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Paul D. Garvin, M.D.; Gerald M. Frumess, M.D.
JAMA. 1935;104(26):2333-2334. doi:10.1001/jama.1935.92760260001008.
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During the last few years extensive studies have been made on the circulating antibody (atopic reagin) usually present in atopy, as well as the reaction of the sensitized tissue when brought in contact with the atopen.

The discovery by Prausnitz and Küstner1 in 1921 that the normal skin can be passively sensitized by the intradermal injection of serum containing atopic reagin has been utilized for the diagnosis of atopic conditions. Walzer2 in 1926 demonstrated that the passive transfer site often reacts in the characteristic manner when the specific atopen is ingested orally instead of injected into the sensitized area.

The histologic picture of the allergic wheal has recently been studied by Kline and his associates.3 They find that the essential picture is an inflammation of the dermis and subcutaneous tissue, with edema, vascular engorgement and leukocytosis. At first the eosinophilic leukocytes predominate (first hour), but later the polymorphonuclear neutrophilic and


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