This is one of the vitamins that form food supplement for man: others are Vitamin B1 [thiamin], Vitamin B2 [riboflavin], vitamin B3 [niacin], vitaminB5 [pantothenic acid], folic acid and vitamin B6 [pyridoxine]. These are important supplements that are required for the maintenance of metabolism in the organisms; they act as coenzymes and cofactors in various anabolic and catabolic reactions essential for the survival of cells, and the organism [1.4].
Of peculiar interest for this article is Vitamin B12. The reason for choice of this, among other things is because of the devastating medical cases including neural tube defects, irreversible Vitamin B12 neuropathy that may arise as a result of deficiency. It would be considered under the following headings: source, metabolism [structure, absorption, transport, biochemical function] and deficiency.
STRUCTURE : There are a variety of forms in which Vitamin B12 exists: as methylcobalamin in human plasma, as deoxyadenosylcobalamin in human tissue, as hydroxocobalamin for treatment, and cyanocobalamin in study of Vitamin B12 activity. All have the same basic structure: cobalt is at the centre of a corrin ring which is attached to a nucleotide.
ABSORPTION: A normal diet contains a large excess of vitamin B12 compared with daily needs. B12 is combined with the parietal cell-produced glycoprotein, intrinsic factor. The IF-B12 complex binds to a specific receptor in the distal ileum called Cubilin. Vitamin B12 is absorbed here at the distal ileum.
TRANSPORT: Vitamin B12 is absorbed into portal blood through the circulation from the intestine to the liver via the portal vein. Here it becomes attached to the plasma-binding protein transcobalamin II [TCII] which delivers B12 to the bone marrow and other tissues, where it is utilized for biosynthetic functions .
BIOCHEMICAL FUNCTION: Vitamin B12 is a coenzyme for two biochemical reactions in the body. First, it acts in the form of methylcobalamin as a cofactor for methionone synthase, the enzyme responsible for the conversion of homocysteine to methionine; methyl tetrahydrofolate
is used as methyl donor during the reaction. Second, it acts as deoxyadenosylB12 where it acts as cofactor for the conversion of methylmalonyl conenzyme A to succinyl coA .
CAUSES: In this part of the world, perincious anemia is the commonest cause of Vitamin B12 deficiency . In this condition, autoimmune reactions on the gastric mucosa cause production of antibodies against parietal cell products, intrinsic factor and its receptors; females are more affected and it is usually associated with other autoimmune conditions such as vitiligo, Hashimoto thyroiditis, thyrotoxicosis, etc. Other causes include malabsorption secondary to gastrectomy, congenital abnormailtiy of the IF, chronic tropical sprue, Crohn’s disease, intestinal stagnant loop syndrome such as stricture .
EFFECTS: Vitamin B12 deficiency causes megaloblastic anaemia ; it features include signs and symptoms of anaemis such as anorexia, easy fatiguability, pallor of skin and mucous membrane and malaise. Others are glossitis, angular stomatitis, purpura and lemon-tint jaundice.
Severe Vitamin B12 deficiency may cause a progressive neuropathy affecting the peripheral sensory nerves and dorsolateral columns of the spinal cord . The neuropathy is usually symmetrical and affects the lower limbs than the upper limbs. These changes are irreversible. The cause of this is usually accumulation of s-adenosyl homocysteine in nervous tissue. In a pregnant woman, the fetus is predisposed to neural tube defects .
LABORATORY FINDINDS: Blood file shows macrocytosis; the mean corpuscularf volume > 95fL. The macrocytes are oval. There are hypersegmented neutrophils, leucopenia and thrombocytopenia .
TREATMENT: Diagnosis is confirmed by absorption tests including schilling test. treatment is by taking Vitamin B12 preparations .
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