Explain the effect of Deficiency of pyridoxine?

A deficiency of vitamin B6 alone is uncommon because it usually occurs in association with a deficit in other B-complex vitamins. Early biochemical changes include decreased levels of plasma pyridoxal 5'-phosphate (PLP) and urinary 4-pyridoxic acid. These  are followed by decrease in synthesis of transaminuses (aninotransferases) and  other enzymes of amino acid metabolism such hat there is an increased presence of  xanthurenate in the urine and a decreased glutamate conversion to the anti-  neurotransmitter α-aminobutyrate.  Hypovitaminosis B⁶ may often occur with riboflavin deficiency, because riboflavin is needed for the formation of the coenzyme PLP.

Infants are especially susceptible to insufficient intakes, which can lead to epileptic form convulsions. Skin changes include dermatitis with cheilosis and glossitis.  Moreover, there is usually a decrease in circulating lymphocytes and sometimes a normochromic, microcytic, or sideroblastic anaemia as well. The sensitivity of such systems as sulphur amino acid metabolism to vitamin B₆ availability is reflected in homocysteinaernia. A decrease in the metabolism of glutamate in the brain, which is found in vitamin B₆ insufficiency, reflects a nervous system dysfunction. As is the case with other micronutrient deficiencies, vitamin B₆ deficiency results in an impairment of the immune system. Of current concern is the pandemic-like occurrence of low vitamin B6 intakes in many people who eat poorly (e.g. people with eating disorders). Vitamin B6 deficiency has also been observed in south-east Asian school children (infected with hookworm), elderly Europeans (Dutch), and in some individuals with hyperhomocysteinaemia or who are on chronic haemodialysis. Several medical conditions can also affect vitamin B₆ metabolism and thus lead to deficiency symptoms.