So we have a picture of anaphylaxis as a sensitiveness to bacterial poisons or to foods or drugs that are harmless to most people expressing itself as an urticaria, an arthritis, an asthma or hay fever. But this is the very group of symptoms on which de Mussy based his theory of gout. When we add that this sensitiveness or anaphylaxis is hereditary and that it is aggravated by foods, drugs, or pollens that are harmless to most people, I submit that we have a pretty picture of the gouty diathesis; for the gouty diathesis, too, is a susceptibility to arthritis, to urticaria, and to asthma from causes that do not trouble other people, and in gout, too, this weakness is hereditary. One thinks of the gouty patient who cannot take iron or digitalis because it aggravates the gouty pain and of the attack of gout that is brought on by a glass of champagne or a piece of beef or a few strawberries that the majority of mankind can take freely without harm. Now, if urticaria, eczema, arthritis, asthma and hay fever form a picture of anaphylaxis, and if these symptoms also form the picture of the gouty diathesis, is it not probable that one of these pictures can be explained in the terms of the other? If the anaphylaxis to the diphtheria antitoxin, horse serum, can develop arthritis, is it not probable that the most striking feature of gout, the inflammation of the joint, is also an anaphylaxis to poisons yet unknown to us but the same poisons that make the gouty urticaria and asthma? What if gout should prove to be a sensitization or anaphylaxis to uric acid that does not exist in the non-gouty? This would explain the puzzle of one patient full of gouty pains with very little uric acid in his blood while another patient, like the leukæmic, has a blood full of uric acid that does not trouble him. =The Mechanism of Anaphylaxis in Hay Fever.= The anaphylaxis theory of hay fever is based on the observation that the epithelial cells of the mucous membranes of the eyes, nose, and throat have not lost their primitive power of digesting foreign protein.