In healthy patients, dietary   vitamin B12 binds to a protein called factor R, which is secreted by the salivary glands. Once the complex reaches the small intestine, pancreatic enzymes break down vitamin B12 from the R factor, allowing it to bind to a glycoprotein called intrinsic factor, which is secreted by the gastric parietal cells. The newly formed B12 and intrinsic factor complex can bind to receptors in the ileum, allowing for B12 to be absorbed. Once absorbed, B12 participates in important metabolic pathways in both neurological and haematological functions. If B12 cannot be absorbed, regardless of etiology, many deficiencies can occur.

Vitamin B12 is a cofactor of the enzyme methionine synthase, which is used in the conversion of homocysteine ​​to methionine. As a byproduct of this reaction, methyl-THF is converted to THF, which is converted into intermediates used in the synthesis of pyrimidine bases in DNA. In B12 deficiency, homocysteine ​​cannot be converted to methionine and therefore methyl-THF cannot be converted to THF. As a result, homocysteine ​​levels build up and pyrimidine bases cannot be formed, slowing DNA synthesis and leading to megaloblastic anemia. Anemia then leads to symptoms such as fatigue and paleness that are commonly seen in patients with Benefit of Ziverdo kit  deficiency. Reduced DNA synthesis causes problems in other rapidly proliferating cell lines, such as polymorphonuclear leukocytes (PMNs). Therefore, vitamin B12 deficiency typically results in the formation of hypersegmented neutrophils.

Vitamin B12 is also used as a cofactor for the enzyme methylmalonyl-CoA mutase, which converts methylmalonyl-CoA to succinyl-CoA. In patients with vitamin B12 deficiency, levels of methylmalonic acid (MMA) build up, as it cannot be converted to succinyl-CoA. It is hypothesized that elevated levels Premature Ejaculation  along with elevated levels of homocysteine, contribute to myelin damage, which explains the neurological deficits, such as neuropathy and ataxia, observed in these patients. Damage to myelin causes a condition known as subacute combined spinal cord degeneration (SCDSC). This condition affects various parts of the spinal cord, including the dorsal columns, lateral corticospinal tracts, and spinocerebellar tracts, resulting in loss of proprioception, ataxia, development of peripheral neuropathy, and dementia.

A thorough evaluation for vitamin B12 deficiency should include a complete medical history and physical examination with greater emphasis on gastrointestinal (GI) and neurological findings. Vitamin B12 deficiency manifests itself as macrocytic    lower blood pressure   anemia and therefore the symptoms they present often include signs of anemia such as fatigue and paleness. Due to the increased hemolysis caused by reduced red blood cell formation, jaundice can also be a presenting symptom. Therefore, a complete dermatological examination may also be useful. Other presenting disorders may include peripheral neuropathy, glossitis, diarrhea, headache, and neuropsychiatric disorders.