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tion of the percomorph liver oil dosage the pruritus subsided within a few days. Bone tenderness, irritability and weakness disappeared rapidly, and within a month recovery was apparently complete. Roentgenographic examination of the long bones on May 28, 1949, revealed that both ulnas were normal. COMMENT In reviewing the cases reported previously it is noteworthy that the correct diagnosis was usually made in retrospect after additional history was obtained (perhaps with difficulty) from Periosteal elevation and thickening along the shafts of both ulnas. the parents. This point was emphasized by Dr. J. M. Lewis,6 who related the difficulty he experienced in getting a mother to admit the administration of large doses of vitamin A to her baby. However, with the persistent extremely high vitamin A concentrations in the plasma (600 U. S. P. units per cubic centimeter) as well as roentgenographic changes in the long bones, he was convinced of the likelihood of hypervitaminosis A and finally obtained admission that the infant had received 1 to 2 teaspoons (5 to 10 cc.) of vitamin A and D concentrate for several months.The members of the medical profession have long been concerned with the diseases resulting from insufficient vitamin intake. Recently we have appreciated the serious dangers of overdosage with vitamin D. We are now seeing cases of disturbed physiologic conditions following excessive dosage of vitamin A. Fortunately, recovery has been prompt and apparently complete on the withdrawal of the vitamin. In experimental animals lethal doses of vitamin A have been administered.In man the possibility of permanent hepatic damage must at least be considered.Administration of large doses of vitamin A may be well tolerated for long periods of time. When it is ingested in large quantities it is rapidly removed from the blood and stored in the liver, maintaining normal blood levels. Hypervitaminosis A has not been produced in controlled cases of excessive vitamin A administration over a period of several months. This observation led Josephs 1 to suggest that in patients in whom clinical hypervitaminosis A develops there may be either an intrinsic alteration in the regulatory mechanism of vitamin A storage and metabolism or an alteration that is a consequence of vitamin A overdosage. Others have suggested that clinical hypervitaminosis A develops only after the liver is loaded with the vitamin so that it is no longer able to remove from the circulation 7 the excessive amount ingested.The etiologic basis of the clinical observations in hypervitaminosis A is still obscure. The skin and hair changes in man and experimental animals are suggestive of vitamin A deficiency. Josephs1 suggests that the elevated phosphatase level, which is probably responsible for the bone changes, may be secondary to hepatic damage produced by overdosage with the vitamin. SUMMARY A case of probable hypervitaminosis A has been reported. The clinical observations followed remarkably those described previously in 4 patients by Josephs, Toomey a...

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