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
Overview
Pathophysiology
- 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.