EVER since Verzar (1) suggested the possibility of adrenocortical hypofunction as an etiologic factor in celiac disease of children and adults, many investigators have speculated about a similar possibility for sprue. Investigation of this theory has not been undertaken until now in our institution because all efforts have been concentrated on the therapeutic angle. The only pertinent information we could find was a personal statement by Koppisch who, in a review of 1,400 consecutive autopsies, found 17 cases of sprue. The duration of the disease could not be ascertained in 5 cases. In the others it varied from four months to five years. Histologic sections were available from 13 of these cases, alterations being found in all but one, which was normal. The periadrenal fat showed serous atrophy, generally advanced. The cortical lipoids had undergone depletion and the zona glomerulosa and fasciculata were atrophic. This condition was most marked in the superficial portions of the cortex, where the cords of cells were usually very narrow. The interstitial tissue of the atrophied parts was broadened by edema. In the case with the most advanced atrophy there was actual loss of portions of the cords of cells, which had been replaced by very loose and edematous areolar tissue. These alterations were not specific, since they resembled those found in other cases of cachexia.