Vitamin B12 deficiency – Cobalamin is a cobalt-containing vitamin, essential for nucleic acid metabolism and myelin formation. (Cyancobalamin is the therapeutic preparation, used to treat Vitamin B1, deficiency).
Widely present in animal sources, Vitamin B12 is absent in plant foods, but may be endogenously synthesized by colonic bacteria.
Vitamin B12 absorption requires hydrolysis by gastric acid and combination with a specific protein in stomach – intrinsic fhctor of castle (IFc). This B12-Ifc complex attaches to specific receptor sites in terminal ileum, where B12 component is absorbed, transported in bound form with a plasma protein — Transcobalamin II and stored in tissues, bound to another protein – Transcobalamin I.
Etiology: Vitamin B12 deficiency is rarely dietary due to extremely low requirements (<1-5 jig/day), usually caused by congenital/acquired defects in its absorption e.g. Congenital IFc deficiency or juvenile pernicious anemia, malabsorption disorders, Immerslund syndrome i.e. IFc-B12 receptor deficiency, and congenital transcobalamin deficiency.
Clinically, Vitamin B12 deficiency presents with a triad of — a) Megaloblastic anemia, b) Glossitis, and c) Signs of demyelination e.g. ataxia, parasthesia, hypo/ hyperreflexia (Subacute combined degeneration of cord).
Diagnosis is usually based on —
a) Megaloblastic anemia on smear that does not respond to folic acid therapy, supported by
b) Low serum Vitamin B12 levels (<100 pg/mi)
c) Methylmalonic aciduria (>3.5 mg/day).
Schilling test is used to confirm Vitamin B12 deficiency as well as to differentiate between Ifc deficiency and malabsorption defects.
Management of Vitamin B12 deficiency: Oral Vitamin B12 therapy is generally useless, due to defective absorption. Cases without neurological signs are treated by life-long monthly therapy with IM Vitamin B12 (1 mg), while those with neurological signs need daily therapy during first two weeks, followed by monthly injections.
Check the below advice from doctor on Vitamin B12 deficiency -