Vitamin B12 deficiency pathophysiology

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Nabeel Ahmed, M.B.B.S

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## Overview

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## Pathophysiology

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* Dietary Vitamin B12 binds to salivary R factor then the complex arrives at small intestine.[1]
* In duodenum Vitamin B12 is detach from R- factor by pancreatic proteases.
* Now free B12 binds to intrinsic factor which is secreted by gastric parietal cell.
* The intrinsic factor - B12 complex is absorbed in the ileum.
* Absorbed vitamin B12 is use in metabolic pathways which is important for neurologic and hematologic function if vitamin B12 is deficit regardless of the cause many impairments may occur .
* Vitamin B12 is a cofactor for the enzyme methionine synthase which convert homocysteine to methionine as a result methyl- THF is converted to THF which is use in synthesis of pyrimidine base of DNA.
* In B 12 deficiency homocysteine accumulate which cause megaloblastic anemia and hypersegmented neutrophils.
* Vitamin B 12 is a cofactor for enzyme methylmalonyl-COA mutase , which converts methylmalonic-COA to succinyl-COA. In B 12 deficiency methylmalonic acid (MMA ) will accumulate. MMA and elevated level of homocysteine cause damage of myelin as a result subacute combined degeneration of spinal cord ( SCDSC ) occur . This affects dorsal columns, lateral corticospinal tracts and spinocerebellar tract as result loss of proprioception , ataxia , peripheral neuropathy and dementia.

## References

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1. ↑ Ankar A, Bhimji SS. PMID 28722952. Missing or empty `|title=` (help)

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