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Last Updated: Aug 29, 2019
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B12 deficiency: a silent epidemic with serious consequences
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B12 deficiency and unsteadiness
Timothy c. Hain, md page last modified: december 19, 2014
Vitamin b12 deficiency is common in the population over 80 (about 10%). It can be a cause of unsteady gait (ataxia), sometimes accompanied by anemia (macrocytic), and loss of position sense. When associated with spinal cord disease, it is sometimes termed" subacute combined degeneration. The ataxia is called a" sensory ataxia, because it appears to be related to loss of position sensation from the feet. A list of diseases that can present with a similar picture is given below:
Subacute combined degeneration (b12 deficiency)
Tabes dorsalis (neurosyphilis)
Fredreich' ataxia (a cerebellar disorder), with damage with sensory input to the cerebellum.
Peripheral neuropathy (common)
Thoracic spinal cord lesions (very rare)
Subacute sensory loss (a rare paraneoplastic syndrome).
The term subacute combined degeneration was coined by russell, batten and collier in 1900 to describe pathological changes in the spinal cord. While changes in the posterior columns are emphasized in clinical accounts, pathologically the lateral and anterior columns are also often affected. The peripheral nerves are generally unaffected. B12 deficiency is a risk factor for cognitive decline (i. E. Dementia)
Causes of b12 deficiency
Decreased intake (e. G. Vegetarians)
Malabsorption
Autoimmune (pernicious anemia)
Stomach and small bowel disorders (e. G. Gastritis, surgery)
Medication interaction (e. G. Metformin, medications that reduce stomach acidity)
Over consumption (blind loop)
B12 is available only from animal sources and thus strict vegetarians are at a risk of deficiency. B12 is bound to animal protein and released by gastric acid. When taken as part of food, b12 is released from food by a combination of gastric acid and pepsin (an enzyme).
A medication for diabetes, metformin, reduces absorption of b12.
Gastric conditions contributing to b12 deficiency include various stomach diseases that impair release of b12 from food
Pernicious anemia (pa) accounts for 15-70% of b12 deficiency. This an autoimmune disorder where antibodies are made to intrinsic factor. Oral supplements are less effective in pa than other modes of administration.
Diagnosis of b12 deficiency
B12 deficiency is usually detected through a b12 blood level. Typical lower limits of normal are 200 pg/ml. A cbc test may show macrocytic anemia.
Because b12 is stored in the liver, it takes about 2 years following a sudden cessation of intake for signs of deficiency to arise.
Treatment of b12 deficiency
There are presently a variety of options.
Oral therapy involves giving 1 to 2 mg (1000 mcg) of b12 daily. Oral therapy is usually as effective as the others noted below
Monthly injections of b12 are traditional. The first injection is generally 1000ug, and subsequent ones are 100.
Nasal b12 is also now available as an alternative to injection in persons who do not respond to oral therapy.
================================================
B12 deficiency and unsteadiness
Timothy c. Hain, md page last modified: december 19, 2014
Vitamin b12 deficiency is common in the population over 80 (about 10%). It can be a cause of unsteady gait (ataxia), sometimes accompanied by anemia (macrocytic), and loss of position sense. When associated with spinal cord disease, it is sometimes termed" subacute combined degeneration. The ataxia is called a" sensory ataxia, because it appears to be related to loss of position sensation from the feet. A list of diseases that can present with a similar picture is given below:
Subacute combined degeneration (b12 deficiency)
Tabes dorsalis (neurosyphilis)
Fredreich' ataxia (a cerebellar disorder), with damage with sensory input to the cerebellum.
Peripheral neuropathy (common)
Thoracic spinal cord lesions (very rare)
Subacute sensory loss (a rare paraneoplastic syndrome).
The term subacute combined degeneration was coined by russell, batten and collier in 1900 to describe pathological changes in the spinal cord. While changes in the posterior columns are emphasized in clinical accounts, pathologically the lateral and anterior columns are also often affected. The peripheral nerves are generally unaffected. B12 deficiency is a risk factor for cognitive decline (i. E. Dementia)
Causes of b12 deficiency
Decreased intake (e. G. Vegetarians)
Malabsorption
Autoimmune (pernicious anemia)
Stomach and small bowel disorders (e. G. Gastritis, surgery)
Medication interaction (e. G. Metformin, medications that reduce stomach acidity)
Over consumption (blind loop)
B12 is available only from animal sources and thus strict vegetarians are at a risk of deficiency. B12 is bound to animal protein and released by gastric acid. When taken as part of food, b12 is released from food by a combination of gastric acid and pepsin (an enzyme).
A medication for diabetes, metformin, reduces absorption of b12.
Gastric conditions contributing to b12 deficiency include various stomach diseases that impair release of b12 from food
Pernicious anemia (pa) accounts for 15-70% of b12 deficiency. This an autoimmune disorder where antibodies are made to intrinsic factor. Oral supplements are less effective in pa than other modes of administration.
Diagnosis of b12 deficiency
B12 deficiency is usually detected through a b12 blood level. Typical lower limits of normal are 200 pg/ml. A cbc test may show macrocytic anemia.
Because b12 is stored in the liver, it takes about 2 years following a sudden cessation of intake for signs of deficiency to arise.
Treatment of b12 deficiency
There are presently a variety of options.
Oral therapy involves giving 1 to 2 mg (1000 mcg) of b12 daily. Oral therapy is usually as effective as the others noted below
Monthly injections of b12 are traditional. The first injection is generally 1000ug, and subsequent ones are 100.
Nasal b12 is also now available as an alternative to injection in persons who do not respond to oral therapy.