Pyridoxine Deficiency
The early description of a pyridoxine deficiency in rats was one of multiple deficiency; other unknown factors were absent from the synthetic diets. At the present there is recognized in rats a specific syndrome representing pyridoxine want. This includes acrodynia, or a typical dermatitis which is generally symmetrical and affects the paws and various parts of the head. Seborrheic lesions are frequent. Edema of the connective tissue layer of the skin is thought to be characteristic. Loss of muscle tonus was observed after long-continued deprivation in rats, and convulsive seizures have been observed. Growth is subnormal on pyridoxine-deficient diets.
All animal species studied show deficiency symptoms, but these vary considerably from one type of animal to another. Mice, for instance, develop fatty livers on a Bs deficiency, while in pigs a microcytic, hypochromic anemia is a characteristic part of the syndrome.
Dogs develop hypochromic anemia, high serum iron levels, and atherosclerosis. Monkeys develop dermatitis, lymphocytopenia, and atherosclerosis. Many species, including man, excrete extra xanthurenic acid in the urine during a deficiency state following a test dose of tryptophan.
Human Bs deficiency may be more prevalent than was generally recognized. Hunt reviewed a number of cases of apparent B6 deficiency. In 1951 an out-break of deficiency in infants was observed in various parts of the country. The cardinal symptom in these infants was convulsions, although only a small per cent of the infants developed the deficiency to such an extent. It was soon determined that the deficiency resulted from the use of a commercial liquid, infant-feeding mixture, which during processing had had the Bs content reduced to very low levels. A. change in diet or administration of pyridoxine promptly relieved the symptoms.
In normal tryptophan metabolism very small amoWlts of xanthurenic acid air formed and creted in the urine. In B6 deficiency larger amounts are excreted. The determination of ::rinary xanthurenic acid after administering tryptophan to a human or animal (load test) gives an indication of the nutritional status with respect to vitamin B6' It has been found by ssey and co-workers and others that some infants require more pyridoxine than others to prevent xanthurenic acid excretion after a tryptophan load. In Hunt's review it is pointed out at some infants given quantities ofB6 sufficient for the majority of the infantile population likely to suffer convulsions.
A number of experimental human deficiencies have been reported. Cheslock and McCully maintained eight college students on a diet low in B6 for 52 days. The blood level of B6 dropped zero within four weeks. Lymphocyte counts decreased in five of the subjects, but no dermal symptoms were evident. Xanthurenic acid excretion increased markedly after a tryptophan load.
Vilter and others induced human deficiency with the antagonist deoxypyridoxine Lymphupenia (reduced,white cell count) was the most common rmding in the blood studies. Clinical symptoms included seborrheic dermatitis, usually about the eyes, in the eyebrows, and at the angles of the mouth.
Hodges and co-workers also produced a deficiency state in humans and found a slight impairment in antibody formation. Large amounts of xanthurenic acid were excreted after tryptophan ingestion, but the ability to convert the amino acid into N-methylnicotinamide was not altered. Will and associates showed low transaminase blood levels in such patients.
upplements of other B vitamins had no effect on skin, mucous membranes, -or' peripheral nerve lesions, whereas all lesions responded promptly to 5 mg of pyridoxine, pyridoxal, or pyridoxamine daily.
A case of hypochromic anemia that did not respond to iron therapy was successfully treated with 20 mg per day of pyridoxine given orally.
