Deficiency

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Deficiency of vitamin Bj2 produces two diseases in humans, megoblastic anaemia and a specific neuropathy or subacute combined degeneration of the spinal cord. These complications are seen mainly in pernicious anaemia, first described by James Coombe in 1824 (Wickramasinghe, 1995). The disease is usually fatal in 1-3 years and was first understood by George Minot and William Murphy (1926) who demonstrated that feeding a daily diet of lightly cooked beef liver induced a remission of the anaemia. Subsequently, the beef was shown to have an extrinsic factor (vitamin B12) which required an intrinsic factor (IF) for its normal absorption. IF was produced by normal stomachs but not by those with pernicious anaemia. IF was shown to complex with vitamin Bj2 for uptake and transport by a specific receptor on the ileal enterocytes in the terminal ileum of humans (Weir and Scott, 1995).

The body has no mechanism to control the effects of vitamin Bj2 deficiency. It may be associated with clinical complications such as atheroma, causing coronary thrombosis, stroke, and peripheral vascular disease, neural tube defects or hepatic drain on the stores by steatosis.

The most important causes of Bj2 deficiency are the various forms of intestinal malabsorption of which the autoimmune disease, pernicious anaemia, is the most common. Autoantibodies are produced against the parietal cells of the stomach so the cells can no longer produce IF or hydrochloric acid (HCl). Patients with hypochlorhydria, such as the elderly and postgastrectomy patients, may exhibit malabsorption of dietary cobalamin and a lack of IF prevents absorption of vitamin B12.

Reduced secretion of pancreatic enzymes and bicarbonate leads to impaired digestion of haptocorrins (Hc) (also called R binders, TC I and III or cobalaphilin) and elevation of intestinal pH. Haptocorrins are glycoproteins which bind to vitamin Bj2 in the terminal ileal cells and transport it in the plasma to the cells of the body. Raised pH and low pancreatic enzymes result in cobalamin malabsorption because the transfer of cobalamin from dietary haptocorrins binders to IF is impaired.

Grasbeck-Immerslund syndrome (Weir and Scott, 1999) is a rare congenital disorder where the ileal receptor is either missing or malfunctioning.

Bacterial overgrowth (Weir and Scott, 1999) of the small intestine by colonic bacteria at concentrations greater than 108 organisms/L can result in Bj2 deficiency caused by competitive uptake of vitamin Bj2 by the micro-organisms.

Patients with AIDS are known to develop plasma vitamin Bj2 deficiency (Weir and Scott, 1999); however, the pathogenic significance of this still needs to be determined. The condition is thought to be due to failure of the IF-Bj2 complex uptake by the ileal intrinsic factor enterocyte cell wall receptor.

The condition, transcobalamin II (TC II) deficiency (Weir and Scott, 1999), usually presents within the first or second month of life. TC II transports co-balamin from the ileum to the liver where it can be stored or to the tissues where it can be used. Deficiency results in a potentially lethal effect. Early symptoms are vomiting, weakness, failure to thrive and megaloblastic anaemia. The TC defect can be due to TC II being absent or it may be immunologically normal but fail to bind cobalamin, or it may bind cobalamin but fail to be taken up by the cell wall receptor.

Several drugs, such as colchicine, neomycin, p-aminosalicylate and alcohol cause vitamin Bj2 malabsorption (Halsted and McIntyre, 1972). In addition, commonly used antacid drugs, such as cimetidine, ranitidine and omeprazole, decrease gastric acid essential for the absorption of vitamin B12 from food. The anaesthetic nitrous oxide is known to inactivate methionine synthesis by oxidising vitamin Bj2 to an inactive form. Prolonged exposure to nitrous oxide has been shown to cause neuropathy and subacute combined degeneration of the spinal cord in humans (Layzer et al, 1978).

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