JAMA. 1925;84(10):753. doi:10.1001/jama.1925.02660360035015.
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The theories of the pathogenesis of the type of chronic polyuria familiarly known as diabetes insipidus have proved to be singularly elusive. There is evidence of long standing character that experimental injury to different parts of the brain may be followed by an increased urinary output, usually of a transitory nature. Presently it was observed that experimental procedures on and about the hypophysis cerebri are frequently followed by excessive thirst and polyuria. This seemingly close relationship between the pituitary structures and diabetes insipidus has been accentuated by the independent discoveries that extracts of the posterior lobe may have a somewhat transient diuretic effect, and that therapeutically the administration of the extracts of the posterior lobe are effective in controlling the secretion of urine in cases of diabetes insipidus or in the experimental polyurias caused by operations on the hypophysis.1 Furthermore, in some instances of diabetes insipidus, lesions have been


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