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The search for the etiology of the various forms of osteochondritis has led some authors to believe that rickets is a causative factor. Clinical and roentgenologic studies,1 however, have failed to substantiate this assumption. A review of the literature shows that the few desultory studies on the inorganic blood chemistry, based on a limited number of cases, have given conflicting results.Seldowitz and Zimtbaum2 concluded that their study of the inorganic composition of the blood, that the efficacy of antirachitic therapy in their single case of Koehler's disease of the tarsal scaphoid and that the histologic evidence of osteoid tissue and irregular calcification gleaned from the literature pointed toward the rachitic nature of the disease. Durham and Outland,3 in a study of six cases of Perthes' disease and one case each of apophysitis of the os calcis and of Osgood-Schlatter's disease, concluded: (1) that Perthes' disease is

Since the presentation of a case of nephritis associated with rachitic changes in the long bones by Lucas1 in 1883, the subject of renal rickets has been widely discussed in English and American literature. Its pathology and chemical physiology, as well as the various etiologic factors involved, have been carefully considered by Parsons,2 Mitchell,3 Schoenthal and Burpee,4 Hamperl and Wallis,5 Shelling and Remsen6 and others. In brief, this disturbance is characterized by chronic renal disease, dwarfism, hyperphosphatemia, azotemia, changes in the skeleton simulating those in infantile rickets, chronic acidosis and, finally, uremia and death.Of late, several cases have been reported in which the clinical and roentgenologic findings simulated those of renal rickets, except for the absence of azotemia and the presence of hypophosphatemia instead of the usual hyperphosphatemia. De Toni7 presented an unusual case of rickets associated with albuminuria, glycosuria, hypophosphatemia and

The ions of calcium, magnesium, potassium, and sodium may be involved singly or in combination in the alteration of neuromuscular irritability in infants and children. Of these the role of magnesium in the neonatal period has received the least attention.Although hypocalcemia is generally considered the most important factor responsible for initiating tetany, the level of other cations may under certain conditions influence the production of tetanic manifestations. It has been demonstrated by several investigators that for normal neuromuscular activity a certain ratio of the concentrations of serum potassium and calcium should exist. Harrison et al1,2 reported that when their patients with sprue had hypokalemia they showed none of the manifestations of tetany even though hypocalcemia was present. Engle et al3 demonstrated that administration of potassium salts to asymptomatic hypocalcemic and hypokalemic patients may induce active tetany. Harbaugh and Dennis4,5 noted, in their studies in cattle with

We have used the constant volume apparatus of Van Slyke and Neill in the estimation of potassium in solutions whose inorganic composition approximates that of serum. The potassium is precipitated as the potassium-sodium cobalti-nitrite compound, essentially as in the original method of Kramer and Tisdall.1The precipitate is decomposed with sodium hydroxide as suggested by Clausen,2∗and the nitrogen of the sodium and potassium nitrite is liberated by adding a solution of urea and sulphuric acid.3†The amount of nitrogen is then determined in the constant volume apparatus. It is possible to determine from 0.07 to 0.45 mg. potassium, with an error not exceeding 0.01 mg.One cc. of the potassium solution is measured into a 15 cc. graduated centrifuge tube, containing 1 cc. of water. One cc. of the sodium-cobalti-nitrite reagent is added slowly, drop by drop, and the solution thoroughly mixed after each drop. At the end of 45 minutes, the volume is made up to 5 cc. with water and the contents mixed again and centrifuged for one-half hour at a speed of about 1800 revolutions per minute.All but 0.3 cc. of the supernatant fluid is pipetted off so as not to disturb the precipitate. Five cc. of water are allowed to run in slowly. The stream is controlled in such a way that the added water is thoroughly mixed with the residual reagent and the precipitate is not disturbed. The procedure is repeated twice, making three washings in all. In the third washing, the water is added in such a way as to gently agitate the upper portion of the precipitate. The tube is centrifuged for 5 minutes.

TO THE EDITOR:— A scientific fact is unaltered by the question of its parenthood, but for the sake of historical accuracy we wish to call your attention to what appears to us to be an accidental oversight by two of your contributors. Drs. C. L. Spingarn and S. H. Geist in The Journal of Dec. 30, 1939, gave an able discussion of the effect of hyperparathyroidism in the mother on the developing embryo. They state that Bakwin (Tetany in Newborn Infants, J. Pediat.14:1 [Jan.] 1939) called attention to the existence of hypoparathyroidism in the newborn. Permit us to say that three years before the appearance of Bakwin's publication we established by means of chemical and metabolic studies the existence of hypoparathyroidism in a 7 weeks old infant (Infantile Tetany, Am. J. Dis. Child.51:816 [April] 1936). We wish to repeat that, while the question of priority may not be important, the added evidence which we presented to favor the thesis of Drs. Spingarn and Geist is of sufficient importance to merit your attention.