[7][8][2] The deficiency may occur in pernicious anemia, following surgical removal of the stomach, with fish tapeworm, or due to bowel cancer.

[14][15] Cyanocobalamin is usually prescribed after surgical removal of part or all of the stomach or intestine to ensure adequate serum levels of vitamin B12.

[16] Cyanocobalamin is also produced in the body (and then excreted via urine) after intravenous hydroxycobalamin is used to treat cyanide poisoning.

[17] Possible side effects of cyanocobalamin injection include allergic reactions such as hives, difficult breathing; redness of the face; swelling of the arms, hands, feet, ankles or lower legs; extreme thirst; and diarrhea.

[18] Treatment of megaloblastic anemia with concurrent vitamin B12 deficiency using B12 vitamers (including cyanocobalamin), creates the possibility of hypokalemia due to increased erythropoiesis (red blood cell production) and consequent cellular uptake of potassium upon anemia resolution.

[19] When treated with cyanocobalamin, patients with Leber's disease may develop serious optic atrophy, possibly leading to blindness.

After consumption the cyanide ligand is replaced by other groups (adenosyl, methyl) to produce the biologically active forms.

[27] This effect may be due to the strong coordination between benzimidazole and the central cobalt atom, pulling it down into the plane of the corrin ring.

These compounds are converted to cyanocobalamin by addition of potassium cyanide in the presence of sodium nitrite and heat.

Since multiple species of Propionibacterium produce no exotoxins or endotoxins and have been granted GRAS status (generally regarded as safe) by the United States Food and Drug Administration, they are the preferred bacterial fermentation organisms for vitamin B12 production.

The MMACHC gene product catalyzes the decyanation of cyanocobalamin as well as the dealkylation of alkylcobalamins including methylcobalamin and adenosylcobalamin.

[36] Cyanocobalamin is added as an ingredient to fortify[37] nutrition in products such as baby formula, breakfast cereals and energy drinks as well as livestock feed.

When the conversion of propionyl-CoA to succinyl-CoA in the mitochondria fails due to Vitamin B12 deficiency, elevated blood levels of methylmalonic acid (MMA) occur.

Processing of cholesterol and protein gives propionyl-CoA that is converted to methylmalonyl-CoA, which is used by MUT enzyme to make succinyl-CoA.

Intestinal absorption of vitamin B12 requires successively three different protein molecules: haptocorrin, intrinsic factor and transcobalamin II.