Although, in the prolonged lipidic stage, a certain specificity for particular antigens can be recognized, the antiheterogeneous response in general represents rather a nonspecific effort of the organism to resolve the problems caused by the presence of any heterogeneous factors as such.

Before going further, we want to emphasize some important characteristics of this antiheterogeneous response related to organization. The catabolic processes present in the first phase appear to result in part from the direct hydrolytic process and in part from the biological intervention of the products of hydrolysis, especially fatty acids. The hydrolytic enzymatic process is homotropic in nature by definition, as it breaks down different constituents, liberating groups with anionic and cationic character.

Enhancing the catabolic character of the first phase processes are the anionic groups which appear to have a predominant role. The second phase, a reparative one, is anabolic and therefore, heterotropic in character.

The study of the antiheterogeneous response emphasizes another fundamental characteristic of the processes. A basic difference exists between the direct effects induced by the intervening agent and those resulting from the defense processes themselves. A direct effect of a noxious intervention corresponds to heterogenization of the constituents. Some changes will appear through this heterogenization itself, others through the defense processes which represent the response of the organism to the heterogenization. While the first corresponds to a direct action, the last is catalogued as antigenic, its manifestations being grouped as defense processes. The same substance can have a direct action and an antigenic one revealed principally through the manifestations which it induces. A direct action can be noted instantaneously if the changes induced are sufficiently intensive. The antigen effects always require a certain time before manifestations appear. This time can range from a few minutes for the first enzymatic response to hours or days for the prolonged response.

An important feature of the prolonged stage is that it persists as long as the noxious agent is present. This is evident in cases in which the noxious agent can be suppressed through external intervention. For example, with suppression of microbial activity by antibiotics, the corresponding clinical condition disappears. Of more interest is the effect of antimicrobial and antitoxic immune sera. Administration of a specific serum, if it can neutralize the noxious agent, produces a curative effect at this stage. In a short time, symptoms disappear and the organism reverts to normal. Although nonspecific, the prolonged antiheterogeneous reaction shows such a straight correlation with the presence of the antigen as to make us designate this stage as primary or toxic. In this stage, the organism reacts with clinical manifestations of disease if the antigen is capable of inducing sufficient noxious changes; if not, there are no clinical manifestations. Persistence in the organism of an antigen beyond the rapid diphasic phenomenon indicates, in general, an incapacity of the organism to achieve its disposal successfully. The need for more complex means to combat the antigen becomes imperative.

With or without clinical manifestations—that is, even without a primary toxic stage of the disease—as long as the antigen has not been fully neutralized, the organism will still try to resolve its intervention and return to normal, resorting to other means. It will produce antibodies with a certain degree of specificity toward the antigen. Two kinds of antibodies will be manufactured and will differ in their fundamental characteristics, the time of their appearance, and their role in the defense processes.