Most observers who have written on the subject of infantile tetany connect the cause with a disturbance of the calcium metabolism, the greater number believing it to be due to a deficiency of calcium in the tissues. The intimate association of rickets and tetany, in the former of which there is a definite disturbance of calcium, has been sufficient to suggest to many that the same salt is probably instrumental in the causation of tetany. The favorable influence of calcium on tetany, which will be discussed subsequently, gives weight to the view that a deficiency of calcium may play a part in the production of tetany.Kassowitz 1 and his adherents have insisted that tetany is just a symptom of rickets. From extensive clinical, and a few metabolism, observations, we are inclined to regard this statement as correct. We have not yet seen a case of tetany that did not show some clinical signs of rickets. Our observations do not coincide with Howland and Marriott's to the effect that tetany is found occasionally in infants who present no signs of rickets. There is still considerable diversity of opinion regarding the thera¬ peutic employment of calcium, and not sufficient use made of the most effective remedy, cod liver oil and phosphorus. It was after a con¬ sideration of these two points, combined with the statement made by Howland and Marriott2 that calcium given by mouth has a very prompt effect in preventing all of the symptoms of active tetany, that we were prompted to undertake this investigation.From the wards and laboratories of the
In those cases in which it was possible to study the complete salt metabolism, a plan similar to that outlined in a previous paper 1 was followed. This, in brief, consisted of the careful determination of all sodium and chloride ingested and excreted during a three or four day period, following a preliminary period of three days on the same diet. Blood was withdrawn in the middle of the metabolism period. Complete balance experiments were not always possible, and in many such cases the daily excretion of chlorides and the effect of added sodium chloride on its excretion were studied. Such patients were always on "salt-free" diets consisting largely of milk at first, and later of vegetables, fruit, cereals and, later on, added protein. When figures for the intake are given in the latter cases, they represent approximate values only, obtained by computation of their amounts from tables of normal values and the measurement of the amounts ingested. Blood determinations were usually made when fasting, but in some cases this was impossible and little difference was noted when the venipuncture was nearer a meal time. METHODSBlood sodium was determined by the method of Kramer and Tisdall2 and the chlorides by that of Rappleye.3 Sodium in the food, feces and urine was determined by the standard gravimetric methods for estima¬ tion of potassium and sodium, cobalti nitrite being used instead of platinic chloride for the precipitation of potassium. The sodium values were obtained by deducting the potassium from the total. The urinary
The studies reported in this paper were undertaken in consequence of some clinical and chemical observations made by us on the condition of chronic intestinal indigestion, particularly in relation to treatment with special high protein diets.1 It seemed desirable to attempt to explain certain apparently contradictory phenomena, and if possible to formulate a rational explanation of the successful use of extremely high protein diets in overcoming this condition.The first question that comes to mind concerns the well-known characteristics of the typical feces, namely, mushy consistency, often acid reaction, suggesting abnormal fermentative activity in the intestinal tract, but accompanied almost invariably by a markedly putrefactive odor. How are the symptoms of two antagonistic forms of bacterial activity to be accounted for? That a fermentative condition prevails is supported by the abdominal distension characteristic of the condition, and by the exaggeration of symptoms when more carbohydrate is added to the diet. That putrefactive activities are also concerned seems to have been indicated by Herter's 2 findings of indolic and phenolic sub¬ stances in the urine and of aromatic oxyacids in the feces in chronic intestinal indigestion. Other questions arise in connection with the type of food used to bring about improvement. A high protein diet would naturally tend to overcome the excessive fermentation, but why at the same time does it not encourage the putrefactive processes? Further, the importance of the ingestion of large amounts of a specific organism, namely, Streptococcus lacticus (Micrococcus ovalis) in the
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