Histologic Changes in Livers of Pyridoxine-Deprived Baboons-Relation to Alpha1 Fetoprotein and Liver Cancer in Africa

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Abstract
Liver histology was described in 10 baboons intermittently fed a balanced artificial diet lacking only pyridoxine for 2–6 years. Half developed increased amounts of alpha, fetoprotein (AFP) in their sera and had multiple atypical hyperplastic nodules regarded in some as neoplastic or premalignant. The animals had megalocytosis and anisocytosis, multinucleosis, abnormal mitoses, liver cell plates more than 2 cells thick, and sheets of bile ductule cells. All these features combined suggested neoplasia. These striking changes occurred in animals that had received no carcinogenic substance, but were only deprived of pyridoxine. Five other baboons totally deprived of pyridoxine died within 6–8 months, with rapidly developing hepatocellular injury. None had atypical hyperplastic nodules, abnormal liver cell plates, increased bile ductule cells, or AFP, and there were no signs of tumors, probably because they died too soon. In 15 other baboons given aflatoxin Bh the liver chang,s were not as severe as those seen in the animals given the pyridoxinedeprived diet alone, and they had no atypical hyperplastic nodules, thickened liver cell plates, or AFP. In all animals deprived of pyridoxine, the serum B6 levels fell from a normal range of 200–350 ngjml to 5–15 ng/ml; increased tryptophan metabolites appeared in the urine. Pyridoxine deficiency or its antagonists may be associated with upsets in immunologic competence, as in other states of malnutrition.

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