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The biochemical techniques described can furnish information as to the dietary supply of vitamin B6provided to the body through reflections in blood levels or in urine excretion rates of the vitamin. Such measurements would not, for the most part, distinguish between a dietary deficiency and abnormal conditions, such as poor absorption, abnormal utilization, dependency syndromes, or drug interactions. Nevertheless, such measurements can be helpful in indicating the possibility of a vitamin B6deficiency. More specific indications of an inadequacy of vitamin B6intake or reduced tissue reserves can be obtained with biochemical tests that reveal metabolic changes such as the tryptophan load test or blood transaminase activity measurements. The detection of metabolic changes indicates with a greater degree of certainty that a state of deficiency in vitamin B6exists more than does the mere reduction of the vitamin in biological fluids.Information obtained from performing the various biochemical tests must be interpreted and evaluated in terms of significance and compared with normal standards developed for appropriate sex and age groups. Such standards of reference are usually difficult to construct because of limited information as to normal values and ranges for various age groups, especially for children. Nevertheless, in Table 4 an attempt has been made to construct tentative guidelines for some of the biochemical measurements employed in evaluating vitamin B6nutritional status in the adult human. With additional controlled human studies on vitamin B6metabolism and with the use of the various biochemical measurements in field studies, improvements in the guidelines will be possible, particularly those applicable to children.

Experimental scurvy was investigated in five volunteer, adult, male human subjects who were maintained on a diet devoid of vitamin C. The metabolism of the vitamin was followed through the use of isotopically labeled ascorbic acid during the depletion and repletion of these subjects.The radioisotope data obtained on each subject showed that there was direct relationship between clinical signs of scurvy and the pool size of ascorbic acid. There was also a definite relationship between the whole blood ascorbic acid values and the body pool of ascorbic acid when the body pool was in excess of 300 mg. Reductions in the ascorbic acid body pool below a level of 300 mg and until repleted back again to this level were not associated with any further changes in whole blood ascorbic acid levels. Frank signs of clinical scurvy were observed in all subjects when the body pool of ascorbic acid had been depleted to a level of 300 mg. Upon repletion of the ascorbate pool beyond a level of 300 mg, clinical symptomatology of scurvy began to recede. The rate of depletion was an exponential process, whereas the rate of repletion of ascorbic acid was found to be a linear process and proportional to the level of daily ascorbic acid intake. When the subjects were fed high intakes of ascorbic acid, only a limited quantity of the ingested vitamin equilibrated with the ascorbate body pool.

Clinical and histopathologic toxicity studies were conducted on fourteen fat emulsions including Lipomul, Intralipid, Lipofundin and cottonseed or soybean oil emulsions prepared commercially or experimentally for intravenous use. These emulsions were administered to rabbits and/or rats in a daily dose of 2.0 to 3.0 gm. of fat per kg. of body weight. Clinical studies included observation of the animals' general reaction to the infusion, local reaction at the site of injection, variation in body weight, and weekly hemograms and urinalyses. The animals were sacrificed at least ten days after infusion and a detailed necropsy was performed. No gross lesions could be attributed to the fat emulsion. However, histopathologic examination revealed the deposition of intravenous fat pigment in the liver and spleen of every animal. The most pigment was found in animals given cottonseed oil emulsions and the least in animals given emulsion SR-151. Lipoid granulomas were observed in all test animals except those given emulsion SR-141. Mild hepatic fibrosis was observed in animals receiving Lipofundin. Adverse clinical reactions in rabbits included death in two animals, produced by Lipofundin K399, and hyperpyrexia, anorexia, decreased water intake, weight loss, and decrease in hemoglobin and hematocrit following infusion. The best performance in rabbits was obtained with Intralipid 293011 and in rats with SR-4734-107A. Although Lipofundin was well tolerated by rats, in general, soybean oil-egg yolk phosphatide-glycerol type emulsions produced the least adverse physiologic and histopathologic changes in the test animals.