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JAMA. 1895;XXV(12):503-504. doi:10.1001/jama.1895.02430380033004.
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Among the morbid entities whose pathogeny is still obscure, the disease first described by the English clinician Addison, in 1855, and since known by his name is not the least interesting. Characterized by marked emaciation, asthenia, toxemic symptoms, vomiting, diarrhea, bradycardia, etc.,—and, generally, by melanoderma or bronzing of the skin, its exact causation is still unknown, but the coöperation of physiologic chemistry and clinical and experimental pathology has furnished clews which lead us to believe that the solution of the problem is near at hand.

The theories to account for the origin of the disease may be divided into three groups—the capsular, nervous and toxic. The capsular theory, which was advanced by Addison, accounts for the disease by the degenerative changes in the suprarenal capsules. Shortly after the appearance of Addison's work, Brown-Séquard undertook a series of experimental researches which may be summed up as follows:1 1, the suprarenal capsules


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