Vitamin B12 Deficiency

Vitamin B12 Deficiency

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  Vitamin B12 Deficiency: Recognitionand Management SAMAH AL SHKAILI R3
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  Vitamin B 12 •Vitamin B12 (cobalamin) is a water-soluble vitamin obtained through the ingestion of fish, meat, and dairy products, as well as fortified cereals and supplements. • It is coabsorbed with intrinsic factor, a product of the stomach's parietal cells, in the terminal ileum after being extracted by gastric acid. • Vitamin B12 is crucial for neurologic function, red blood cell production, and DNA synthesis, and is a cofactor for three major reactions: the conversion of methylmalonic acid to succinyl coenzyme A; the conversion of homocysteine to methionine; and the conversion of 5-methyltetrahydrofolate to tetrahydrofolate.
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  Risk Factors forVitamin B12 Deficiency Decreased ileal absorption • Crohn disease • Ileal resection • Tapeworm infection Decreased intrinsic factor • Atrophic gastritis • Pernicious anemia • Postgastrectomy syndrome (includes Roux-en-Y gastric bypass) • Genetic
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  Inadequate intake • Alcoholabuse • Patients older than 75 years • Vegans or strict vegetarians (including exclusively breastfed infants of vegetarian/vegan mothers) Prolonged medication use • Histamine H2 blocker use for more than 12 months • Metformin use for more than four months • Proton pump inhibitor use for more than 12 months Risk Factors for Vitamin B12 Deficiency
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  Clinical Manifestations ofVitamin B12 Deficiency Cutaneous • Hyperpigmentation • Jaundice • Vitiligo Gastrointestinal • Glossitis Hematologic • Anemia (macrocytic, megaloblastic) • Leukopenia • Pancytopenia • Thrombocytopenia • Thrombocytosis
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  Clinical Manifestations ofVitamin B12 Deficiency Neuropsychiatric • Areflexia • Cognitive impairment (including dementia-like symptoms and acute psychosis) • Gait abnormalities • Irritability • Loss of proprioception and vibratory sense • Olfactory impairment • Peripheral neuropathy
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  Clinical Manifestations ofVitamin B12 Deficiency • Maternal vitamin B12 deficiency during pregnancy or while breastfeeding may lead to:  neural tube defects,  developmental delay,  failure to thrive,  hypotonia, ataxia,  anemia.
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  Screening • persons ataverage risk of vitamin B12 deficiency is not recommended to be screen. • Screening should be considered in patients with:  risk factors suspected clinical manifestations
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  • Serum vitaminB12 levels may be artificially elevated in patients with alcoholism, liver disease, or cancer because of decreased hepatic clearance of transport proteins and resultant higher circulating levels of vitamin B12. • If Normal Vitamin B12 level in suspected patient , a serum methylmalonic acid level is an appropriate next step , It is a more direct measure of vitamin B12's physiologic activity.
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  Pernicious anemia • refersto one of the hematologic manifestations of chronic auto-immune gastritis, in which the immune system targets the parietal cells of the stomach or intrinsic factor itself, leading to decreased absorption of vitamin B12. • Asymptomatic autoimmune gastritis likely precedes gastric atrophy by 10 to 20 years, followed by the onset of iron-deficiency anemia that occurs as early as 20 years before vitamin B12 deficiency pernicious anemia.
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  Treatment • Vitamin B12deficiency can be treated with intramuscular injections of cyanocobalamin or oral vitamin B12 therapy. • Guidelines from the British Society for Haematology recommend injections three times per week for two weeks in patients without neurologic deficits. • If neurologic deficits are present, injections should be given every other day for up to three weeks or until no further improvement is noted
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  Treatment • In general,patients with an irreversible cause should be treated indefinitely, whereas those with a reversible cause should be treated until the deficiency is corrected and symptoms resolve. • If vitamin B12 deficiency coexists with folate deficiency, vitamin B12 should be replaced first to prevent subacute combined degeneration of the spinal cord. • The British Society for Haematology does not recommend retesting vitamin B12 levels after treatment has been initiated • No guidelines address the optimal interval for screening high-risk patients.
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  Treatment routes • A2005 Cochrane review involving 108 patients with vitamin B12 deficiency found that high-dose oral replacement (1 mg to 2 mg per day) was as effective as parenteral administration for correcting anemia and neurologic symptoms. • There is insufficient data to recommend other formulations of vitamin B12 replacement (e.g., nasal, sublingual, subcutaneous). • The British Society for Haematology recommends intramuscular vitamin B12 for severe deficiency and malabsorption syndromes, whereas oral replacement may be considered for patients with asymptomatic, mild disease with no absorption or compliance concerns.
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  Prevention • consider screeningpatients for vitamin B12 deficiency if they have been taking proton pump inhibitors or H2 blockers for more than 12 months, or metformin for more than four months. • recommended dietary allowance is 2.4 mcg per day for adult men and nonpregnant women, and 2.6 mcg per day for pregnant women • The American Society for Metabolic and Bariatric Surgery recommends that patients who have had bariatric surgery take 1 mg of oral vitamin B12 per day indefinitely.
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  Reference • Vitamin B12Deficiency: Recognition and Management • Am Fam Physician. 2017 Sep 15;96(6):384-389