IIYPERSENSITIVENESS, PROTEIN INTOXICATION 221 



slight albuminuria and cylindruria and occasionally with an impairment 

 of the excretion of phenolsulphonephthalein by the kidneys. In the 

 patients who presented edema with gain in weight during the serum sick- 

 ness, the plasma chlorids were below normal. There was no noticeable 

 retention of nitrogenous products in the blood of these patients as estimated 

 by the non-protein nitrogen of the blood and by the blood urea. No ac- 

 curate observations have been made upon the nitrogen balance in the 

 period of serum sickness, and it is, therefore, impossible to determine 

 whether the same loss of nitrogen occurs in the human being during this 

 period as has been described in animals following shock, nor have careful 

 studies been made of the alterations in the serum ferments. Therefore, 

 the field of protein metabolism in this disease is practically unexplored. 



The few observations upon the coagulation of the blood would indicate 

 that, even in patients who develop a purpuric eruption during the course 

 of serum disease, the normal factors concerned in the coagulation of the 

 blood are not disturbed. The resistance of the capillaries of the skin 

 to injury or increased intravascular tension, however, may be diminished 

 in patients who develop purpura during the course of the illness. 



Much discussion has arisen as to the exact mechanism by which serum 

 disease is brought about. As was originally shown by von Pirquet and 

 Schick, and has been demonstrated by Hamburger and Moro, Weil, C. 

 Wells, and Francione, specific precipitins for horse serum occur in the 

 circulating blood of the patient during or following the serum illness. It 

 was at first believed that the appearance in the circulation of these pre- 

 cipitins and their subsequent union with the antigen in this situation were 

 responsible for the disease, but later observations have not upheld this 

 view and the observations of Longcope and Rackemann, Weil, and Mac- 

 kenzie and Leake would indicate that the appearance of circulating pre- 

 cipitins as well as other antibodies such as the anaphylactic antibody are 

 the result rather than the cause of serum disease and act in the capacity of 

 a protective mechanism to rid the body of antigen and thus bring about 

 a spontaneous cure of the disease. It has further been shown by Mac- 

 kenzie and Leake, that in the small group of patients who are insusceptible 

 to serum disease, even when large amounts of foreign serum are given, 

 that these antibodies are not demonstrable in the circulating blood, or 

 appear in slight concentration and that the antigen or horse serum con- 

 tinues to* circulate as an innocuous substance for weeks or months. They 

 suggest that the person susceptible to serum disease possesses some 

 mechanism which prevents the union of antigen (horse serum) with the 

 body cells, but the exact explanation of this mechanism is as yet lacking. 



Though many factors concerning the development and the recovery 

 from serum sickness are still very obscure, the study of this disease has 

 been aided by the fact that fairly well defined, though complicated pro- 

 tein substances have been introduced in known quantities into the cir- 



