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 Vitamin B12 deficiency is a common
cause of macrocytic anemia and has
been implicated in a spectrum of
neuropsychiatric disorders
 The role of B12 deficiency in
hyperhomocysteinemia and the
promotion of atherosclerosis is only now
being explored.
 Diagnosis of vitamin B12 deficiency is
typically based on measurement of serum
vitamin B12 levels; however, about 50
percent of patients with subclinical
disease have normal B12 levels.
 A more sensitive method of screening for vitamin
B12 deficiency is measurement of serum
methylmalonic acid and homocysteine levels,
which are increased early in vitamin B12
deficiency.
 Use of the Schilling test for detection of pernicious
anemia has been supplanted for the most part by
serologic testing for parietal cell and intrinsic
factor antibodies. Contrary to prevailing medical
practice, studies show that supplementation with
oral vitamin B12 is a safe and effective treatment
for the B12 deficiency state.
 Even when intrinsic factor is not present to aid in
the absorption of vitamin B12 (pernicious anemia)
or in other diseases that affect the usual
absorption sites in the terminal ileum, oral therapy
remains effective.
Clinical Manifestations
Hematologic
 Megaloblastic anemia
 Pancytopenia (leukopenia,
thrombocytopenia)
Neurologic
 Paresthesias
 Peripheral neuropathy
 Combined systems disease (demyelination of
dorsal columns and corticospinal tract)
Psychiatric
Vitamin B12 Deficiency
Vitamin B12 Deficiency
Vitamin B12 Deficiency
Vitamin B12 Deficiency
Vitamin B12 Deficiency
Follow-Up
 Vitamin B12 deficiency associated with
severe anemia, correction of the
deficiency state should lead to a marked
reticulocytosis in one to two weeks
 In mild vitamin B12 deficiency, we
recommend repeat measurements of
serum vitamin B12, homocysteine, and
methylmalonic acid levels two to three
months after initiating treatment.

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Vitamin B12 Deficiency

  • 2.  Vitamin B12 deficiency is a common cause of macrocytic anemia and has been implicated in a spectrum of neuropsychiatric disorders  The role of B12 deficiency in hyperhomocysteinemia and the promotion of atherosclerosis is only now being explored.  Diagnosis of vitamin B12 deficiency is typically based on measurement of serum vitamin B12 levels; however, about 50 percent of patients with subclinical disease have normal B12 levels.
  • 3.  A more sensitive method of screening for vitamin B12 deficiency is measurement of serum methylmalonic acid and homocysteine levels, which are increased early in vitamin B12 deficiency.  Use of the Schilling test for detection of pernicious anemia has been supplanted for the most part by serologic testing for parietal cell and intrinsic factor antibodies. Contrary to prevailing medical practice, studies show that supplementation with oral vitamin B12 is a safe and effective treatment for the B12 deficiency state.  Even when intrinsic factor is not present to aid in the absorption of vitamin B12 (pernicious anemia) or in other diseases that affect the usual absorption sites in the terminal ileum, oral therapy remains effective.
  • 4. Clinical Manifestations Hematologic  Megaloblastic anemia  Pancytopenia (leukopenia, thrombocytopenia) Neurologic  Paresthesias  Peripheral neuropathy  Combined systems disease (demyelination of dorsal columns and corticospinal tract) Psychiatric
  • 10. Follow-Up  Vitamin B12 deficiency associated with severe anemia, correction of the deficiency state should lead to a marked reticulocytosis in one to two weeks  In mild vitamin B12 deficiency, we recommend repeat measurements of serum vitamin B12, homocysteine, and methylmalonic acid levels two to three months after initiating treatment.