Type I: Acute allergic reaction (anaphylactic type)
Type II: Cytotoxic type
Type III: Immune complex reaction
Type IV: Delayed reaction mediated by cells
The classification by pathomechanisms systematizes the multitude of allergic diseases. It has been applied for more than three decades and has proven scientifically instructive:
Type I—acute allergic reaction (anaphylactic type): IgE-mediated degranulation of mast cells and consequent release of mediators. The classical allergy symptoms such as hay fever, urticaria, Quincke's edema, allergic asthma, etc. (Fig. 5.2) fall into this category.
Type Il—cytotoxic type: Antibodies, directed toward antigens on the surface of specific cells, cause cell destruction. This category includes blood type incompatibilities, hemolytic anemia, allergic agranulocytosis or thrombocytopenia, etc.
Type Ill—immune complex reaction: Circulating immune complexes activate the complement system as well as neutrophilic granulocytes and thrombocytes. An immediate reaction leads to “immune complex anaphylaxis,” a delayed reaction to “serum sickness,” and similar types of reactions.
Type IV—reaction mediated by cells: This group contains immune reactions that are mediated by sensitized T-lymphocytes. Among these allergies are contact eczema and a number of drug eruptions.
(Recently two more types have been suggested: Type V, certain granulomatous reactions, for example after injections; Type VI, “stimulatory hypersensitivity”, for example as seen in autoimmune diseases of the thyroid. Both types may only be relevant for the highly specialized clinical field.)
Fig. 5.2 Immunological mechanism of a Type I allergy (according to Roitt, Brostoff, and Male: Kurzes Lehrbuch der Immunologie (Short Treatise of Immunology), 1987.
Type I reactions are by far the most important for the medical practitioner. Separated into two big groups, they are discussed in the following chapters.
Over the course of the last few years, we have gained many new perspectives regarding the subject of allergies. Consequently, we now know that the type and frequency of contact with the allergen, in the case of Type I allergies, plays a more significant role than previously assumed. That is why we distinguish between acute, more or less episodic and superficially occurring allergies, and chronic allergy forms that profoundly affect the body for extended periods of time. This has proven to be practical and didactically fruitful.
Acute allergies are the domain of clinical allergology. They can usually be diagnosed by means of traditional testing methods. Their interrelations can be seen clearly.
Acute allergies are understood to be allergic reactions to substances to which sensitization has occurred. The body is only occasionally or temporarily exposed to those substances.
Among the acute allergies are most of the inhalation allergies such as pollinosis and allergy to animal epithelia, chemicals, fragrances etc. Also contained in this group are acute reactions to the ingestion of allergens (e.g., macular, papular, urticarial exanthema and edemic reactions after ingesting strawberries, peaches, pharmaceuticals). Figure 5.3 shows a typical example from the medical practice. In the second part of the book we will discuss the individual clinical symptomatology in more detail.
Fig. 5.3 Example demonstrating acute drug eruption: Acute occurrence of symmetrical, urticarial exanthema after ingesting Ospen syrup. Primarily affected are the extremities.
We are no longer talking about acute reactions to certain allergens, but about the long-term effects of allergies to substances that the body is more or less continuously exposed to.
People with a genetic predisposition often develop chronic allergies in their early childhood. They are caused by sensitization to a staple food that is frequently ingested (usually daily), or by a substance continuously present in the body (e.g., candida in the case of chronic intestinal mycosis, mercury in people with amalgam fillings).
Frequent or continuous contact with the allergen masks the allergy. An immediate connection between symptoms and allergen is often indiscernible.
Cow's milk is usually the first foreign protein a baby, in our culture, will be exposed to. (All industrially manufactured baby food, with the exception of special diet foods, is made with cow's milk.)
Wheat is second. As flour, semolina, flakes, etc., it is also an ingredient in many baby foods. By the second year of life it has become a substance that is ingested daily in the form of bread, pastries, pasta, etc.
Due to primarily positive test results, chicken eggs are often accused of being an allergy-provoking antigen. In our experience they are responsible for triggering central allergies only in exceptional cases. The informative statistics by Gerrard, Hattewig and co-workers were previously mentioned. They confirm our observations that many people have built up specific antibodies to chicken egg protein (resulting in positive tests), though only a small number display actual relevant allergic symptoms.
Interestingly, meat— of whatever kind—does not play a role as a central allergen. Mackarness, one of the few physicians in the US recognizing and accepting these correlations, believes that human beings were initially designed to be meat eaters and were accustomed to a diet of primarily fatty meats for hundreds of thousand of years. His “stone-age diet” produced sometimes surprising results with chronic food allergies.
Regardless of whether human beings were originally meat eaters or not, which is still periodically the subject of debate, it seems important to note that today cow's milk and wheat are by far the most important triggers for central allergies. They are virtually the only foods that we have all ingested daily since early childhood. Accordingly, the reactions they cause occur frequently although they are usually not easily recognizable as milk or wheat allergies.
It is one phenomenon of our present times that scientific medicine still ignores the actual interrelations despite tremendous investment into major and extensive research for neurodermatitis, colitis, etc. Doubtlessly, the main reason for this is the unreliability of traditional test methods with regards to food allergies. A negative test result seems to be enough to prohibit any further deliberations as to whether or not it might be an allergy.
Why are the interrelations so difficult to recognize in the case of chronic allergies? The one term central to this issue is masking.
The American physician, Herbert Rinkel recognized this phenomenon and, very fittingly, coined this term after having dramatically experienced it himself. One of his students, Richard MacKarness, tellingly describes Rinkel's experiences in his book Allergie gegen Nahrungsmittel und Chemikalien (Allergies to Foods and Chemicals) (1986).
As a medical student, Rinkel had little money. Over the course of several years, his main diet consisted of eggs, which his father, a Kansas farmer, sent him in large quantities to help save money. Rinkel became increasingly unwell. He developed an unusually heavy nasal catarrh with unbelievable