An indication of a vitamin B6 deficiency is elevated urinary levels of xanthurenic acid and kynurenic acid, indicating incomplete conversion of tryptophan. For status evaluation, Driskell (1984) concluded that the best assessment parameter for vitamin B6 status in clinical cases is measurement of either the coenzyme stimulation of erythrocyte alanine aminotransferase activity or PLP level.
In growing pigs, clinical signs of vitamin B6 deficiency include a poor appetite, slow growth (Illus. 2), microcytic hypochromic anemia, epileptic-like fits or convulsions (Illus. 3), fatty infiltration of the liver, diarrhea, rough hair coat, scaly skin, a brown exudate around the eyes, demyelination of peripheral nerves and subcutaneous edema (Bauernfeind, 1974; Braunlich, 1974; Cunha, 1977). Hughes and Squibb (1942) reported many of these deficiency symptoms and also an unsteady gait in pyridoxine-deficient pigs. Almost identical symptoms of B6 deficiency were reported in baby pigs (Lehrer et al., 1951). Follis and Wintrobe (1945) reported specifically on the effects of pyridoxine deficiency on the nervous tissues. Myelin degeneration of the peripheral portion of the sensory nerve was observed to be the initial neural change in pyridoxine-deficient animals. Based on morphologic data the preliminary site of injury in pyridoxine-deficient animals is in the myelin sheath and axon. Like some other vitamins, vitamin B6 deficiency reduces the immune responses of the pig (Harmon et al., 1963). The first and most conspicuous sign in baby pigs that vitamin B6 is insufficient is a loss of appetite that may appear in less than two weeks if the deficiency is severe. This is accompanied by reduced growth, vomiting, diarrhea, and a peculiar compulsion to lick.