Since the publication of Cheadle's paper' in 1903, the presence of excess of fat in the foeces has attracted much notice as the most characteristic signi of the metabolic disturbainee in cceliac disease. It ha,s beein recognized that associated with this disturbance of fat absorption, there occuirs also a defective retention of minerals and an excessive loss of nitroge.n in the feeces. In consequence some attention hias been paid to the effect of varying the composition of the dietarv, especially fromi the therapeuitic standpoint. The interrelationship of the disturbanices in the absorption of the various elements of the diet is a m4atter of importance both from the practical point of view, an(d l)ecause of the possible value in the explanation of other metabolic disor(lers.Parsons2 has already indicated the importa,nce of vitanmin D in the preventioni of cceliac rickets, showing that the continued absence of this vitanmin from the fat-poor diets used in treatment is the cause of the rickets of convalescence. The series of observations detailed in this paper are published in the hope that some further light nay be throwin onl the und(lerlying chemical pathology of the cceliac state. A more complete understanding of the disorder should ultimately prove of value in the prevention and cure of the disease.Metabolic studies in eoliae disease are subject to the great disadva,ntage that sudden changes oecur in the condition of the patient although the diet is constant and the environment unaltered. Accordingly it is difficult to determine whether differences in the metabolic findings are to be attribuited to changes in food or other treatment, or to nattural aggravation or amelioration of the condition. In these investigations as unich care as possible was taken to rule out the idiopathic changes in the severity of the disease. A brief description of the salient featuires of the case-histories of the patients is appended at the end of the paper (see Appendix). It is proposed in the first place to summarize the metabolic findings with regard to the various forms of foodstuffs and thereafter to discuiss the bearing of these results on the chemical pathogenesis of coeliac disease.
Acidosis is so frequently put forward as the underlying pathological condition in such a variety of disorders that it is important to appreciate what actually are the metabolic manifestations of the acidotic state. Clinically one seldom if ever has an opportunity of studying acidosis uncomplicated by some such other factor as inanition or toxaemia. It is therefore advisable in an investigation of the metabolic reactions to a disturbance in acid-base equilibrium to have these secondary factors as far as possible excluded. This can only be done when the acidosis is induced in a healthy individual with the minimal amount of upset especially as regards food-intake, and such a condition is most nearly attained in the acidosis produced by the ingestion of ammonium chloride. Haldane' was the first to show that ammonium chloride taken in large amounts led to a marked acidosis owing to its ammonium moiety being converted to urea. Since then many papers have been published dealing with changes following the administration of this substance.The present research was undertaken primarily with the object of studying the changes in mineral metabolism during acidosis and, if possible, of correlating these changes with other metabolic phenomena. Most workers are agreed that there is an increased output of lime in the urine during acidosis. The effect on the faecal excretion of lime and the influence of the acidotic state on phosphorus metabolism have not, however, been clearly determined. Steenbock, Nelson and Hart2 have pointed out the detrimental effect of acid-forming diets on calcium retention and calcification in animals. Sawyer, Bauman and Stevens3 found an increased urinary output of calcium and phosphorus in two children during a period of high fat intake: in only one, however, was there an increase in the fwecal amounts of these substances, while in the other there was a decrease. In a study of acid and base-forming diets in adult women Bogert and Kirkpatrick4 did not obtain a constant change in the amount of feecal calcium during the period ofLcid-forming diet although the urinary lime was always increased.
In many diseases, particularly in those with a tendency to spontaneous cure, various therapeutic agents have been unjustifiably credited with possessing valuable curative properties. In perhaps no instance is this more striking than in the case of rickets, in which claims have been made for the efficacy of many different forms of treatment. Much of the misLnderstanding in the question in the case of rickets has arisen from the want of certainty in the examples tested whether the disease was in a progressive or a retrogressive stage. At the outset therefore of any investigation it is essential that we have standards by which this matter may be decided, and the present communication deals with this aspect of the problem, namely, the relative value of different methods of determining the phase of the disease. It has frequently been the custom to decide whether an individual example ot rickets were active or healing from an isolated radiological examination. We have not infrequently noted, however, that a case of rickets which has been
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