January 17, 1931


JAMA. 1931;96(3):196-197. doi:10.1001/jama.1931.02720290040013

Clinical phenomena are interpreted in terms of the physiologic and biochemical knowledge of the time, so that with the growth of basic knowledge earlier interpretations may become obsolete. A slight change in the sequence with which clinical discoveries are made may conceivably result in establishing different forms of therapy. In no field is this better illustrated than in the field of hereditary and acquired protein sensitivity.

The observation that animals can be sensitized to specific foreign proteins was made by bacteriologists and was quite naturally interpreted in terms of their theory of infection. They postulated that protein sensitivity is an immunologic phenomenon, a specific lowering of normal bodily defense, and embodied this hypothesis in the term "anaphylaxis" (ana, without; phylaxis, protection). The logical therapy, therefore, was protein immunization. However, many paradoxes and inconsistencies were soon reported, such as protein sensitivity in demonstrably immune animals ("Theobald Smith phenomenon"), necrotizing local anaphylaxis

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