In March, 1916,1we published our first report on the treatment of hay-fever by injections of specific antigens. We analyzed the literature and our own clinical experience for results in the treatment of hayfever patients with pollen extracts alone, and with bacterial vaccines alone, and we concluded that neither method had given completely satisfactory therapeutic results. We suggested the theory that hay-fever symptoms could be explained by the conception of the disease as a combined state of hypersensitiveness to various pollens and a condition of nasal infection, or, as called by Adami,2"subinfection." There can be no doubt that each hay-fever patient represents a state of hypersensitiveness to a definite pollen, as can easily be proved by ocular or dermal tests with pollen extracts; but there are at least theoretical considerations indicating the presence of a complicating infection. Furthermore, because of the inconclusive results of pollen therapy and
These results seem definitely to show, through animal experiments, that phagocytic immunity is to a high degree specific for the organism used in immunization, and that the amount of opsonin produced in the process depends to a great extent on the virulence of the organism. The negative results obtained with post-critical sera do not mean that opsonins may not be present (our five positive cases indicate their presence), but they emphasize strongly the fact that they are not formed to any great extent. Therefore this study adds further support to the view that although opsonic immunity is produced in pneumonia, it is not the only means of defense possessed by the body, and by itself it cannot explain the crisis.
The relations between the kidney and sugar excretion form interesting chapters in the study of diabetes and of less well-known glycosurias. The general conception that the kidney is practically passive in diabetes has been disputed. In 1897 Lépine1reported the case of a woman dying in coma, whose blood contained 1.6 per cent, sugar and whose kidneys were enormous and showed a high grade of interstitial inflammation. Richter,2in 1900, in a critical review of the relation between kidney and glycosuria, concluded that renal diseases may have a favorable effect on glycosuria, and that in kidney diseases the permeability of the renal filter to sugar seemed diminished. Von Noorden3also considers that a diseased kidney shows a diminished permeability to sugar. Weiland4has shown that in cases of acute nephritis the blood-sugar level is low, and in chronic interstitial nephritis it reaches the upper limits of
While Daly and one of us1were studying the thyroid during pregnancy, we became interested in our office practice in the frequent occurrence of the clinical syndrome resembling mild hyperthyroidism without changed basal metabolic rate. Patients presenting this group of symptoms were usually seen in office practice and practically never in hospital wards. The clinical picture presented by these patients was similar to if not identical with the syndrome long known and described by various authors under the names of irritable heart, effort syndrome, neurocirculatory asthenia, autonomic imbalance and sympathicotonia.2They also closely paralleled some of the cases described by Miller3in his study of mild hyperthyroidism. Almost all the patients had goiters, for which reason we decided to use iodine therapeutically. Results more than vindicated this practice. None of the patients used in this study had shown abnormal metabolic rates. We nevertheless thought that by the
The diagnosis of renal glycosuria is based on the syndrome of (1) glycosuria without hyperglycemia, (2) glucose excretion almost entirely independent of carbohydrate intake, and (3) absence of diabetic symptoms. To these data should be added, I think, a fourth, namely, that such patients do not subsequently develop diabetes mellitus or show a disturbance of carbohydrate metabolism similar to that found in diabetes mellitus. Not many reported cases have been observed long enough to answer either of the latter two questions. Garrod's1case was observed six years, Goto's2five years. Allen, Wishart and Smith3have recently recorded three cases of renal glycosuria, and have discussed the unsatisfactory nature of this interesting anomaly. It is the purpose of this paper to place on record four cases, patients who have been under observation for from two to eight years since the onset of the disease and on two of whom late metabolic
In the first communication we showed both by quotations from the literature and by our experiments that certain obese persons maintained body weight on diets below their calculated caloric requirements.1To explain this apparent anomalous balance between caloric intake and energy expense, we made an intensive study of the specific dynamic action of foods in persons of widely varying body build. The results of this study will be published shortly. A rather large and interesting series of basal metabolism readings were accumulated during this research, and since the subject of the basal metabolism in obesity cannot be considered closed we present in this paper our data on the basal metabolism in obesity. REVIEW OF THE LITERATURE Before the development of modern methods of studying gaseous exchange and the accumulation of more accurate standards of comparison, the literature on the metabolism of obesity contains much conjecture and a few isolated studies.
II Uniformity of methods of procedure of the test for hyperglycemia after glucose ingestion has resulted in rather uniform conclusions regarding the test. Hopkins,1Hamman and Hirschman,2Janney and Isaacson,3Williams and Humphreys4showed that the normal individual usually reacted to a given dosage of glucose by a maximum rise in one-half hour and almost immediate drop after the half hour. The maximum rise rarely exceeded 0.16. Bailey5reports a normal alimentary glucose test in which the blood sugar in the whole blood was 0.172 in thirty-five minutes, 0.22 in one hour, and 0.216 in one hour and twenty-five minutes after the ingestion of 75 gm. of glucose. This type of curve is considered by most authors as distinctly abnormal, both in regard to the height which it reached and to the length of time it took before returning to normal. The diabetic curve is characterized by a rise at
The incidence of the combination of pregnancy and hyperthyroidism is very low. Javert reports 18 cases of hyperthyroidism in 23,439 pregnancies (0.076 per cent), McLaughlin and McGoogan 19 cases in 6,112 (0.3 per cent). We have been able to find reports of less than 10 cases of hyperthyroidism in pregnancy treated with thiouracil—so far without any toxic effect on either mother or child. However, since the drug has caused a number of complications, we might anticipate the probability of toxicity in a certain percentage of mothers. Experimental studies of the effect of thiourea on pregnant rats indicate the possibility of damage to the offspring, with characteristic thyroid hyperplasia and retardation of development. For these reasons we have been hesitant about employing thiouracil in cases of hyperthyroidism complicated with pregnancy, and in all cases except the 1 here reported we have followed older measures of therapy as adapted to the individual.
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