Vitamin B12 deficiency using the more sensitive combined indicators (4cB12), in the management of T2DM patients on metformin.

Acute lymphoblastic leukemia and vitamin B12 deficiency secondary to a gastric intrinsic factor gene mutation

2012 ◽  
Vol 59 (4) ◽  
pp. 766-767 ◽  
Author(s):  
Ayesha Zia ◽  
Tunç Fışgın ◽  
Catherine Sokolowski ◽  
Stephan M. Tanner ◽  
Süreyya Savaşan
Keyword(s):  
Acute Lymphoblastic Leukemia ◽  
Vitamin B12 ◽  
Gene Mutation ◽  
Lymphoblastic Leukemia ◽  
Intrinsic Factor ◽  
Vitamin B12 Deficiency ◽  
Factor Gene ◽  
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.

scholarly journals Congenital Pernicious Anemia with Coexistent Transitory Intestinal Malabsorption of Vitamin B12

Blood ◽  
1967 ◽  
Vol 30 (4) ◽  
pp. 495-502 ◽  
Author(s):  
BEATRICE C. LAMPKIN ◽  
ALVIN M. MAUER
Keyword(s):  
Vitamin B12 ◽  
Pernicious Anemia ◽  
Intrinsic Factor ◽  
Vitamin B12 Deficiency ◽  
Gastric Fluid ◽  
Intestinal Malabsorption ◽  
Gastrointestinal Series ◽  
Schilling Test ◽  
B12 Deficiency ◽  
Vitamin B12 Absorption

Abstract Pernicious anemia with coexistent transitory intestinal malabsorption of vitamin B12 has been established in adults. In this report a child with congenital pernicious anemia was documented to have had transitory selective intestinal malabsorption of vitamin B12. The diagnosis of congenital pernicious anemia was established by the age of the patient, absence of intrinsic factor in gastric fluid, lack of antibodies to intrinsic factor and parietal cells, presence of HCl in gastric fluid, and normal gastric biopsy. The xylose excretion test, 72-hour fecal fat determination, upper gastrointestinal series, and biopsy of the jejunum were normal, but the Schilling test was abnormal with hog intrinsic factor of known potency on two occasions, indicating selective malabsorption of vitamin B12. Seven months after therapy the Schilling test was still abnormal without intrinsic factor, but was normal with both human and hog intrinsic factor. The normal absorption with intrinsic factor after therapy is indicative that the selective malabsorption which was originally present was probably a consequence of the vitamin B12 deficiency resulting from lack of intrinsic factor. In patients with abnormal radioactive vitamin B12 absorption tests with administration of intrinsic factor, coexistent pernicious anemia must be excluded by demonstration of intrinsic factor in gastric fluid.

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