Vitamin B12 (Cobalamin) Deficiency Anemia:
can also cause a demyelinating disorder involving the peripheral nerves and, ultimately and most importantly, the spinal cord
Vitamin B12 is abundant in all animal foods, including eggs and dairy products, and is resistant to cooking and boiling.
Even bacterial contamination of water and nonanimal foods can provide adequate amounts.
It is stored in the liver, which normally contains reserves that are sufficient to support bodily needs for 5 to 20 years
As a result, deficiencies due to diet are rare and are virtually confined to strict vegans
Metabolism of vitamin B12:
Peptic digestion releases dietary vitamin B12, which then binds to salivary B12-binding proteins called cobalophilins, or R binders.
R-B12 complexes are transported to the duodenum and processed by pancreatic proteases; this releases B12, which attaches to intrinsic factor secreted from the parietal cells of the gastric fundic mucosa.
The intrinsic factor-B12 complex passes to the distal ileum and attaches to the epithelial intrinsic factor receptors, which leads to absorption of vitamin B12.
The absorbed B12 is bound to transport proteins called transcobalamins, which then deliver it to the liver and other cells of the body.
Pathogenesis of B12 deficiency:
Three types of antibodies have been found in pernicious anemia
parietal canalicular antibodies, which bind to the mucosal parietal cells;
blocking antibodies, which block the binding of vitamin B12 to intrinsic factor; and
binding antibodies that react with intrinsic factor-B12 complex and prevent it from binding to the ileal receptor.
An occurrence of pernicious anemia with other autoimmune diseases such as Hashimoto thyroiditis, Addison disease, and type I diabetes mellitus is well documented
gastrectomy (which leads to loss of cells producing intrinsic factor) or
resection of ileum (which prevents absorption of intrinsic factor-B12 complex), and in
disorders that involve the distal ileum (such as Crohn disease, tropical sprue, and Whipple disease
In individuals older than 70 years of age, gastric atrophy and achlorhydria can interfere with the production of acid and pepsin, which are needed to release the vitamin from its bound form in the diet.
Vitamin B12 is required for recycling of tetrahydrofolate
pallor, easy fatigability, and, in severe cases, dyspnea and even congestive heart failure. The increased destruction of erythroid progenitors may give rise to mild jaundice. Gastrointestinal symptoms
The principal neurologic lesions associated with vitamin B12 deficiency are demyelination of the posterior and lateral columns of the spinal cord, sometimes beginning in the peripheral nerves. In time, axonal degeneration
spinal cord disease begins with symmetric numbness, tingling, and burning in feet or hands, followed by unsteadiness of gait and loss of position sense, particularly in the toes
Diagnosis is made by
(1) low serum vitamin B12 levels,
(2) normal or elevated serum folate levels,
(3) serum antibodies to intrinsic factor,
(4) moderate to severe megaloblastic anemia,
(5) leukopenia with hypersegmented granulocytes, and
(6) a dramatic reticulocytic response (within 2-3 days) to parenteral administration of vitamin B12.