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Visual-Evoked Potential in Neuro-Ophthalmology
Published in Vivek Lal, A Clinical Approach to Neuro-Ophthalmic Disorders, 2023
Vitamin B12 is a common cause of myeloneuropathy and occasionally cognitive and behavioral change. B12 deficiency occurs in the patients who are unable to absorb it because of gastrointestinal disease, intrinsic factor deficiency, and widely variety of genetic and/acquired causes. Low vitamin B12 level is associated with megaloblastic anemia, involvement of posterior and lateral column of spinal cord and peripheral nerve resulting in subacute combined degeneration of the spinal cord (SACD). Vitamin B12 deficiencies usually manifest with sensory ataxia (distal paresthesia, joint position, and vibration sense impairment), spasticity and weakness, rarely optic neuropathy and may be the presenting sign of pernicious anemia [29]. Vitamin B12 deficiency results in bilateral prolongation of P100 latency, but the abnormality is generally asymptomatic. Visual acuity, field of vision, and color vision testing are normal. In a study on 17 patients with B12 deficiency neurologic syndrome, P100 latency was prolonged in 10 patients (17 eyes). There was no visual symptom and vision testing was also normal. After 6 months of treatment P100 latency improved in all except four eyes (Figure 3B.5). VEP changes were related to duration of illness [30].
Dementia/Cognitive Decline
Published in Charles Theisler, Adjuvant Medical Care, 2023
Cyanocobolamin: Metabolic disorders such a vitamin B12 deficiency cause dementia and must be corrected if present.8 Older adults on a vegetarian or vegan diet have an increased risk of vitamin B12 deficiency. Certain drugs (metformin, proton pump inhibitors, and histamine [H-2] receptor antagonists) can also lead to a B12 deficiency. A typical dose for vitamin B12/cyanocobolamin is 1,000–2,000 mcg/day.
Assessing and managing pain
Published in Nicola Neale, Joanne Sale, Developing Practical Nursing Skills, 2022
Lindsey Pollard, Harriet Barker
Entonox is a 50:50 mixture of nitrous oxide and oxygen delivered through a handheld mask or mouthpiece. If the person becomes drowsy, because of the drug, their hand and therefore the delivery set will fall away. As such, Entonox is another form of PCA. It should not be used by people with Vitamin B12 deficiency and caution should be applied to those at risk of deficiency (Schug et al. 2020). It is effective for mild to moderate, short-lasting pain and is used by paramedics, in emergency care, for procedural pain and during labour. There is no absolute contraindication for the use of Entonox in the first 16 weeks of pregnancy (BOC 2016)
Serum Levels of Thyroid Hormone, Vitamin B12, Vitamin D3, Folic Acid, and Ferritin in Chalazion
Published in Ocular Immunology and Inflammation, 2022
Vitamin B12 is a water-soluble vitamin that is very important for the proper function of the human body. The main rationale to evaluate vitamin B12 levels in this study is to understand whether there is vitamin B12 level alteration in the chalazion pathogenesis, which is a lipogranulomatous inflammation. There is limited evidence of the presence of a direct association between vitamin B12 level and inflammation. Al-Daghri et al.18 reported a significant negative correlation between vitamin B12 level and tumor necrosis factor-α (TNF-α), while Young et al.19 reported a similar relationship between vitamin B12 level and C-reactive protein (CRP) for some races in their large population-based study. Some experimental animal studies showed that vitamin B12 deficiency triggers proinflammatory pathways through interleukin-1β (IL-1β), interleukin-10 (IL-10), and monocyte chemoattractant protein-1 (MCP-1).20 Nonetheless, there is not a consensus as to how vitamin B12 deficiency can be a reason for inflammation in human body and to what degree of, if any exists.
Perioperative anemia: clinical practice update
Published in Hospital Practice, 2021
Yogita Sharma Segon, Sara Dunbar, Barbara Slawski
Laboratory findings in Vitamin B12 deficiency: Vitamin B12 deficiency should suspected in patients with: Elevated mean corpuscular volume (MCV)B12 levels of less than 200 pg/mL- Borderline B12 levels ranging from 200 to 300 pg/mL should be followed up by obtaining methylmalonic acid (MMA) levels.Elevated MMA levels of greater than 270 nmol/L are highly suggestive of B12 deficiency [2]. If MMA levels are elevated, consider obtaining anti-parietal cell and anti-intrinsic factor antibodies prior to vitamin B12 supplementation [2].The presence of anti-intrinsic factor antibody is highly specific for pernicious anemia [21]
Fooled by the fragments: vitamin B12 deficiency masquerading as thrombotic thrombocytopenic purpura
Published in Journal of Community Hospital Internal Medicine Perspectives, 2021
Pegah Jahangiri, Rachel Hicks, Prabjot K. Batth, Christopher J. Haas
Vitamin B12 is a water-soluble vitamin with an essential role in DNA synthesis, hematopoiesis, and myelination. Vitamin B12 is a necessary cofactor for the conversion of methylmalonyl coenzyme A to succinyl coenzyme A via methylmalonyl coenzyme A mutase (Figure 2), enabling the breakdown of odd-chained fatty acids and some amino acids. It is also a required cofactor for methionine synthase, which catalyzes the conversion of homocysteine to methionine, ultimately allowing for the generation of tetrahydrofolate, a biologically active form of folate needed in DNA synthesis (Figure 2). Insufficient levels of vitamin B12 lead to reduced function of methylmalonyl coenzyme A mutase and methionine synthase, with a resultant accumulation of the precursors methylmalonyl coenzyme A and homocysteine, respectively. Classically, vitamin B12 deficiency manifests as a macrocytic, megaloblastic anemia and in severe cases, subacute combined degeneration of the posterior columns of the spinal cord. In rare cases, severe vitamin B12 deficiency can present as a pseudo-microangiopathic hemolytic anemia/TTP, characterized by thrombocytopenia and hemolytic anemia (i.e., elevated LDH, low haptoglobin, hyperbilirubinemia, and schistocytes). In contrast to classic microangiopathic hemolytic anemia/TTP, vitamin B12-related pseudo-TTP presents as a macrocytic, megaloblastic anemia with reticulocyte hypoproliferation, elevated levels of homocysteine and MMA, and a low vitamin B12. Management of this masked deficiency requires only vitamin B12 supplementation in contrast to initiation of plasmapheresis required for true TTP.