Studies of the chemical exchanges in scurvy have been surprisingly few. It is a field that should repay investigation, promising to afford a clearer insight into the intermediary metabolism in this disorder. One of the first to touch upon this question was Garrod, who in 1848 reported that there was a diminution of potassium salts in the urine and in the blood of scurvy patients. In 1877 Ralfe confirmed the potassium deficiency in the urine, but denied its importance from an etiologic standpoint, as he was unable to benefit scurvy patients by administering potassium nitrate. He reported an increase of uric acid in the urine, a diminution of the total acidity, and a reduction of the alkaline phosphates. Litten found the analyses of the urine very contradictory in respect to potassium, but stated that beyond a doubt its uric acid content is increased at the height of the disease, although this diminishes rapidly with convalescence. These few and scattered articles comprise the sum of metabolic studies up to the last decade, and even during the succeeding period they have been very few--so few, indeed, that they furnish insufficient data from which to draw conclusions. The first careful study of the mineral metabolism in a case of scurvy is that of Baumann and Howard, published in 1912. Its conclusions are not very definite. They may be summed up by their statement that "chlorin and sodium were retained during the fruit-juice period, but excreted in excess of the intake during the preliminary period," and that "more potassium, calcium and magnesium were retained during the fruit-juice period."