The Treatment of Hay Fever by rosin-weed, ichthyol and faradic electricity / With a discussion of the old theory of gout and the new theory of anaphylaxis

by George Frederick Laidlaw

As we rose in the animal scale, instead of being an amœba of a single cell, we became constructed of millions of tiny cells and began to set aside certain groups of cells to do special work, the eyes for seeing, the ears for hearing, the lungs for breathing, the digestive organs to prepare our food and a sheath of harder cells over the outside of the body that we call our skin and mucous membranes. Specialized as those cells have been for many generations, they have never forgotten that a foreign protein is a food or, perhaps, an enemy, to be split up and decomposed at sight. So, the epithelial cells of the mucous membrane of the nose and eyes, though they have no longer anything to do with digesting our food, secrete a ferment or enzyme that can split up any protein that may happen along. This process is called parenteral digestion or digestion outside of the intestines; and this theory of the parenteral digestion of protein is the foundation of the anaphylaxis theory of hay fever.

During the growing months of the year the air is full of pollen that is blown in everybody's eyes and nose. In that pollen is a proteid that is digested by the secretion of those mucous membranes, proceeding exactly as food is digested in the stomach and intestines, splitting up the complex proteid molecule into simpler groups, and forming both poisonous and non-poisonous substances. In the normal eyes and nose this splitting of the protein proceeds slowly, forming only minute amounts of poison. As absorption from the eyes and nose is slight, no unpleasant effects are produced.

The first step in the development of hay fever is supposed to be a disturbance in this digestion of protein in the eyes and nose, by which larger amounts of poison are formed and absorbed by the mucous membrane, producing the first poisoning, which, like the first injection into the dog, sensitizes the mucous membrane to other doses of the same poison. It is supposed that disturbance in the protein digestion may be caused by stoppage of the nasal passages, with excessive accumulation of proteid, inhalation of excessive amounts of pollen, forming excessive amounts of poison, or, perhaps, insufficient secretion, so that the splitting-up process is not hastened to its conclusion of harmless products. The anaphylaxis theory halts a little at this point and is not exactly clear about the mechanism of that first poisoning.

After the first poisoning, the epithelia are permanently injured and remain more permeable to protein. They also develop the power of making large amounts of the digesting enzyme, which is absorbed into the blood and is supplied to all the tissues of the body, so that all tissues, including the skin, can decompose the pollen protein. Advantage is taken of this distribution of the protective enzyme in the skin reaction, in which a small area of skin denuded of its superficial epithelia reacts in the form of a hive-like swelling when the pollen that originally affected the patient is brought in contact with it.

The next time that the pollen reaches the eyes and nose the mucous membrane is ready for it with an abundant secretion of enzymes to destroy it. In this intense digestion of the proteid, quantities of the poisonous substances are formed which irritate the eyes and nose worse than before, explaining why hay fever becomes worse with successive attacks.

The inherited form of hay fever is explained by the well-known transmission of anaphylaxis to the offspring. The first case in the line of descent must start with a severe poisoning that lays the foundation of the anaphylactic inheritance.

I would submit to the enthusiastic immunologist that this first sensitization which he takes for granted but cannot prove is the weak spot in his hypothesis. This is the point where he needs help, and it is at just this point that de Mussy's neglected theory of gout completes the picture. The immunologist has not explained why I, a boy growing up with other boys, inhaling the same amounts of pollen as they, catching no more colds than they, and never having any serious illness, became sensitive to pollen while the others did not. There is no recollection of any "first poisoning" by pollen that might have started the anaphylaxis. But, says the immunologist, it was your parents who were sensitized and you inherited the anaphylaxis. Now, my parents lived to old age and had no sign of hay fever, though my brother had it and my children are beginning to sneeze and rub their eyes suspiciously in June and August. But if you associate hay fever with the gouty diathesis, as the clinical histories seem to justify, you enlarge immensely your opportunity to prove ancestral sensitization to whatever unknown poison originally produced the gouty sensitization. This view does not restrict you to ancestral hay fever, but extends it to gout or to any equivalent of gout.

The best work in English on hay fever as an anaphylaxis is the monograph of Karl K. Koessler in Forchheimer's Therapeusis of Internal Disease, 1914, Volume 5, page 671, to which the reader is referred for a full discussion of the subject. The same author gives an abstract of his work in the Illinois Medical Journal, 1914, page 120. This article in Forchheimer is the most complete that has been written since Sticker's time and covers the ground from Sticker, who knew not anaphylaxis, to Wolff-Eisner, who is not available in English.

I was gratified to find in Koessler a sympathetic soul. He thinks, as I did, that the monograph of Sticker in Nothnagel is the best review of hay fever that we have. He calls it "a remarkable monograph and the standard work on the subject." But why, oh why, K. K. K., in your own masterly article in Forchheimer, did you follow Sticker all through his historical chapter but leave out all that he says of de Mussy's theory of gout or arthritism as the constitutional basis of hay fever and also leave de Mussy and every reference to his work out of your list of Literature? The German books are more liberal. While most of them ignore de Mussy and his theory in their text, they all list his writings in the Literatur. Has the microbe of bacteriology and the laboratory bitten you so virulently that you can find no place for the gouty diathesis even in an index?

I know that the gouty diathesis is out of date. In fact, all diatheses are out of fashion. Nobody speaks of them now. They went out with the medical philosophies of the eighteenth century. Cellular pathology with its wonderful revelation of the anatomical seat of disease and bacteriology, with its still more wonderful revelation of the external cause of disease, so dazzled the eye and the mind that we forgot that the sensitive animal body behind the attacking microbe had its changes, too, its changes in body chemistry that could not be stated in terms of cells and bacteria. The pendulum is swinging back now to a consideration of the constitution of the body on which the microbe or poison acts, its resistance or immunity, its anaphylaxis or allergie. With these holiday and lady terms, are we not trying to describe what our ancestors knew as diathesis? For what is the old conception of diathesis but just such a hereditary weakness or lack of defense or tendency to disease that our ancestors recognized clinically but could not demonstrate, elusive, difficult to detect, but nevertheless there; like the dog who has been sensitized to an otherwise harmless proteid, who seems well and is well in everything except his susceptibility to that one special cause of disease?